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y4 paediatrics > Surgery > Flashcards

Surgery Flashcards

1
Q

How might peritonitis present?

A

Abdominal pain - widespread at start, may be localised depending on cause
vomiting and nausea
infection symptoms

guarding, rebound tenderness, rigid abdomen, mass

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2
Q

How might you investigate suspected peritonitis?

A
  • urine - Urinalysis and microscopy if indicated, pregnancy test
  • blood - FBC, U&E and creatinine, amylase, glucose, sickle cell status if indicated. Arterial blood gas, LFT. Bone profile (Ca and PO 4 )
  • CXR - pneumoperitoneum
  • AXR - dilated bowel
  • USS - (Pyloric stenosis, intussusception, ovarian pathology)
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3
Q

How might peritonitis be treated?

A
  • abx - cephalosporin
  • surgical washout
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4
Q

What is the pathophysiology of appendicitis?

A

inflammationof theappendix which is a small, thin tube sprouting from thecaecum which becomes inflamed due to infection trapped in the appendix by obstruction - usually by a faecolith or lymphoid hyperplasia

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5
Q

What features in the history may suggest appendicitis?

A

central abdominal pain which later radiates to the right iliac fossa
low-grade pyrexia
minimal vomiting
anorexia

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6
Q

What examination findings would you expect in acute appendicitis?

A
  • tenderness in Mcburney’s point which is a localised area 1/3 distance from ASIS to umbilicus
  • Rovsing’s sign
  • rebound tenderness and percussion tenderness which suggest rupturing of appendix
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7
Q

What are some complications in appendicitis?

A
  • inflammation -> gangrene -> rupture -> peritonitis
  • appendicular mass
  • surgical complications
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8
Q

What differentials must you keep in mind when considering appendicitis?

A
  • ectopic pregnancy
  • ovarian cysts
  • Meckel’s diverticulum
  • mesenteric adenitis
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9
Q

What investigations would you carry out in suspected appendicitis?

A
  • clinical presentation usually
  • CRP raised
  • CT scan
  • USS to exclude ovarian and gynaecological pathology
  • if investigations negative diagnostic laparoscopy
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10
Q

How would you manage appendicitis?

A

laparoscopic appendicectomy with prophylactic abx
- abdominal lavage if perforated
- if abscess suspected IV abx first then surgery 4-6w later

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11
Q

What is biliary atresia?

A

congenital condition where section of bile duct is narrowed or absent resulting in cholestasis where bile cannot be transported from liver to the bowel

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12
Q

What is the classical history of biliary atresia?

A

*presents shortly after birth with significant jaundice, persistent jaundice (>2w)
- white to light yellow stool
- dark urine
- growth and appetite disturbances
*may be healthy babies with pale stool and dark urine

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13
Q

What are some examination findings in biliary atresia?

A
  • jaundice
  • hepatosplenomegaly
    abnormal growth
    cardiac murmurs - if associated syndromes
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14
Q

What are some associated complications with biliary atresia?

A
  • Unsuccessful anastomosis formation
  • Progressive liver disease
  • Cirrhosis with eventual hepatocellular carcinoma
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15
Q

How is biliary atresia investigated?

A
  • levels of conjugated > unconjugated bilirubin
  • serum alpha-1-antitrypsin
  • USS biliary tree and GB
  • percutaneous liver biopsy
  • LFT
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16
Q

What procedure if carried out to treat biliary atresia?

A

Kasai portoenterostomy - EARLY
*attaching section of small intestine to opening of liver, where bile duct normally attaches

done early as over 100 days may cause permanent liver damage - transplant before 12m may be needed

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17
Q

What is the pathophysiology of Hirschsprung’s disease?

A

congenital condition where nerve cells of myenteric plexus are absent in distal bowel and rectum - absence of parasympathetic ganglion cells hence doesn’t relax hence with lack of this stimulation bowel looses motility and cannot pass food along its length

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18
Q

What does the pathophysiology of Hirschsprung’s mean for the neonate?

A

tonic state of bowel means bowel obstruction
which may lead to enterocolitis, perforation, sepsis and even death

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19
Q

How does hirschsprung’s present?

A

*within 2 days
failure to pass meconium, abdominal distension, bilious vomiting

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20
Q

How would you examine a patient with suspected hirschsprung’s?

A

Abdominal examination: grossly distended abdomen, faecal mass in the left lower quadrant, tympanic percussion note

Digital rectal examination: increased anal sphincter tone, empty rectal vault, withdrawal of the examining finger leads to a gush of liquid stool and flatus known as the “blast sign” due to dramatic rectal decompression

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21
Q

What is a complications of Hirschsprung’s?

A

Hirschsprung-associated enterocolitis
- inflammation and obstruction of intestine caused by overgrowth of c.diff, s.aureus

  • 3D Dysmotility, Dysbiosis of the gut microbiome, Defective intestinal barrier function and mucosal immune response
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22
Q

How does Hirschsprung-associated enterocolitis present?

A

fever, abdominal distention, foul smelling diarrhoea often with blood, sepsis

*life-threatening as toxic megacolon and perforation risk

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23
Q

How might you investigate Hirschsprung’s?

A

rectal biopsy with acetylcholinesterase (AChE) staining - Absence of colonic ganglion cells
OR suction rectal biopsy
abdominal XR - intestinal obstruction and demonstrating HAEC

FBC, sepsis screen, electrolytes, TFT, ABG

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24
Q

How is hirschsprung’s managed?

A

intravenous broad-spectrum antibiotics (e.g. metronidazole), fluid resuscitation, routine colonic irrigation, nasogastric/orogastric bowel decompression and making the patient nil-by-mouth for complete bowel rest

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25
Q

What is the definitive management for Hirschsprung’s?

A

surgical removal of the aganglionic segment, followed by a pull-through of the proximal healthy bowel down to the anal canal with preservation of sphincter function
+ washout to prevent HAEC

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26
Q

What are some pads causes of intestinal obstruction?

A

meconium ileus
hirschsprung’s
oesophageal atresia
duodenal atresia
intussusception
imperforate anus
malrotation
strangulated hernia

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27
Q

How might intestinal obstruction present?

A
  • persistent vomiting - maybe bilious bright green bile (distal to the ampulla of Vater)
  • abdominal pain with distension
  • failure to pass stools or wind
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28
Q

What are the common principles of managing intestinal obstructions?

A
  • referral to paediatric surgical unit
  • NBM and insertion of NGT to help drain stomach and stop vomiting
  • IV fluids to correct dehydration and electrolyte imbalances to keep them hydrated while waiting for definitive management
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29
Q

What is intussusception?

A
  • telescoping or invagination of one part of the bowel into another bowel, ie bowel folds inwards
  • this thickens size of bowel and narrows the lumen at folded area leading to palpable mass in the abdomen and obstruction to faecal passage
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30
Q

What are some common causes of intussusception?

A

henoch-schonlein purpura, cystic fibrosis, intestinal polyps, Meckel diverticulum (most common)

31
Q

How might intussusception present?

A

*infants 6 months to 2 years
- parent report child - sudden onset of inconsolable crying episodes
- concurrent viral upper respiratory infections preceding illness
- severe, colicky abdominal pain
- later stages - redcurrant jelly stool (blood and mucus)
- older children - vomiting and abdominal pain
*intestinal obstruction presentation

32
Q

What is the classic text-book presentation of intussusception?

A
  • RUQ mass on palpation - sausage shaped
  • redcurrant jelly stool
33
Q

What are some complications associated with intussusception?

A
  • obstruction (common cause of this in children is intussusception)
  • perforation as it invaginates further, stretching and constricting blood supply, venous congestion
  • dehydration and shock due to third spacing fluid loss within intussusception —> hypovolaemic shock
34
Q

How would you investigate intussusception?

A
  • USS doughnut or target sign
  • contrast enema
  • AXR for obstruction
35
Q

What is the management for intussusception?

A
  • non-operative - fluid resuscitation, NGT insertion to decompress obstructed bowel
  • therapeutic enema to reduce the telescoping
  • surgical reduction
  • surgical resection if bowel gangrene
36
Q

What is the pathophysiology of pyloric stenosis?

A

hypertrophy (thickening) and therefore narrowing of pylorus is called pyloric stenosis this prevents food travelling from stomach to the duodenum

*pyloric sphincter is a ring of smooth muscle that forms the canal between the stomach and duodenum

37
Q

Why doesn’t pyloric stenosis present at birth?

A

not seen from birth as sphincter continues to grow after birth, hence classically presenting around 3-6 weeks

38
Q

What is the classic history of pyloric stenosis?

A
  • projectile vomiting of non-billions milk content
  • failure to thrive
39
Q

What is the classic examination finding in pyloric stenosis?

A
  • peristalsis seen in observing abdomen
  • firm, round mass can be felt in upper abdomen, feels like large olive—> hypertrophic muscle of pylorus
    • best felt after feed
40
Q

What are some other differentials to consider when thinking pyloric stenosis?

A
  • raised intracranial pressure - differential for projectile vomiting
  • meningitis - vomiting in baby so LP done to rule out, much more acute in presentation
  • gastroenteritis
  • GORD
  • over-feeding
  • sepsis
  • UTI
  • food allergy
  • malrotation if bilious vomiting
41
Q

How might to investigate pyloric stenosis?

A
  • test feeding performed with NGT and stomach aspirated
  • LP to rule out meningitis and CT head to rule out raised ICP
  • blood gas analysis - hypochloraemic (low chloride) metabolic alkalosis due to vomiting HCl
    • hypokalaemia as kidneys exchange potassium to retain protons to compensate
  • USS - hypertrophy of pyloric muscle, doughnut or target sign
42
Q

How might you manage pyloric stenosis (non-surgical)?

A
  • non surgical: stop feeds, correct metabolic abnormalities, NGT, blood gases etc
43
Q

What is the definitive management of pyloric stenosis?

A

laparoscopic pyloromyotomy (Ramstedt’s pyloromyotomy)
*resume feeding after 6h unless mucous membrane perforation
*Post–operative vomiting is common after surgery, due to gastric distension and dysmotility, and is not necessarily a sign of incomplete myotomy

44
Q

What are some post-op complications for pyloric stenosis?

A
  • Wound dehiscence
  • Infection
  • Bleeding
  • Perforation of mucous membranes
  • Incomplete myotomy
45
Q

What is a volvulus? and what does it lead from?

A
  • intestinal malrotation is a birth defect, this happens when the intestinal tract doesn’t form as it should
  • this presents as a volvulus when baby is born
46
Q

What is the pathophysiology of intestinal malrotation and volvulus?

A

lack of intestinal fixation to the retro-peritoneum and a narrow midgut mesenteric base that predisposes to a twisting of the small bowel in the form of midgut volvulus

47
Q

How does a volvulus present?

A

bilious vomiting
abdominal pain and cramping
D+C
rectal bleed or bloody stool
*could be intermittent obstruction

distention, tenderness, drawing up legs, failure to thrive, tachycardia, body stools

48
Q

What investigations would you undertake for a suspected volvulus?

A
  • upper GI contrast studies
  • CT abdomen with contrast
  • abdominal XR
  • FBC
  • blood gas
  • flexible sigmoidoscopy
49
Q

How is a volvulus managed?

A

NGT decompression, IVF, prophylaxis abx

surgical management
- Ladd’s procedure to divide lands bands and widen base of mesentery
- appendicectomy
- ileostomy if necrotic

50
Q

What is the normal descent of testes? and what is cryptorchidism?

A
  • normal - testes develops in the abdomen and gradually migrates down through the inguinal canal and into scrotum before birth
    • testis pulled by gubernaculum within processes vaginalis

*failed to reach the bottom of the scrotum by 3 months of age

51
Q

What are the 3 types of failure of descent of testes?

A
  • true undescended - absent from scrotum but lies along line of testicular descent (incomplete processes vaginalis)
  • ectopic - testis found away from normal path of descent (abnormal position of processes vaginalis)
  • ascending - testis previously identified in the scrotum undergoes secondary ascent out of the scrotum
52
Q

What are some risk factors for cryptorchidism?

A

prematurity, low birth weight, having abnormal genitalia, having first degree relatives with cryptorchidism, maternal smoking during pregnancy

53
Q

How would you examine a presentation of cryptorchidism?

A

💁🏽‍♂️ lie child flat and keep relaxed

  • warm hands, palpate laterally with left hand, from inguinal ring and work along canal to pubic symphysis
  • from other hand palpate scrotum
  • should feel like enlarged lymph node, deeper location
  • if found check if it can be milked down to base, and if so diagnose retractile testis
  • if in groin along canal - inguinal undescended testis
54
Q

What might b/L cryptorchidism indicate?

A

congenital adrenal hyperplasia

55
Q

What are the differentials for cryptorchidism?

A
  • normal retractile testis - in boys who have not reached puberty, its normal for testes to move out of scrotum into canal when cold or when cremasteric reflex activated
  • true undescended testis
  • ectopic testis
  • absent
  • BL impalpable testes
56
Q

when would you worry about cryptorchidism?

A

unilateral - NICE CKS now recommend referral should be considered from around 3 months of age, with the baby ideally seeing a urological surgeon before 6 months of age

bilateral - Should be reviewed by a senior paediatrician within 24hours as the child may need urgent endocrine or genetic investigation

57
Q

What are some reasons for the correction of cryptorchidism?

A

Reduce risk of infertility
Allows the testes to be examined for testicular cancer - 40 times as likely to develop testicular cancer (seminoma)
Avoid testicular torsion
Cosmetic appearance

58
Q

How is cryptorchidism managed?

A

Orchidopexy at 6- 18 months of age - consists of inguinal exploration, mobilisation of the testis and implantation into a dartos pouch
Intra-abdominal testis should be evaluated laparoscopically and mobilised

  • After the age of 2 years in untreated individuals the Sertoli cells will degrade and those presenting late in teenage years may be better served by orchidectomy than to try and salvage a non functioning testis with an increased risk of malignancy
59
Q

What is testicular torsion?

A
  • Mobile testis rotates on the spermatic cord
  • Leads to reduced arterial blood flow, impaired venous return, venous congestion, resultant oedema & infarction to the testis within hours
60
Q

What is the pathophysiology of testicular torsion ?

A
  • Males with a horizontal lie to their testes are more prone to developing testicular torsion - ‘bell-clapper deformity’ lacks normal attachment to tunica vaginalis hence more mobile
  • in neonates the attachment between scrotum and tunica vaginalis is not fully formed and entire testis and tunica vaginalis can tort - extra-vaginal torsion
61
Q

How might testicular torsion present?

A
  • Sudden onset severe unilateral testicular pain
  • associated N&V
  • referred abdominal pain
62
Q

What are some examination findings for testicular torsion?

A
  • testis will have a high position with a horizontal lie
    • try and confirm normal position with patient or parent
  • swollen and tender
  • cremasteric reflex is absent
  • negative Prehn’s sign - pain continues despite elevation of testicle
63
Q

How might you investigate testicular torsion?

A
  • clinical - straight to theatre
  • doppler ultrasound to investigate potential compromised blood flow
  • urine dipstick to assess for infection
64
Q

How is testicular torsion managed?

A
  • Surgical emergency – urgent surgical exploration of the testis within 4-6h window
  • Strong analgesia and anti-emetics pre=operatively
  • nil by mouth and maintenance fluids
  • Torsion in confirmed intra-operatively = bilateral orchidopexy
  • Testis is non-viable = an orchidectomy may be warranted
65
Q

What is a hernia?

A

protrusion of viscus through a defect of walls of its containing cavity, inguinal hernia viscus if intra-abdominal contents like bowel, containing cavity is abdomen and protrusion is into the inguinal canal

66
Q

What is the pathophysiology of the most common type of inguinal hernia?

A
  • indirect inguinal hernias common in children where contents protrude through deep inguinal ring into inguinal canal, through superficial inguinal ring into groin
  • this is due to incomplete closure of out-pouching of peritoneum called processus vaginalis after descent of testes in utero
67
Q

How might an inguinal hernia present?

A
  • groin swelling
  • nausea, vomiting
  • constipation
  • inguinal/ inguino-scrotal mass that cannot ‘get above’
    • reducible when lying flat
    • does not transilluminate
    • positive cough reflex
  • when strangulated, irreducible and tender tense lump with pain out of proportion to clinical signs + features of bowel obstruction
68
Q

How is an inguinal hernia managed?

A
  • surgical repair of hernia - herniotomy
    • performed on all full-term male infants with asymptomatic reducible inguinal hernias
  • emergency surgical repair in irreducible ones, to prevent bowel and testicular ischaemia
69
Q

What is the pathophysiology of epididymorchitis?

A

Usually caused by local extension of infection from the lower urinary tract either via enteric or non-enteric organisms which spreads to epididymis and testicle

  • In younger boys, it can be caused by a urinary tract infection and may be linked to a structural problem in the genitourinary system
  • In older boys and teens, could be an STI, most often caused by gonorrhoea or chlamydia hence are bacterial infections
  • It’s most often seen in teen boys ages 14 and older or in younger children are at risk if they have had a urinary tract infection
  • mumps to TB?
70
Q

How might epididymorchitis present?

A
  • Pain and swelling in the testicles
  • nausea and vomiting
  • Fever
  • Feeling of heaviness in the testicles
  • Fluid leaking from the urethra
  • Blood in the semen
  • Lump in the testicles
  • Pain during urination or ejaculation
71
Q

What are some examination findings seen in Epididymo-orchitis?

A
  • red & swollen, very tender
  • reactive hydrocoele
  • urethral discharge
  • Cremasteric reflex which is intact in cases of epididymitis
  • Prehn’s sign (supine & scrotum is elevated by the examiner -> relieved by elevation)
72
Q

How might Epididymo-orchitis be investigated?

A
  • urine dip - infection
  • assess STI potential and do a screen
  • First-void urine should be collected and sent for NAAT for suspected non-enteric epididymitis
  • Routine bloods
  • Imaging – typically a clinical one, however USS of the testes can be useful to confirm the diagnosis & rule out any complication like an abscess
73
Q

How is Epididymo-orchitis managed?

A
  • antibiotics and analgesia
    • If an enteric organism is suspected, fluoroquinolones are the preferred antibiotic, as they have excellent penetration into the testes
  • If your teen has an STI, make sure they tell any sexual partners who had contact within 60 days before symptoms
  • chronic epididymitis that prove to be refractory to all other therapy and have a persistent pain,orchiectomymay be warranted in rare cases
74
Q
A

y4 paediatrics (16 decks)

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