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4th Year > Paeds - Surgery (teachmepaeds) > Flashcards

Paeds - Surgery (teachmepaeds) Flashcards

1
Q

What is the pathophysiology of appendicitis?

A

Luminal obstruction, usually secondary to faecolith or lymphoid hyperplasia or impacted stool.
(Rarely appendiceal or caecal tumour)

When obstructed, bacteria congregate in the appendix and multiply = acute inflammation

Reduced venous drainage and localised inflammation can result in increased pressure = ischaemia

If untreated, ischaemia within the appendiceal wall = necrosis = perforation

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2
Q

How would appendicitis typically present?

A

dull poorly localised peri-umbilical pain that migrates
to sharp well localised RIF pain

vomiting, anorexia, nausea, diarrhoea, constipation

Rebound tenderness and percussion pain over McBurneys point

Guarding

Rovsings sign (RIF pain on palpation of LIF)

Psoas sign (RIF pain on extension of R Hip)

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3
Q

What are some investigations you would do for suspected appendicitis?

A

1st line = US to minimise radiation exposure in kids
(CT Can help)

Urinalysis + preg test in women

FBC, CRP, B-HCG

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4
Q

What risk stratification score would you use in kids?

A

Shera Score

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5
Q

How would you manage appendicitis?

A

Gold standard = Laparoscopic appendectomy

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6
Q

What is Hirschsprung’s disease?

A

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

3 types = short segment, long segment, total colonic aganglionosis disease

short segment (85%) = aganglionosis is restricted to rectosigmoid part of colon

long segment = aganglionosis extends past rectosigmoid portion to splenic flexure

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7
Q

How would Hirschsprung’s disease present?

A

Typically presents around 2 days

Classic triad:

  • Abdo distension
  • Bilious vomiting
  • Failure to pass meconium within 48 hours of birth

Failure to pass faeces = dilation of proximal bowel = palpated in Lower Left Abdo

Rectal exam = empty rectal vault

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8
Q

What is the pathophysiology of Hirschsprungs?

A

The aganglionic segment of the bowel remains in a tonic state, leading to failure in peristalsis and bowel movements.

Stasis and resultant increased intraluminal pressure can lead to decreased blood flow and deterioration of mucosal layer.
Stasis of faeces leads to bacterial proliferation (esp C Diff, S Aureus) = Hirschsprung’s enterocolitis (complication that can lead to sepsis)

Faeces in the rectum fails to trigger relaxation of the internal anal sphincter due to the aganglionosis.
Accumulation of faeces in the rectosigmoid region can cause functional obstruction.

It can lead to proximal bowel dilation = abdo distension.

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9
Q

What are some differentials for Hirschsprungs?

A

Meconium plug syndrome = failure to pass meconium until passage of plug.
(do barium enema or water-soluble contrast enema)

Meconium Ileus = s bowel impacted by meconium.
(do a water-soluble contrast enema)

Intestinal atresia = congenital malformation of intestine resulting in obstruction

Anorectal malformation
(differentiated by physical exam of rectum)

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10
Q

How would you investigate Hirschsprungs?

A

Gold Standard = Rectal Suction Biopsy to test submucosa for ganglionic cells
(Stain biopsy with acetylcholinesterase. Will show aganglionosis, no ganglion cells in submucosal and myenteric plexus, with several hypertrophied nerve bundles stained +ve brown for acetylcholinesterase)

Plain Abdo Xray

Contrast Enema to rule out differentials
(will show short transition zone between proximal end of colon and narrow distal end of colon. Rectal diameter similar or equal to sigmoid colon is suggestive of Hirschsprung’s)

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11
Q

How would you manage Hirschsprungs?

A

IV Antibiotics
NG Tube
Bowel decompression

Surgery to resect aganglionic section of bowel and connect the unaffected bowel to the dentate line

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12
Q

What is intussusception?

A

Telescoping of one part of the bowel into another.

Most commonly ileo-colic type where the distal ileum passes into the caecum through the ileo-caeceal valve.

typically between 5-7 months of age

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13
Q

How would intussusception present in a child?

A

Hx

  • sudden onset inconsolable crying episodes
  • pallor and child may draw knees up to chest to help pain
  • child returns to normal self between episodes
  • in later stages, child can pass stools with “red-currant jelly” consistency due to blood and mucus

Exam

  • distension
  • palpable “sausage shaped” abdo mass in RUQ (ileo-caecal)
  • Peritonism
  • Presence of bowel sounds
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14
Q

How would you investigate suspected intussusception?

A

Abdo US is preferred and is more sensitive.

  • Doughnut/ Target sign on transverse plane
  • Pseudokidney sign on longitudinal plane

Abdo XRay can confirm

  • curvilinear outline of intussusception
  • absence of bowel gas in colon distal to intussusception
  • Riglers sign if perforation has occured

Contrast enema can diagnose intussusception.
However contraindicated in perforation/ peritonitis.

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15
Q

How would you manage intussusception?

A

Fluid Resus, NG can help decompress

Non surgical = Air or contrast enema to reduce intussuscepted bowel

Surgical reduction = reduce bowel and resect necrotic areas.

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16
Q

What is pyloric stenosis?

A

progressive hypertrophy of pyloric muscle causing gastric outlet obstruction.

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17
Q

How does pyloric stenosis present?

A

Onset of vomiting at 2-8 weeks (gets gradually more frequent and more intense until projectile, non-bilious, 30-60mins after a feed, baby remains hungry, sometimes haematemesis)

hunger, weight loss, dehyration, lethargy, infrequent/ absent bowel movements

Exam =
Visible peristalsis,
enlarged pylorus “olive” palpated in RUQ or epigastrium (best palpated at start of a feed)

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18
Q

How would you investigate pyloric stenosis?

A

Test feed with NG tube in situ and stomach aspirated
(palpate for “olive” while feeding and observe for visible peristalsis)

Ultrasound of abdo
(shows hypertrophy of pyloric muscle, thickness >3mm, length >15mm, diameter >11mm5)

Blood gas shows Hypokalaemic, Hypochloraemic Metabolic ALKALOSIS
(HypoCh and MA due to vomiting acid, HypoK due to kidney exchanging K+ to retain protons to compensate)

19
Q

How would you manage pyloric stenosis?

A

NG tube and 4 hourly aspirations.

Rehydration at 150ml/kg/day using crystalloids

correct any underlying metabolic abnormalities.

ABG, U&Es

Surgery = Ramstedt’s Pyloromyotomy
(can resume feeding after 6 hours)

20
Q

Define Balanitis Xerotica Obliterans

A

At birth, there are adhesions between the prepuce and glans of the penis.
These gradually break down to allow the foreskin to be retracted.
(By 16, only 1% of phimosis persists)

Pathalogical Phimosis is usually due to “BXO”, which is keratinisation of the tip of the foreskin so scarring occurs and prepuce can not be retracted.

21
Q

How would BXO present?

A

Hx

  • ballooning of foreskin during micturition
  • scarring of the urethral meatus = irritation, dysuria, haematuria, local infection
  • episodes of urinary obstruction if prepucial scarring is extensive

Exam
- white fibrotic scarred preputial tip
(A physiological phimosis may be non-retractile but will not have scarring or meatal involvement)

22
Q

How would you manage BXO?

A

Circumcision

Send foreskin to histopathology

23
Q

What is Cryptorchidism?

A

Congenital absence of one or both testes in the scrotum due to failure of the testes to descend during development

(They are usually pulled down by the gubernaculum within the processes vaginalis)

24
Q

How would cryptorchidism present?

A

Hx = ask if the testis has ever been seen or palpated within the scrotum
(eg. newborn check, a warm bath)

Exam

  • 80% of undescended testis are palpable
  • lie child flat on bed, use warm hands to palpate
  • if testis can be milked down to base of scrotum = retractile testis
  • if it is pulled down but under tension in the base = “high testis”
  • if found along inguinal canal but cannot be brought down further = “inguinal undescended testis”
  • if not palpable = ectopic, intra-abdo, absent, impalpably small
25
Q

How would you manage cryptorchidism?

A

Urgent referral to senior paediatrician within 24 hours if associated DSD suspected, associated ambiguous genitalia or hypospasdias or bilateral undescended testis.
= could be congenital adrenal hyperplasia
(risk of salt losing crisis = high dose NaCl therapy, glucose monitoring and steroid replacement)

At 3 months after birth if still undescended, refer for definitive intervention occurring at 6-12 months old.

DSD = disorder of sex development

26
Q

What kind of interventions are available for cryptorchidism?

A

Based on clinical findings:

If palpable = open orchidopexy

If intra-abdo = Fowler-Stephens procedure

If atrophic testis = remove it, groin exploration

27
Q

What is Epididymitis

A

Inflammation of the epididymis,
usually from local extension of infection from the lower urinary tract (bladder/urethra)
or a complication of Mumps Viral Infection

28
Q

How would mumps orchitis present?

A

Unilateral/ Bilateral orchitis

Fever

4-8 days after onset of mumps parotitis

29
Q

How does epididymitis present?

A
  • unilateral scrotal pain and swelling
  • red and swollen and tender on palpation
  • fevers and rigors
  • dysuria, storage LUTS, urethral discharge

Cremasteric reflex is intact

Prehn’s sign is positive (elevate scrotum on supine patient. pain is relieved by elevation)

30
Q

How would you investigate epididymitis?

A

US Doppler can confirm diagnosis

Urine dipstick and Culture

First void urine
(Nucleic Acid Amplification Test for n gonorrhoea, c trachomatis, m genitalium)

Blood cultures and FBC, CRP

31
Q

How would you manage epididymitis?

A

Antibiotics and analgesia

Enteric organisms = Ofloxacin 200mg PO BD for 14 days

STI organisms = Ceftriaxone 500mg IM single dose
or Doxycycline 100mg PO 2x daily for 10-14 days
(+ Azithromycin 1g PO single dose if gonorrhoea)

32
Q

What is hypospadias?

A

A Congenital defect causing urethral meatus to be located at an abnormal site

(eg. underside of penis rather than at the tip)

Thought to occur due to arrest of penile development, resulting in hypoplasia of ventral tissue of the penis

33
Q

How would hypospadias present?

A

Hx

  • abnormal urinary flow (eg. not form tip of penis)
  • abnormal penile curvature during erections

3 key features

  • ventral opening of urethral meatus
  • ventral curvature of the penis or “Chordee”
  • dorsal hooded foreskin
34
Q

What is an important differential diagnosis to rule out?

A

Disorder of Sex Development (DSD)

DSD can be associated with unilateral/bilateral undescended testis.

Congenital adrenal hyperplasia a common cause of DSD.
It can lead to salt wasting crisis due to cortisol and aldosterone deficiency with androgen excess.

35
Q

How would you manage hypospadias?

A

Urethroplasty

  • will bring meatus to the glans of the penis
  • chordee is corrected to straighten the penis
  • dorsal foreskin is managed with circumcision or reconstruction
36
Q

What are some complications of managing the hypospadias?

A

Short term

  • urethral catheter can block
  • urethral catheter can cause pain and bladder spasms
  • bleeding and infection

Long term

  • urethral fistula
  • meatal or urethral stenosis
37
Q

What is testicular torsion?

A

Spermatic cord and its contents twist within the tunica vaginalis.

Reduced arterial blood flow, impaired venous return, venous congestion, resultant oedema, infarction to the testis.

38
Q

Who is at risk of testicular torsion?

A

males with a “bell-clapper deformity” or a horizontal lie to their testes

neonates where the attachment between the scrotum and TV is not fully formed
so the entire testis and tunica vaginalis can tort (extra-vaginal torsion)

Previous testicular torsion

Fhx of Testicular torsion

Undescended testes

39
Q

How would testicular torsion present?

A

sudden onset severe unilateral testicular pain and swelling

nausea and vomiting secondary to pain

testis will have a high position and horizontal lie

Absent cremasteric reflex and
Negative Prehn’s sign

40
Q

Describe torsion of the hydatid of morgagni

A

H of M is a remnant of the Mullerian duct and can become torted, presenting similarly.

Scrotum is less erythematous with a normal lie of the testis.

“Blue dot sign” can be present in the upper half of the hemiscrotum.
(This is the visible infarcted hydatid.)

41
Q

How would you investigate testicular torsion?

A

Doppler US to investigate compromised blood flow to testis
(high sensitivity and specificity)

Urine dipstick

Take to theatre for scrotal exploration

42
Q

How would you manage testicular torsion?

A

4-6 hour window from onset of symptoms before significant ischaemic damage.

Urgent surgical exploration.

  • Once confirmed = bilateral orchidopexy
  • If testis is non-viable = orchidectomy

analgesia and anti-emetics

43
Q

When would you suspect malrotation?

A
  • Bowel obstruction (initially tinkling bowel sounds and then absent, abdo distension)
  • Bilious or blood stained vomit
  • tachycardia and HTN due to abdo pain
  • peritonitis
  • ischaemic bowel (eventually results in tachy + hyPOtension)
44
Q

What is malrotation?

A

Basically a volvulus

Ileocaecal and Duodenaljejunal flexure are predisposed to volvulus.

It is a surgical emergency!

  • NMB
  • NG Tube
  • Ladd Procedure

4th Year (17 decks)

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