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Paediatrics > Surgery > Flashcards

Surgery Flashcards

1
Q

acute apendicitis

A

…

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2
Q

gastroschisis definition

A

full thickness abdominal wall defect in which foetal organs protrude outside the abdomen with no protective membrane covering it. Direct intestinal exposure to amniotic fluid in utero leads to chemical reactions, creating a thick inflammatory film or peel over the bowel

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3
Q

prevalence gastroschisis

A

1-6 per 10000 live births

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4
Q

gastroschisis patho

A

unknown
possible..compromised vascular supply to anterior abdo wall, defect in primordial umbilical ring, or abdnormal involution of R umbilical vein so weakened point at risk of rupture

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5
Q

risk factors gastroschisis

A

Maternal smoking (possibly due to placental insufficiency and abnormal development of the vascular system)
Maternal age <20 years old
Environmental exposures e.g. Nitrosamines
Maternal cyclooxygenase inhibitors use e.g. aspirin and ibuprofen

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6
Q

clinical features gastroschisis

A

can be present visible at birth or detected on prenatal USS at 20 weeks
often found to R of umbilicalcord
organs involed - S and L intestines, liver, stomach
swollen/thickened intestines
abdo cavity may appear smaller
intestinal malrotation sometimes - intestinal atresia

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7
Q

gastroschisis v omphalocoele

A

omphalocoele - no membrane covering abdo contents
extra intestinal or structural abnormalities

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8
Q

gastroschisis investigations

A

mainly clinical diagnosis
alpha fetoprotein - elevated
routine USS in 2nd trimester - detected
Ultrasonography - echogenic and dilated loops of bowel freely floating in amniotic fluid
coloured doppler - localise herniation

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9
Q

immediate management gastroschisis

A

fluid resus
maintain temp
sterile, clear covering over herniated contents

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10
Q

definitive management gastroschisis

A

surgery - protrude and close abdo wall
may need to be staged if large - nvolve placing the bowel in a clear sac called a silo, which is tightened until there is enough space to reduce the bowel completely
then NG tube and parenteral feeding

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11
Q

complications gastroschisis

A

Abdominal Compartmental Syndrome
Persistent bowel dysfunction
Wound infection
Necrotizing Enterocolitis
Short gut syndrome
Abdominal Compartmental Syndrome

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12
Q

prognosis gastroschisis

A

87-100% survival rates
intestinal atresia - poor prognostic factor

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13
Q

hirschsprung’s disease definition

A

also known as congenital aganglionic megacolon disease, is a congenital disease in which ganglionic cells fail to develop in the large intestine. This commonly presents as delayed or failed passage of meconium around birth.

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14
Q

prevalence hirschsprung’s disease

A

1 case per 1500-1700
median age 2 days
males 4 times more likley

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15
Q

genes hirschprung’s disease

A

those that encode the proteins for the RET signaling pathway and endothelin type B receptor pathway. The strongest association with Hirschsprung’s, is the Receptor tyrosine kinase (RET) gene, a proto-oncogene on chromosome 10q11. HD is strongly associated with chromosomal abnormalities, with 10-15% HD cases associated with trisomy 21 (Down Syndrome)

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16
Q

hirschsprung’s disease subtypes

A

short-segment - most common
long segment - aganglionosis extends past rectosignoid portion of colon to splenic flexture
total colonic aganglionosis disease - entire colon affected

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17
Q

hirschsprung’s disease pathophysiology

A

ganglionic cells of the myenteric and submucosal plexuses in the bowel aren’t present proximally from the anus to a variable length along the large intestine.
The most common accepted aetiology of this disease is due to the arrest of the neuroblast, derived from neural crest cell migration in fetal development between week 8 to 12.

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18
Q

hirschsprung’s enterocolitis

A

Increased intraluminal pressure can lead to decreased blood flow and deterioration in the mucosal layer. This stasis can lead to bacterial proliferation and the subsequent complication of Hirschsprung’s enterocolitis, which has a mortality rate of 25-30%. If not recognised early this can lead to sepsis and death

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19
Q

risk factors hirschsprung’s disease

A

males
chromsomal abnormalities - down’s
family hx - mutations

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20
Q

25% have classic triad in hirscsprung’s

A

failure to pass (within 48 hrs) meconium
abdo distention
billous vomiting

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21
Q

examination hirschsprung’s diease

A

faecal mass palpated in left lower abdomen
tympanic abdomen
empty rectal vault…forceful discharge of gas and faecal material

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22
Q

ddx hirschprung’s disease

A

meconium plug syndrome
meconium ileus
intestinal atresia

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23
Q

hirschsprung’s disease investigations

A

gold standard: rectal suction biopsy to confirm aganglionosis using acetylcholinesterase
contrast enema - short transition between proximal end of colon and narrow distal end of colon plus rectal diameter equal to sigmoid colon
laparatomy - if perfortation present as enema contraindicatedr

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24
Q

rectal suction biopsy guidelines

A

clinical features indicated, otherwise avoided:
Delayed passage of meconium (more than 48 hours after birth in term babies)
Constipation since first few weeks of life
Chronic abdominal distension plus vomiting
Family history of Hirschsprung’s disease
Faltering growth in addition to any of the previous features

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25
Q

management hirschsprung’s

A

IV abx
NG
bowel decompression
definitive - surgery - resecting aganglionic section and connecting unaffected bowel to dentate line

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26
Q

complications hirschsprung’s

A

Hirschsprung associated enterocolitis (HAEC) - c.diff, s.aureus
complications of surgery - constipation, enterocolitis, perianal abscess, faecal soiling, adhesions

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27
Q

risk factors inguinal heria

A

prematurity
male
fhx

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28
Q

management inguinal hernia

A

surgical repair - herniotomy on ful term male infants with asx reduciable hernias
emergency surgery if irreducible…testicular ischaemia

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29
Q

intussusception definition

A

the movement or ‘telescoping’ of one part of the bowel into another. The proximal bowel segment is referred to as the intussuceptum whilst the distal segment as intussucipiens

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30
Q

epidemiology intussception

A

5-7 mths of age
boys twice as more likely

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31
Q

pathophysiology intussception

A

leads to intestinal obstruction
up to 90% are ileo colic type -distal ileum passes into caecum through ileo-caecal valve

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32
Q

risk factors intessuscption

A

most are idiopathic
rotaviruses increase risk
pathological causes include Meckel diverticulum (most common)
Polyps
Henoch-Schönlein purpura
Lymphoma and other tumors
Post-operative

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33
Q

when pathological cause suspected in intussception

A

if child older
high recurrence rate

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34
Q

hx intrussception

A

sudden onset inconsolable crying episodes
pallor
draw up kneeds
normal inbetween episodes
lethargic
anorexic
red current consistency - blood and mucus stooll
older - obstruction features

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35
Q

examination intussecption

A

Distention
A palpable ‘sausage-shaped’ abdominal mass which can be found in the right upper quadrant (ileo-ceceal type)
Signs of peritonism
Presence of bowel sounds
dehydration and shock

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36
Q

ddx intessception

A

colic
testicular torsion
appendicitis

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37
Q

diagnosis intussception

A

abdo USS - dougnut/target sign on transverse plane and pseudokidney sign on longitudinal plane
AXR - distented small bowel loops, outline intussuception, rigler’s sign
contrast enema

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38
Q

management intussception

A

fluid resus
NG tube
non op reduction - air or contrast enema. c/i if perforation or peritonitis
surgical reduction - manually reduce and resection of necrotic bowel

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39
Q

complications intussception

A

obstruction -surgical emergency
perforation - venous congestion and oedema within bowel wall..necrosis and perforation
dehydration and shock

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40
Q

omphalocoele definition

A

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

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41
Q

prevalence omphalocele

A

1 in 5000 live births

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42
Q

pathophysiology

A

During normal development of the intestines, the midgut begins to elongate at around 6 weeks gestation. However, at this time the liver and stomach are also growing, meaning there is not enough room in the abdomen to accommodate the midgut. In order to continue developing, the midgut herniates through the umbilical ring out of the abdomen into the umbilical cord (called physiological umbilical herniation). During the 10th week, the abdomen has enlarged enough for the midgut to return (3).

The exact cause of omphalocele is unknown (4), however the main theory is failure of this normal intestinal migration back into the abdominal cavity, and persistence of the physiological umbilical herniatio

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43
Q

risk factors omphalocele

A

maternal smoking
maternal age >40 yrs
chromosomal abnormalities - triosomy,turners, klinefelters

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44
Q

clinical features omphalocele

A

4-12cm abdo wall defects located centrally within umbilical cord
protective membranes surroudning
healthy intestines

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45
Q

ddx omphalocele

A

gastroschisis
cloacal exstrophy
physiological gut herniation

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46
Q

omphalocele investigations

A

clinical diagnosis
prenatal USS or birth
alpha fetoprotein elevated
chromosomal abnormalities - chronic villus sampling or amniocentesis

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47
Q

immediate management omphalocele

A

fluid resus
temp
NG tube
neonatal ICU

48
Q

definitive management omphalocele

A

reduction of bowel into abdo cavity and closure of skin and fascia
agents to promote epithelisiation - silver impregnated dressings or povidone iodine solutions
if ruptured membrnaous sac - immediate surgery

49
Q

complications omphalocele

A

ruptured
abdominal compartmental syndrome

50
Q

prevalence pyloric stenosis

A

1 in 500-1000 live births
4 males for every 1 female

51
Q

pathophysiology pyloric stenosis

A

progressive hypertrophy of the pyloric muscle, causing gastric outlet obstruction. The aetiology remains unknown

52
Q

risk factors pyloric stensois

A

male
family hxl

53
Q

clinical features pyloric stenosis

A

4-6 weeks of age
non bilious vomiting after every eed
projectile vomiting
haematemesis
weight loss
dehydration
visible peristalysis and palpable olive shaped pyloric mass

54
Q

ddx pyloric stenosis

A

Gastroenteritis
Gastro-oesophageal reflux, including Sandifer syndrome
Over-feeding

55
Q

investigations pylotic stenosis

A

test feed with NG in situ and stomach aspirated. while feeding palpated for mass and observe for visible peristalsis
USS - hypertrophy
blood gas - low K, low Cl, met alkalosis from vomiting

56
Q

management pyloric stenosis

A

correct underlying metabolic abnormalities
10-20ml/kg fluid boluses
NG tube - aspirated every 4 hrs
Ramstedt’s pyloromyotomy

57
Q

complications of pyloric stenosis

A

Pre-operative:

Hypovolaemia
Apnoea – secondary to hypoventilation associated with metabolic acidosis
Post-operative:

Wound dehiscence
Infection
Bleeding
Perforation
Incomplete myotomy

58
Q

glioma define

A

all primary brain tumours that originate from neuroepithelial glial cells (including ependymal cells, astrocytes, oligodendrocytes and astrocytes)

59
Q

most common type of brain tumour in children

A

low grade glioma

60
Q

clinical features glioma

A

seizures*, cranial nerve palsies or visual field defects, language dysfunction, or features of raised intracranial pressure.

61
Q

investigations glioma

A

CT with IV contrast
biopsy to confirm

62
Q

low grade gliomas management

A

watch aand wait
total or partial debulking
radiotherapy

63
Q

high grade gliomas management

A

total or partial decompressive tumour debulking
both chemo and radiotherapy

64
Q

prognosis glioma

A

low grade - 15-16yrs
high - 15-18 mths

65
Q

hydrocephalus definition

A

the accumulation of cerebrospinal fluid (CSF) within the cerebral ventricles

66
Q

hydrocephalus pathophysiology

A

obstructive - blockage to natural ventricular drainage system and CSF flow - tumour, cysts
communicating - reduced absorbance of CSF by arachnoid villi - infective menginitis, SAH, normal pressure hydrocephalus

67
Q

normal pressure hydrocephalus triad

A

triad of Parkinsonian gait, urinary incontinence, and dementia.

68
Q

clinical features hydrocephalus

A

N+V
headache
worse in morning
altered GCS
blurred vision
abnormal gait
incontineence
papilloedema

69
Q

investigations hydrocephalus

A

CT - enlargement of ventricles, loss of sulcal gyral pattern, CSF exudation

70
Q

pattern of ventricular enlargement

A

Generalised ventricular dilatation suggests a communicating hydrocephalus
Dilated lateral and third ventricle:
With a normal fourth ventricle suggests aqueduct stenosis
With dilated fourth ventricle suggests a posterior fossa mass

71
Q

management hydrocephalus

A

insertion of external ventricular drain
debulking of tumour, endoscopic third ventriculostomy or choroid plexis resection

72
Q

routes of pathogen spread CNS infections

A

1) haematogenous spread via the choroid plexus, (2) direct extension from adjacent tissues, and (3) inoculation from interventional procedures or surgery

73
Q

extradural abscess

A

develops following neurotrauma, surgery (such as following a craniotomy), or direct spread from sinusitis or mastoiditis. The condition often presents with localised pain over the affected region and can present concurrently with osteomyelitis of the cranial vault. The most common causative organisms are Streptococci and S. aureus.

74
Q

subdural empyema

A

develops as direct spread from sinusitis (particularly frontal sinusitis) or from chronic otitis media, extending to the subdural space via the emissary veins or as a result of retrograde thrombophlebitis.

75
Q

cerebral abscesses

A

direct spread from sinusitis, haematogenous spread from a septic focus*, or following a penetrating wound to the head or following neurosurgical procedures.

The most common causative pathogens are S. pneumoniae and S. aureus. On cross-sectional imaging, cerebral abscesses will present as discrete lesions with an enhancing rim

76
Q

ventriculitis

A

inflammation of the ependymal cells which lines the cerebral ventricles. It often develops secondary to pre-existing infections (e.g. meningitis), however may develop from those with external ventricular drains (EVD) in-situ or following intracranial surgery

77
Q

clinical features CNS infections

A

new onset confusion
reduced GCS
headache
features of sepsis
raised ICP
seizures
pyrexia
focal neurological deficit

78
Q

risk factors CNS infections

A

extremes of age, recent neurosurgical procedure, intravenous drug use, the presence of any long-term intracranial devices, or immunosuppresion

79
Q

investigations CNS infections

A

routine bloods
blood cultures
CSF samples
CT

80
Q

management CNS infections

A

fluid resus
IV abx
hyperosmolar agents
anti epileptics
surgical intervention is definitive

81
Q

balanitis xerotica obliterans pathophysiology

A

adhesions between prepuce and glans of penis. over time - gradually breaks down. mean age of foreskin retraction is 10.4 yrs, can be normal up to age of 8 and 1% have phsyiological phimosis at age 16. Around 95% of pathological phimosis is due to the process ‘Balanitis xerotica obliterans’ (BXO); where keratinisation of the tip of the foreskin causes scaring and the prepuce remains non-retractile

82
Q

hx BXO

A

ballooning of foreskin during micrturition
irritation
dysuria
haematuria
local infection

83
Q

examination BXO

A

white, fibrotic scarred preputial tip
hard to visualise meatus

84
Q

management BXO

A

circumcision
foreskin to histopathology to confirm diagnosis

85
Q

complications BXO

A

day case procedure…dissolvable stitches
small risk of bleeding and infection
swelling and serous discharge
if left untreated - meatal stenosis, phimosis, erosions of glans and prepuce

86
Q

cryptochordism definition

A

failure of testicular descent into scrotum

87
Q

3 types of cryptochorisim

A

True undescended testis: where testis is absent from the scrotum but lies along the line of testicular descent
Ectopic testis: where the testis is found away from the normal path of decent
Ascending testis: where a testis previously identified in the scrotum undergoes a secondary ascent out of the scrotum.

88
Q

pathophysiology cryptochordism

A

the testis descends from the abdomen to the scrotum, pulled by the gubernaculum, within the processes vaginalis. This process is incomplete in the context of true undescended testis; or tracks to an abnormal position in an ectopic testis. However, particularly with bilateral cryptorchidism, hormonal causes such as androgen insensitivity syndrome or disorder of sex development must also be excluded

89
Q

risk factors cryptochordism

A

prematurity,
low birth weight,
having other abnormalities of genitalia (i.e. hypospadias)
having a first degree relative with cryptorchidism.

90
Q

hx cryptochoridism

A

if the testis has ever been seen or palpated within the scrotum, such as in the newborn check - warm bath?

91
Q

exam cryptochordism

A

To start, have the infant/child laid flat on the bed, aim to keep the child as comfortable and relaxed as possible. With warm hands, palpate laterally with your left hand, from the inguinal ring and work along the inguinal canal to the pubic symphysis, from there your other hand can be used to palpated the testis in the scrotum. If found, one should attempt to see if the testis can be gently milked down to the base of the scrotum, in which case a diagnosis of retractile testis can be made, if it is pulled down but under tension in the base, this commonly referred to as a ‘high scrotal’ or simply ‘high testis’.

Sometimes the testis may be found within the groin, along the inguinal canal, but cannot bring it further, therefore an ‘inguinal undescended testis’ has been found.

92
Q

cryptochordis ddx

A

normal retratile testis
true undescended testis
ectopic testis

93
Q

initial management cryptochordism

A

undescended testis associated with ambiguous genitalia or hypospadias, or bilateral undescended testis are found: urgent referral to senior paediatrician within 24 hours

94
Q

monitoring cryptochordism

A

At birth – review at 6-8 weeks of age

At 6-8 weeks – if fully descended, no further action. If unilateral, re-examine at 3 months

At 3 months – If testis is retractile, advise annual follow up (due to risk of ascending testis). If undescended, refer to paediatric surgery/urology for definitive intervention – ideally occurring 6 – 12 months of age.

95
Q

definitive management cryptochordism

A

examination under anaesthesia followed by laprascopy
open orchidopexy if palpable
if intra abdo - fowlder stephens procedure
groin exploration if atrophic testis

96
Q

surgical complications cryptochoridism

A

infection
bleeding
wound dehiscence
resricular atrophy
testicular re ascent

97
Q

complications of undescended testis

A

impaired fertility
testicular cancer -2-3x more common
torsion

98
Q

hydrocele definition

A

collection of fluid that builds up in the remnants of the processus vaginalis

99
Q

2 types of hydrocele

A

communicating - the persistence of a patent processus vaginalis (PPV), allowing the free flow of peritoneal fluid from peritoneum to the tunica vaginalis. If the connection is large enough, an inguinal hernia may occur due to the protrusion of intra-abdominal content
non communicating - imbalance between production and absorbance of serous fluid

100
Q

aetiology hydrocele

A

congenital
malignancy
testicular torsion
trauma
inection

101
Q

clinical features hydrocele

A

non-tender, smooth and transilluminates. There is notable scrotal enlargement following exertio

102
Q

hydrocele ddx

A

inguinal hernia
testicular cancer
epididymitis

103
Q

investigations hydrocele

A

USS scan but clinical diagnosis

104
Q

management hydrocele

A

reassurance
surgery - open/laparoscopic PPV (patent processus vaginalis) ligation is offered electively to children in whom hydrocele persists beyond 2 years. Exploratory laparoscopy can be indicated if the hydrocele is large, infected, recurrent or to rule out secondary pathology

105
Q

hypospadias definition

A

a congenital defect causing the urethral meatus to be located at an abnormal site, usually on the under side of the penis rather than at the tip

106
Q

epidemiology hypospadias

A

1 in 300 male births
incidence increasing

107
Q

pathophysiology hypospadias

A

due to arrest of penile development, leading to hypoplasia of the ventral tissue of the penis

108
Q

clinical features hypospadias

A

abnormal urine flow - not from tip
abnormal penile curvature during erections
1) Ventral opening of the urethral meatus

2) Ventral curvature of the penis or “Chordee”

3) Dorsal hooded foreskin

109
Q

classification hypospadias

A

Glandular, coronal, shaft (distal, mid, proximal), scrotal, perineal

110
Q

hypospadias risks

A

Congenital Adrenal Hyperplasia is a diagnosis that must not be missed and should be considered in females with ambiguous genitalia. If not detected early this can lead to a salt wasting crisis due to cortisol and aldosterone deficiency with androgen excess.

111
Q

investigations hypospadias

A

Detailed history and examination
Karyotype
Pelvic ultrasound scan
Urea and Electrolytes
Endocrine hormones: Testosterone, 17 alpha-hyroxyprogesterone, LH, FSH, ACTH, renin, aldosterone

112
Q

hypospadias management

A

urethroplasty
Performed as a single stage or a 2-stage repair, using a graft. This is preferentially a preputial graft harvested from the foreskin hence the need to advise against circumcision

113
Q

short term complications hypospadias

A

This urethral catheter may block, requiring further management such as flushing. The urethral catheter may also become displaced or kinked and therefore there should be careful inspection if not draining. also may cause pain and bladder spasms
tx with anticholingerics
bleeding, infection

114
Q

long term complications hypospadias

A

urethral fistula
meatal and urethral stenosis

115
Q
A

Paediatrics (17 decks)

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