Surgery Flashcards

(115 cards)

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
management hirschsprung's
IV abx NG bowel decompression definitive - surgery - resecting aganglionic section and connecting unaffected bowel to dentate line
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complications hirschsprung's
Hirschsprung associated enterocolitis (HAEC) - c.diff, s.aureus complications of surgery - constipation, enterocolitis, perianal abscess, faecal soiling, adhesions
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risk factors inguinal heria
prematurity male fhx
28
management inguinal hernia
surgical repair - herniotomy on ful term male infants with asx reduciable hernias emergency surgery if irreducible...testicular ischaemia
29
intussusception definition
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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epidemiology intussception
5-7 mths of age boys twice as more likely
31
pathophysiology intussception
leads to intestinal obstruction up to 90% are ileo colic type -distal ileum passes into caecum through ileo-caecal valve
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risk factors intessuscption
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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when pathological cause suspected in intussception
if child older high recurrence rate
34
hx intrussception
sudden onset inconsolable crying episodes pallor draw up kneeds normal inbetween episodes lethargic anorexic red current consistency - blood and mucus stooll older - obstruction features
35
examination intussecption
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
36
ddx intessception
colic testicular torsion appendicitis
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diagnosis intussception
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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management intussception
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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complications intussception
obstruction -surgical emergency perforation - venous congestion and oedema within bowel wall..necrosis and perforation dehydration and shock
40
omphalocoele definition
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
41
prevalence omphalocele
1 in 5000 live births
42
pathophysiology
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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risk factors omphalocele
maternal smoking maternal age >40 yrs chromosomal abnormalities - triosomy,turners, klinefelters
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clinical features omphalocele
4-12cm abdo wall defects located centrally within umbilical cord protective membranes surroudning healthy intestines
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ddx omphalocele
gastroschisis cloacal exstrophy physiological gut herniation
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omphalocele investigations
clinical diagnosis prenatal USS or birth alpha fetoprotein elevated chromosomal abnormalities - chronic villus sampling or amniocentesis
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immediate management omphalocele
fluid resus temp NG tube neonatal ICU
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definitive management omphalocele
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
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complications omphalocele
ruptured abdominal compartmental syndrome
50
prevalence pyloric stenosis
1 in 500-1000 live births 4 males for every 1 female
51
pathophysiology pyloric stenosis
progressive hypertrophy of the pyloric muscle, causing gastric outlet obstruction. The aetiology remains unknown
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risk factors pyloric stensois
male family hxl
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clinical features pyloric stenosis
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
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ddx pyloric stenosis
Gastroenteritis Gastro-oesophageal reflux, including Sandifer syndrome Over-feeding
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investigations pylotic stenosis
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
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management pyloric stenosis
correct underlying metabolic abnormalities 10-20ml/kg fluid boluses NG tube - aspirated every 4 hrs Ramstedt's pyloromyotomy
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complications of pyloric stenosis
Pre-operative: Hypovolaemia Apnoea – secondary to hypoventilation associated with metabolic acidosis Post-operative: Wound dehiscence Infection Bleeding Perforation Incomplete myotomy
58
glioma define
all primary brain tumours that originate from neuroepithelial glial cells (including ependymal cells, astrocytes, oligodendrocytes and astrocytes)
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most common type of brain tumour in children
low grade glioma
60
clinical features glioma
seizures*, cranial nerve palsies or visual field defects, language dysfunction, or features of raised intracranial pressure.
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investigations glioma
CT with IV contrast biopsy to confirm
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low grade gliomas management
watch aand wait total or partial debulking radiotherapy
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high grade gliomas management
total or partial decompressive tumour debulking both chemo and radiotherapy
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prognosis glioma
low grade - 15-16yrs high - 15-18 mths
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hydrocephalus definition
the accumulation of cerebrospinal fluid (CSF) within the cerebral ventricles
66
hydrocephalus pathophysiology
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
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normal pressure hydrocephalus triad
triad of Parkinsonian gait, urinary incontinence, and dementia.
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clinical features hydrocephalus
N+V headache worse in morning altered GCS blurred vision abnormal gait incontineence papilloedema
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investigations hydrocephalus
CT - enlargement of ventricles, loss of sulcal gyral pattern, CSF exudation
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pattern of ventricular enlargement
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
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management hydrocephalus
insertion of external ventricular drain debulking of tumour, endoscopic third ventriculostomy or choroid plexis resection
72
routes of pathogen spread CNS infections
1) haematogenous spread via the choroid plexus, (2) direct extension from adjacent tissues, and (3) inoculation from interventional procedures or surgery
73
extradural abscess
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
subdural empyema
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
cerebral abscesses
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
ventriculitis
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
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clinical features CNS infections
new onset confusion reduced GCS headache features of sepsis raised ICP seizures pyrexia focal neurological deficit
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risk factors CNS infections
extremes of age, recent neurosurgical procedure, intravenous drug use, the presence of any long-term intracranial devices, or immunosuppresion
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investigations CNS infections
routine bloods blood cultures CSF samples CT
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management CNS infections
fluid resus IV abx hyperosmolar agents anti epileptics surgical intervention is definitive
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balanitis xerotica obliterans pathophysiology
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
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hx BXO
ballooning of foreskin during micrturition irritation dysuria haematuria local infection
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examination BXO
white, fibrotic scarred preputial tip hard to visualise meatus
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management BXO
circumcision foreskin to histopathology to confirm diagnosis
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complications BXO
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
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cryptochordism definition
failure of testicular descent into scrotum
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3 types of cryptochorisim
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.
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pathophysiology cryptochordism
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
risk factors cryptochordism
prematurity, low birth weight, having other abnormalities of genitalia (i.e. hypospadias) having a first degree relative with cryptorchidism.
90
hx cryptochoridism
if the testis has ever been seen or palpated within the scrotum, such as in the newborn check - warm bath?
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exam cryptochordism
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.
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cryptochordis ddx
normal retratile testis true undescended testis ectopic testis
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initial management cryptochordism
undescended testis associated with ambiguous genitalia or hypospadias, or bilateral undescended testis are found: urgent referral to senior paediatrician within 24 hours
94
monitoring cryptochordism
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.
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definitive management cryptochordism
examination under anaesthesia followed by laprascopy open orchidopexy if palpable if intra abdo - fowlder stephens procedure groin exploration if atrophic testis
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surgical complications cryptochoridism
infection bleeding wound dehiscence resricular atrophy testicular re ascent
97
complications of undescended testis
impaired fertility testicular cancer -2-3x more common torsion
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hydrocele definition
collection of fluid that builds up in the remnants of the processus vaginalis
99
2 types of hydrocele
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
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aetiology hydrocele
congenital malignancy testicular torsion trauma inection
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clinical features hydrocele
non-tender, smooth and transilluminates. There is notable scrotal enlargement following exertio
102
hydrocele ddx
inguinal hernia testicular cancer epididymitis
103
investigations hydrocele
USS scan but clinical diagnosis
104
management hydrocele
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
hypospadias definition
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
epidemiology hypospadias
1 in 300 male births incidence increasing
107
pathophysiology hypospadias
due to arrest of penile development, leading to hypoplasia of the ventral tissue of the penis
108
clinical features hypospadias
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
classification hypospadias
Glandular, coronal, shaft (distal, mid, proximal), scrotal, perineal
110
hypospadias risks
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
investigations hypospadias
Detailed history and examination Karyotype Pelvic ultrasound scan Urea and Electrolytes Endocrine hormones: Testosterone, 17 alpha-hyroxyprogesterone, LH, FSH, ACTH, renin, aldosterone
112
hypospadias management
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
short term complications hypospadias
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
long term complications hypospadias
urethral fistula meatal and urethral stenosis
115