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Y4 paeds > Surgery > Flashcards

Surgery Flashcards

1
Q

When is peak incidence of appendicitis

A

age 10-12

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2
Q

What causes appendicitis

A

Caused by luminal appendix obstruction by a faecolith, normal fecal matter or lymphoid hyperplasia due to a viral infection

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3
Q

What signs/ symptoms are on the paediatric appendicitis score?

A
  • cough/ percussion pain (2pts)
  • hopping tenderness in RLQ
  • anorexia
  • pyrexia
  • nausea/ vomiting
  • right iliac fossa tenderness
  • leukocytosis
  • polymorphonuclear neutrophilia
  • migration of pain
    >5 means appendicitis likely
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4
Q

Give 3 complications of appendicitis

A
  • perforation
  • appendix mas
  • appendic abscess
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5
Q

How is appendicitis managed

A
  • IV fluid resus, abx (piperacillin) and contact surgical team for appendectomy
  • pain control
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6
Q

What causes pyloric stenosis

A

progressive hypertophy of pyloric muscle causing gastric outlet obstruction

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7
Q

How does pyloric stenosis present

A
  • non billious projectile vomiting within 4-6 weeks of age
  • weightloss
  • dehydration
  • visible peristalsis
  • palpable olive sided pyloric mass, best felt during feeds
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8
Q

How should pyloric stenosis be investigated

A
  • test feed performed with NG tube in situ and stomach aspirated
  • USS shows hypertrophy of pyloric muscle
  • blood gasses: hypokalaemia, hypochloraemia, metabokic alkalosis is common due to loss of HCL from repeated vomiting
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9
Q

Give 2 pre op and 2 post op complications of pyloric stenosis

A

Pre: hypovolaemia, met alkalosis and then apnoeas due to hypoventilation because of this
Post: wound dehiscence, infection, bleeding, perforation

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10
Q

How is pyloric stenosis managed?

A
  • correct metabolic abnormalities
  • fluid boluses for hypovolaemia
  • stop oral feeding, pass NG tube and aspirate this 4hrly
  • rehydration
  • blood gasses and u&es done regulalry
  • ramstedt’s pyloromyotomy
  • resume feeding after 6 hrs
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11
Q

What is hirshprungs disease (describe pathophys)

A

Where ganglionic cells of the myenteric and submucosal plexuses in the bowel fail to develop in the large intestine.
The aganglionic segment remains in a tonic state leading to failure in peristalsis and bowel movements.
Faeces in the rectum fail to trigger relaxation of the internal anal sphincter, due to aganglionosis.
The accumulation of faeces in the rectosigmoid region is responsible for the functional obstruction.
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

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12
Q

how does hirshprungs present?

A
  • depends on extent of disease- may be just short section of aganglionic bowel or whole bowel
  • will usually have failure to pass meconium in first 48hrs
  • constipation
  • abdominal distension and vomiting
  • rectal exam reveals empty rectal vault
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13
Q

How is hirschprungs definitively managed?

A

surgery to remove the aganglionic section of bowel

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14
Q

What is a congenital diaphragmatic hernia and what happens because of it?

A
  • developmental defect allowing hernatin of abdominal contents into thorax
  • leads to impaired lung development- pulmonary hypoplasia
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15
Q

How does a congenital diaphragmatic hernia present?

A
  • difficult resus at birth
  • resp distress
  • bowel sounds heard in chest
  • ph <7.3
  • cyanosis
  • associated with trisomy 18 and neural tube defects
  • many picked up on USS before birth
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16
Q

How is a congenital diaphragmatic hernia managed if picked up before and after birth

A

Before: refer to neonate tertiary centre for support at birth- they obstruct trachea w/ balloon surgery
After: insert large bore NG tube when diagnosis is suspected, intubate immediatly to stop air going into bowel & compressing heart and lungs, ventilate gently to prevent pneumothorax, may need ecmo while lung develop. Surgery is needed to reduce the hernia

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17
Q

How urgently should inguinal hernias be repaired in paediatrics?

A

6/2 rule:

  • <6 weeks operate within 2 days
  • <6 months operate within 2 weeks
  • <6 years operate within 2 years
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18
Q

What is intussusception and what age group does it occur in

A

One segment of the bowel invaginates into another, just distal, leading to obstruction and mesentery compression. Occurs in 5-12 month olds usually.

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19
Q

How does intussusception present?

A
  • colicky abdo pain
  • episodic intermittent inconsolable crying
  • early vomiting
  • pr bleed
  • sausage shaped abdo mass
  • dehydration
  • irritable
  • dances sign: absence of bowel in RLQ
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20
Q

How is intussusception managed?

A
  • AXR (RLQ opacification and perforation)
  • drip and suck resus
  • US with reduction by air enema
  • laparoscopic/ laparotomy reduction if enema fails or signs of perforation/ peritonitis
  • CT for lymphoma if age >2
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21
Q

What is gastroschisis

A

congenital defect of the abdominal wall, usually to the right of the umbelical cord insertion, Abdominal contents herniate into the amniotic sac, usually just involving the small intestine but sometimes also the stomach, colon and ovaries. There is no membrane covering.

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22
Q

How is gastroschisis managed?

A
  • cover exposed bowel in cling film at delivery
  • keep baby warm and well hydrated
  • corrective surgery- may be needed to be done in stepwise procedure if abdomen is too small
  • intestinal function is slow to resume and the baby may require TPN for several weeks
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23
Q

What is omphalocele/ exomphalos?

A
  • contents of abdomen herniate into umbilical cord through umbilical ring
  • peritoneum and amnion cover the organs
  • if small may only contain a meckles diverticulum but if larger may contain the stomach, liver and bladder
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24
Q

How is omphalocele managed?

A
  • protect herniated viscera
  • maintain fluid and electrolytes
  • prevent hypothermia
  • gastric decompression
  • prevention of sepsis
  • primary or staged closure
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25
Q

What is oesphageal atresia with TOF?

A

Oesophageal atresia is a congenital abnormality in which there is a blind ending oesophagus.
It can occur in isolation or with one/ more fistulae communicating between the abnormal oesophagus and the trachea, known as a tracheo-oesophageal fistula (TOF)

26
Q

What is vacterl syndrome?

A

3 or more of:

  • vertebral defects eg scoliosis
  • anorectal malformations eg imperforate anus
  • CVS defects: ventricular septal defects
  • oesphageal defects with or w/out TOF
  • renal abnormalities
  • limb deformities
27
Q

How can you distinguish between oesphageal atresia and oesphaeal atresia with TOF?

A

CXR: shows it coiled oesophagus, no air seen in GI= oesophageal atresia + NO TOF. Air in oesophageal pooch= TOF

28
Q

What are the clinical features of oesophageal atresia

A
  • polyhydramnios can be early indicator
  • resp distress
  • recurrent cough
  • increased secretions
  • distended abdomen
  • aspiration and feeding problems
  • impossible to pass NG tube
  • cardiac and other defects often common alongside it
29
Q

How is oesophageal atresia managed?

A
  • stop feeding
    W/ TOF:
  • pre op bronchoscopy can help identify and locate fistula
  • open thoracotomy, fistula tied off and oesphageal anastomosis created between disconnected upper and lower segments
    No TOF:
  • gastrostomy so feeding is possible
  • suctioning of blind ending to prevent aspiration
  • prophylactic abx may be needed
  • then surgery performed to anastomose ends
30
Q

How should malrotation be investigated?

A
  • AXR- usually normal unless complicated

- contrast studies show DJ junction is misplaced

31
Q

How does malrotation present?

A
  • non rotation may be asymptomatic
  • malrotation often leads to intermittent symptoms of obstruction but if a full volvulus develops the obstruction will be complete
  • failure to thrive, anorexia, constipation, blood stools and intermittent apnoea may also be presenting complaints
  • older children may present with cyclical vomiting, recurrent abdo pain, protein - calorie malnutrition or immunodeficiency
32
Q

How is malrotation managed?

A
  • Ladd’s procedure indicated in all even if asymptomatic due to volvulus risk
33
Q

What is acute bacterial adenitis

A
  • characterized by larger nodes >10mm, which are tender and fluctuate.
  • Often associated with fever and warm, erythematous overlying skin.
  • caused by staph aureus or Group A strep
34
Q

What could cause persisting adenitis (>2 weeks)

A 
• Atopic eczema 
• Infectious mononucleosis (EBV), cytomegalovirus
• Mycobacterium tuberculosis
- HIV
• Lymphoma - Hodgkins, Non-Hodgkins
•Leukaemia
•Juvenile chronic arthritis
•SLE
•Kawasaki Disease - unilateral, >15mm, painful nodes
35
Q

How is acute acute adenitis managed?

A
  • if well= oral fluclox for 10 days

- if unwell, neonate or failed oral abx= IV fluclox

36
Q

What causes balanitis xerotica obliterans

A

A skin irritation on the head of the penis- keratinization of the tip of the foreskin causes scarring and the prepuce remains non- retractile- is the leading cause of phimosis.
Peak incidence is 9-11 years
(normal to have non- retractable foreskin aged 2-4- this self-resolve as the prepuce becomes more mobile)

37
Q

How does balanitis and BXO present?

A
  • penile soreness and itching, ouder, diabetes, bleeding, redness, dysuria, difficulty passing urine, non retractile foreskin
  • BXO presents with scaring of urethral meatus irritation, dysuria, haematuria, local infection, ballooning of foreskin during micturition due to subsequent phimosis
  • appear as white, fibrotic and scarred preputial tip- difficult to view meatus
38
Q

how is balanitis XO managed?

A
  • BXO managed with circumcision
  • topical abx to help reduce infection
  • emollients
  • untreated BXO can also lead to meatal stenosis, phimosis, erosions of glands and prepuce and can extend to the urethra
39
Q

What is hypospadias?

A
  • congenital abnormality causing the urethral meatus to be located in an abnormal site
  • usually on underside of the penis rather than tip, due to arrest of penile tissue causing hypoplasia of the ventral tissue of the penis
40
Q

How are hydrospadias classified?

A

By location on penis:

  • glandular
  • coronal
  • distal penile
  • midshaft
  • proximal penile
  • penoscrotal
  • scrotal
  • perineal
41
Q

How does congential adrenal hyperplasia present and what is dangerous about it?

A
  • presents with ambiguous genitalia
  • procosious puberty
  • hair growth early
  • high 17 hydroxyprogesterone
  • can lead to salt wasting crisis due to cortisol and aldosterone deficiency with androgen excess
  • skin pigmentation esp of genitalia
42
Q

How is hypospadias managed?

A
  • urethroplasty: brings the meatus to the glands of the penis, the chordee is also corrected to straighten the penis. The foreskin is either circumcised or reconstructed.
  • if very distal they can sometimes be left alone
43
Q

What is cryptorchidism

A

Undescended testis.
True undescended testis: testis is absent from the scrotum but lies along the line of testicular descent
Ectopic testis: 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

44
Q

What could cause bilateral undescended testis?

A
  • could be idiopathic

- but need to rule out hormonal causes eg androgen insensitivity syndrome and disorders of sex development

45
Q

Give 4 risk factors for cryptorchidism

A
  • prem
  • low birth weight
  • other genitalia abnormalities such as hypospadias
  • having fist degree relative with cryptorchidism
46
Q

How is cryptorchidism managed?

A
  • If bilateral or other features and DSD/ AIS suspected, refer urgently to paeds urology and endocrinology
  • if not review at 6-8 weeks of age as many will descend on their own
  • if unilateral but undescended at this point then wait till 3 months
  • if undescended at this point then refer for surgical correction (will be done between 6-12 months of age)
  • if descended, still needs annual follow up due to risk of ascending testis
47
Q

How does testicular torsion present

A

• Severe sudden onset pain in the affected testicle – makes walking uncomfortable.
• Abdominal pain
• Nausea or vomiting due to the pain
O/E:
• One testis is very hot, tender and inflamed
• Affected testicle usually lies higher and transversely in the scrotum due to the torsion of the cord
• Absent or decrease in cremasteric reflex

48
Q

Give 3 differentials for testicular torsion

A
  • epidiymo- orchitis
  • tumour
  • trauma
  • hydrocele
  • idiopathic scrotal odema (age 2-10 yrs)
  • epididymal appendage (7-12 yrs- can cause less pain and a blue dot visible under scrotum)
49
Q

How is testicular torsion managed?

A
  • analgesia
  • manual rotation of testicle
  • orchidectomy if testis necrotic
  • or testis not necrotic, untwist and fix both to scrotum to stop reoccurring
50
Q

Give 2 RFs for testicular torsion?

A
  • bell clapper deformity (tunica vaginalis joins high on the spermatic cord and wraps almost all the way around leaving the testis free to rotate)
  • cold temperatures
51
Q

Give 5 differentials for testicular masses and how you’d distinguish between them

A

• Cannot get above the lump – inguinoscrotal hernia
• If separate and cystic in nature – epididymal cyst
• If separate and solid – epididymitis or varicocele
• If testicular and cystic – hydrocele
If testicular and solid – tumour, haematocele, granuloma, orchitis

52
Q

How are epididymal cysts managed?

A
  • remove only if has symptoms
53
Q

How are primary hydroceles managed

A

If from birth and associated with patent processus vaginalis: typically resolves in 1st year of life but if it remains >2 yrs then operation indicated.
Theyre more common in younger men, and resolved spontaneously.
Can be secondary to tumour, trauma or infection and can be aspirated or do surgery in this setting.

54
Q

What can cause epididymo- orchitis?

A
  • chlamydia
  • ecoli
  • mumps
  • gonorrhoea
  • tb
55
Q

How does epididymo- orchitis present and how is it investigated?

A
  • sudden onset tender testicular swelling, dysuria, sweats, fever
  • first catch urine sample and look for urethral discharge and screen for STIs
  • abx depends on causative organism
56
Q

What is a varicocele and how are they managed?

A
  • dilated veins of pampinform plexus, left sided more commonly affected
  • feels like bag or worms and get dull ache
  • associated with subfertility
  • surgery and embolisation have little effects
57
Q

What is haematocele and how are they managed?

A
  • blood in tunica vaginalis following trauma

- needs excision and drainage

58
Q

Give 3 differentials for failure to pass meconium?

A
  • hirshprungs
  • ileal atresia
  • meconium ileus (swallowed meconium and causes obstruction) (CF)
  • volvulus
59
Q

How is hirshprungs diagnosed?

A

Sub-mucosal (suction biopsy) or a full thickness rectal biopsy in association with either anorectal manometry or barium enema.
Fuctional obstruction= proximal dilated colon and a distal normal appearing segment which is seen as a transition zone on a barium enema.

60
Q

How is balanitis managed?

A
  • swabs and topical hydrocortisone cream if no improvment in 6 days
  • Hba1c and HIV test
  • clean with water and nappy change freqently
  • bacterial= oral fluclox
  • candidal= imidazole cream
  • irritant/ contact dermatitis= hydrocortisone cream, emollients

Y4 paeds (14 decks)

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