Paeds - Surgery (teachmepaeds) Flashcards
(44 cards)
What is the pathophysiology of appendicitis?
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
How would appendicitis typically present?
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)
What are some investigations you would do for suspected appendicitis?
1st line = US to minimise radiation exposure in kids
(CT Can help)
Urinalysis + preg test in women
FBC, CRP, B-HCG
What risk stratification score would you use in kids?
Shera Score
How would you manage appendicitis?
Gold standard = Laparoscopic appendectomy
What is Hirschsprung’s disease?
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
How would Hirschsprung’s disease present?
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
What is the pathophysiology of Hirschsprungs?
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.
What are some differentials for Hirschsprungs?
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)
How would you investigate Hirschsprungs?
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)
How would you manage Hirschsprungs?
IV Antibiotics
NG Tube
Bowel decompression
Surgery to resect aganglionic section of bowel and connect the unaffected bowel to the dentate line
What is intussusception?
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
How would intussusception present in a child?
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
How would you investigate suspected intussusception?
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.
How would you manage intussusception?
Fluid Resus, NG can help decompress
Non surgical = Air or contrast enema to reduce intussuscepted bowel
Surgical reduction = reduce bowel and resect necrotic areas.
What is pyloric stenosis?
progressive hypertrophy of pyloric muscle causing gastric outlet obstruction.
How does pyloric stenosis present?
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)
How would you investigate pyloric stenosis?
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)
How would you manage pyloric stenosis?
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)
Define Balanitis Xerotica Obliterans
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.
How would BXO present?
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)
How would you manage BXO?
Circumcision
Send foreskin to histopathology
What is Cryptorchidism?
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)
How would cryptorchidism present?
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
