Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Child Health > GI Surgery > Flashcards

GI Surgery Flashcards

1
Q

Appendicitis

A 
Inflammation of appendix 
Gangrene and rupture
Releases faecal contents and infective material into abdomen 
Peritonitis 
Peak age 10-20
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pathophysiology of appendicitis

A

Typically caused by direct luminal obstruction
Secondary to faecolith or lymphoid hyperplasia, impacted stool, appendiceal or caecal tumour
Bacteria multiple, acute inflammation
Reduced venous drainage and localised inflammation
Increased pressures in appendicitis
Ischaemia
Necrosis
Perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Risks factors for appendicitis

A

FH
Ethnicity: Caucasians more common, but ethnic minorities greater risk of perforation
Environmental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Symptoms of appendicitis

A 
Abdominal pain: periumbilical (dull, poorly localised) —> RIF (localised and sharp)
Vomiting
Anorexia
Nausea 
Diarrhoea
Constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Signs of appendicitis

A 
Rebound tenderness (peritonitis)
Percussion pain over McBurney’s point (peritonitis)
Guarding, perforated
Sepsis: tachycardia and hypotension
Appendiceal abscess: RIF mass
Rovsing’s sign
Psoas sign
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Rovsings sign

A

RIF fossa pain on palpation of LIF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Psoas sign

A

RIF pain with extension of right hip

Inflamed appendi abutting psoas major muscle in a retrocaecal position

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acute appendicitis in children

A

Atypical presentations
Check all systems
Genital examination in boys

<6 years and >48hours of symptoms likely to be perforated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

DD of appendicitis

A 
Ectopic pregnancy
Ovarian cysts
Meckel’s diverticulum 
Mesenteric adenitis 
Constipation
Gastroenteritis
Intussusception 
UTI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Ectopic pregnancy

A

Gynaecological emergency

Serum/urine bHCG to exclude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ovarian cysts

A

Pelvic and iliac fossa pain

Especially with rupture or torsion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Meckel’s diverticulum

A

Malformation of distal ileum
2% of population
Can bleed, become inflamed or cause volvulus/ intussusception
Often removed prophylactically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mesenteric adenitis

A

Inflamed abdominal lymph nodes
Abdominal pain, usually in younger children
Associated with tonsillitis or URTI
No treatment required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Laboratory tests for appendicitis

A 
Urinalysis 
Pregnancy test
FBC, CRP
Serum b-HCG
USS if inconclusive 
CT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Risk stratification score appendicitis

A

Shera score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Management of appenditicits

A

Emergency admission to hospital under surgical team
Laparoscopic appendicectomy
Send appendix to histopathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Complications of appendicectomy

A 
Bleeding, infection, pain, scars
Damage to bowel, bladder or other organs
Removal or a normal appendix 
Anaesthetic risks
Venous thromboembolism 
Perforation
Appendix mass: omentum and small bowel adhere to appendix 
Pelvic abscess: fever with palpable RIF mass, mx with ax and drainage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pyloric stenosis pathophysiology

A

Progressive hypertrophy of pylorus
Gastric outlet obstruction
Food ejected into oesophagus
Projective vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Risk factors for pyloric stenosis

A

Male gender

FH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Clinical features of pyloric stenosis

A 
Presents at 4-6weeks
Non-bilious vomiting after every feed
Hungry baby, thin, pale, fails to thrive
Projectile vomiting
Firm round mass in upper abdomen, peristalsis, olive-sized pyloric mass best felt during feed
Haematemesis
Weight loss and dehydration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Blood gas analysis of pyloric stenosis

A

Hypochloric metabolic alkalosis
Baby vomiting HCl

Hypokalaemia as kidneys exchange potassium to retain protons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

DD of pyloric stenosis

A 
Gastroenteritis 
GORD
Over-feeding
Sepsis
UTI
Food allergy
Malrotation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Investigations for pyloric stenosis

A

Test feed with NG in-situ
Stomach aspirated
Palpate for pyloric mass whilst child is feeding
Observe for visible peristalsis
Abdominal USS: hypertrophy of pyloric muscle >3mm thickness, >15mm in length, diameter >11mm
Blood gases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Management of pyloric stenosis

Peri-operative

A

Correct metabolic abnormalities
Patients may required 10-20ml/kg fluid boluses for acute hypovolaemia
Oral feeding should be stopped
NG tube passed and aspirated at 4 hourly intervals
Rehydration at 150ml/kg/day, using crystalloid
Blood gases and U&Es

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Operative management of pyloric stenosis

A

Ramstedt’s pyloromyotomy
Only once fluid and electrolyte abnormalities have been corrected

Laparoscopically or through a supra-umbilical incision
Muscle divided along down to the mucosa
Successful in majority of patients
Babies can resume feeding after 6 hours, may be some residual vomiting
Post-op vomiting common after surgery, due to gastric distension and dysmotility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Complications of pyloric stenosis

A

Pre-op:
Hypovolaemia
Apnoea; hypoventilation from metabolic acidosis

Post-op:
Wound dehiscence
Infection
Bleeding
Perforation
Incomplete myotomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hirschsprung’s disease

A

Congenital aganglionic mega colon disease
Ganglionic cells fail to develop in the large intestine
Delayed or failed passage of meconium around birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hirschsprung disease epidemiology

A

2 days most cases
Male: female 4:1
Genes: RET signalling pathway, endothelin TYB receptor pathway
Receptor tyrosine kinase gene: proto-oncogene on chromosome 10q11
Associated with trisomy 21

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Subtypes of Hirschsprung’s disease

A

Short-segment:
Long-segment:
Total colonic aganglionosis disease;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Short-segment Hirschsprung’s

A

Aganglionosis is restricted to rectosigmoid portion of colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Long-segment Hirschsprung’s

A

Aganglionosis extends past rectosigmoid portion of the colon to the splenic flexure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Total colonic aganglionosis

A

Entire colon affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Pathophysiology of Hirschsprung’s

A

Parasympathetic Ganglionic cells of myenteric and submucosal plexuses in bowel aren’t present proximally from anus to a variable length along large intestine

Arrest of neuroblast from neural crest cell migration in week 8-12 of foetal development
Fails to develop properly: apoptosis, improper differentiation, failure in proliferation

Failure of peristalsis and bowel movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Pathophysiology of Hirschsprung’s enterocolitis

A 
Aganglionic segment
No peristalsis or bowel movements
Faeces fail to trigger relaxation of internal anal sphincter
Accumulation of faeces in rectosigmoid region 
Functional obstruction
Proximal bowel dilatation
Abdominal distension 
Increased intraluminal pressure
Decreased blood flow 
Deterioration in mucosa layer 
Stasis-> bacterial proliferation
Hirschsprung’s enterocolitis
Sepsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Enteric nervous system

A

Vagal segment of neural crest cells which migrate along vagus nerve to enter foregut mesenchymal in cranial-> caudal direction
Myenteric (Auerbach’s plexus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Risk factors

A

Males
Chromosomal abnormalities: Down’s syndrome
Neurofibromatosis
Waardenburg syndrome
MEN TY2
FH: due to mutations in RETproto-oncogene on chromosome 10q11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Clinical features

A 
Delay in passing meconium >48hrs
Abdominal distension and pain
Bilious vomiting
Poor weight gain and failure to thrive
Faecal mass in LLQ
Tympanic abdomen 
Empty rectal vault
Chronic constipation since birth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Triad of Hirschsprung’s

A

Failure to pass meconium
Abdominal distension
Bilious vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Hirschsprung’s-associated enterocolitis

A

Inflammation and obstruction of intestine occurring in 20% of neonates with the disease
Presents 2-4 weeks with fever, abdominal distension, sepsis features, diarrhoea
Life-threatening and can lead to toxic mega colon and perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Hirschsprung’s-associated enterocolitis mx

A

Ax
Fluid resuscitation
Decompression of obstructed bowel

Stool culture
AXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

DD of Hirschsprung’s disease

A 
Meconium ileus 
Intestinal atresia
Intestinal malrotation
Anorectal malformation
Constipation
Meconium plug syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Meconium plus syndrome

A

Symptoms pass after passage of plus

Can be differentiated by barium enema or water-soluble contrast enema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Meconium ileus

A

Distal small bowel impacted by meconium
Abdominal distension and failure to pass meconium
Can be differentiated by radiograph, barium enema, water-soluble contrast enema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Intestinal atresia

A

Congenital malformation
Complete obstruction
Usually involve abdominal distension and failure to pass meconium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Intestinal malrotation

A

Congenital anomaly in the rotation of the midgut during embryological development
Midgut volvulus: bilious vomiting and abdominal distension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Anorectal malformation

A

Anal stenosis
Imperforate anus
Failure to pass meconium and abdominal distension
Can be differentiated by physical examination of rectum that reveals malformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Investigations of Hirschsprung’s

A

Contrast enema: determine transition zone in HD, extent of aganglionosis. Contraindicated in perforation, then need laparotomy

Gold standard: rectal suction biopsy
Test submucosa for ganglionic cells
Without risks associated with general anaesthetic
Give adequate ax and good decompression of bowel
Washouts cannot be performed for 24hrs after procedure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Contrast enema findings Hirschsprung’s

A

Short transition zone between proximal end of colon and narrow distal end of colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Rectal suction biopsy

A

Stain biopsy for acetylcholinesterase
Calretinin staining
Confirm aganglionis, no ganglion cell in both the submucosal and myenteric plexus
Severe hypertrophied nerve bun does that stain positive for acetylcholinesterase
Risk of perforation, bleeding and inadequate sample

50
Q

Rectal suction biopsy should be avoided unless the following clinical features are present

A

Delayed passage of meconium (>48hrs)
Constipation since first few weeks of life
Chronic abdominal distension plus vomiting
FH of Hirschsprung’s
Faltering growth in addition to any of the previous features

51
Q

Mx of Hirschsprung’s

A

IV ax
NG tube insertion
Bowel decompression
Surgery as definitive treatment

52
Q

Surgery for Hirschsprung’s

A

Pull-through procedures:
Swenson
Soave
Duhamel

Resect aganglionic section of bowel
Connect unaffected bowel to dentate line

53
Q

Complications of Hirschsprung’s

A

Hirschsprung’s associated enterocolitis: C.dif, staph aureus, anaerobes
Enterocolitis

Surgery complications:
Constipation
Enterocolitis
Perianal abscess
Faecal soiling
Adhesions
54
Q

Intussusception

A

Telescoping of one part of the bowel into another

Proximal segment: intussusception
Distal segment: intussucipiens

55
Q

Epidemiology of intussusception

A

5-7 months of age

Boys: girls 2:1

56
Q

Pathophysiology of intussusception

A

Intestinal obstruction
90% cases are ileo-colic type
Distal ileum passes into caecum through ileo-caecal valve

57
Q

Risk factors for intussusception

A 
Meckel’s diverticulum 
Polyps
HSP
Lymphomas 
CF
Concurrent viral illness
Post-operative

Consider pathological cause if child is older or has a high recurrence

58
Q

History of intussusception

A

Sudden onset of inconsolable crying episodes
Pallor can be observed
Draw knees into chest
Child returns to normal in between episodes
Lethargic and anorexia
Red-current stools, blood and mucus

Older children: vomiting and abdominal pain

59
Q

Examination of intussusception

A 
Distension
Palpable sausage-shaped abdominal mass in RUQ
Signs of peritonism
Bowel sound 
Check for dehydration/ shock
60
Q

DD of intussusception

A 
Colic 
Testicular torsion
Appendicitis 
Gastroenteritis
Volvulus
61
Q

Diagnosis of intussusception

A

Abdominal US

AXR not recommended due to low sensitivity

Contrast enema

62
Q

AXR intussusception

A

Distended small bowel loops
A curvilinear outline of intussusception
Absence of bowel gas in colon distal to intussusception site
Rigler’s sign if perforation has occurred

63
Q

Abdominal US

A

Doughnut/ target sign on a transverse plane

Pseudo kidney sign on a longitudinal plane

64
Q

Management of intussusception

A

Fluid resuscitation
NG tube to decompress obstructed bowel
Non-operative reduction
Surgical reduction

65
Q

Non-operative reduction

A

Air or contrast enema
Performed by radiologist or paediatric surgeon at time of diagnosis with USS

Contraindications:
Perforation
Peritonitis
Uncorrected shock

66
Q

Surgical reduction

A

If contraindications to enema or enema intervention is unsuccessful
Surgery required to manually reduce intussusception
Resection of areas of necrotic bowel

67
Q

Complications of intussusception

A

Obstruction: surgical emergency
Perforation: blood vessels stretched and constricted, venous congestion, oedema, bowel necrosis and perforation, sepsis
Dehydration and shock: fluid and bowel contents can collect within the intussuception, dehydration and hypovolaemic shock

68
Q

Biliary atresia

A

Section of bile duct is narrowed or absent
Cholestasis
Conjugated bilirubin excreted

69
Q

Pathogenesis of biliary atresia

A

Infectious agents
Congenital malformations
Retained toxins within bile

70
Q

Epidemiology of biliary atresia

A

Extrahepatic biliary atresia more common in females than males
Unique to neonatal children: perinatal form in first two weeks, postnatal form in first 2-8weeks

71
Q

TY1 biliary atresia

A

Proximal ducts patent but common duct obliterated

72
Q

TY2 biliary atresia

A

Atresia of cystic duct and cystic structures are found in portal hepatic

73
Q

TY3 biliary atresia

A

Atresia of left and right ducts to the level of the porta hepatic
Occurs in 90% of cases of biliary atresia

74
Q

Presentation of biliary atresia

A

Presents in first few days of life
Jaundice extending beyond physiological 2 weeks
Dark urine and pale stools
Appetite and growth disturbance

75
Q

Signs of biliary atresia

A

Jaundice
Hepatomegaly with splenomegaly
Abnormal growth
Cardiac murmurs if associated cardiac abnormalities present

76
Q

Investigations biliary atresia

A

Serum bilirubin: conjugated and total
LFT: serum bile acids, aminotransferase
Serum alpha 1-antitrypsin: neonatal cholestasis if deficiency
Sweat chloride test: CF affected biliary tract
USS of biliary tree and liver
Percutaneous liver biopsy with intra-operative cholangioscopy

77
Q

Management of biliary atresia

A

Surgical intervention: Kasai portoenterostomy
Dissection of the abnormalities into distinct ducts and anastomosis creation
Medical intervention: ax coverage and bile acid enhancers following surgery

78
Q

Complications of biliary atresia

A

Unsuccessful anastomosis formation
Progressive liver disease
Cirrhosis with eventual hepatocellular carcinoma

79
Q

Prognosis of biliary atresia

A

Good prognosis if surgery successful

Liver transplant may be required in first 2 years of life

80
Q

Abdominal mass

A 
AAA
Benign tumour
Bowel obstruction
Cancer
Cholecystitis
Congenital anomaly
Diverticulitis 
Enlarged organ
Hydronephrosis
Infection 
Ovarian cysts
Traumatic injury
Uterine fibroids
81
Q

Adrenal causes of abdominal mass

A 
Adrenal carcinoma
Nueroblastomas
Phaeochromocytoma
Adrenal adenoma
Adrenal haemorrhage
82
Q

Gallbladder causes of abdominal mass

A

Leiomyosarcoma
Choledochal cyst
Gall-bladder obstruction
Hydrops

83
Q

GI causes of abdominal mass

A 
Leiomyosarcoma
Non-Hodgkin lymphoma
Appendiceal abscess
Intestinal duplication
Faecal impaction
Meckel’s diverticulum
84
Q

Kidney causes of abdominal mass

A 
Lymphomatous nephromegaly
Renal cell carcinoma
Renal neuroblastoma
Wilms tumour
Hydronephrosis
Multicystic kidney
Polycystic kidney
Mesoblastic nephorma
Renal vein thrombosis
Hamartoma
85
Q

Liver causes of abdominal mass

A 
Hepatoblastoma
Hepatocellular carcinoma
Embryonal sarcoma
Liver metastases
Mesenchymoma 
Focal nodular hyperplasia
Hepatitis
Liver abscess
Storage disease
86
Q

Lower genitourinary tract causes of addo mass

A 
Ovarian germ cell tumour
Rhabdomyosarcoma of bladder
Rhabdomyosarcoma of prostate
Bladder obstruction
Ovarian cysts
Hydrocolpos
87
Q

Spleen causes of abdominal mass

A 
Acute or chronic leukaemia
Histiocyte sis
Hodgkin lymphoma 
Non-Hodgkin lymphoma 
Congestive splenomegaly
Histiocytosis
Mononucleosis 
Portal HTN
Storage disease
88
Q

Miscellaneous causes of abdo mass

A 
Hodgkin lymphoma
Non-Hodgkin lymphoma
Pelvic neuroblastoma
Retroperitoneal neuroblastoma
Retroperitoneal rhabdomyosarcoma
Retroperitoneal germ cell tumour
Teratoma
Abdominal hernia
Pyloric stenosis
Omental or Mesenteric cyst
89
Q

Intestinal obstruction

A 
Physical obstruction 
Prevents flow of faeces through the intestines
Back pressure through GI system
Vomiting
Absolute constipation
90
Q

Causes of intestinal obstruction

A 
Meconium ileus
Hirschsprung’s disease
Oesophageal atresia 
Duodenal atresia 
Intussusception
Imperforate anus
Malrotation of intestines with a volvulus
Strangulated hernia
91
Q

Causes of bilious vomiting in neonates

A 
Duodenal atresia 
Malrotation with volvulus
Jejunum/ ileal atresia
Meconium ileus
Necrotising enterocolitis
92
Q

Presentation of intestinal obstruction

A 
Persistent vomiting
Bilious
Abdominal pain and distension
Failure to pass stools or wind
Abnormal bowel sounds: high-pitched and tinkling
93
Q

Diagnosis of intestinal obstruction

A

AXR
Dilated loops of bowel proximal to obstruction
Collapsed loops of bowel distal to obstruction
Absence of air in rectum

94
Q

Management of intestinal obstruction

A

Paediatric surgical unit
NBM
NG tube to drain stomach and stop vomiting
May also require IV fluids to correct any dehydration and electrolyte disturbance
Keep hydrated while waiting for definitive management

95
Q

Duodenal atresia

A

Higher rate in Down’s syndrome
Presents few hours after birth
AXR: double bubble sign

96
Q

Duodenal atresia mx

A

Duodenoduodenostomy

97
Q

Malrotation with volvulus

A

Caused by incomplete rotation during embryogenesis
Presents 3-7days after birth, peritoneal signs and haemodynamic instability
Upper GI contrast study, DJ flexure is more medially placed, USS may show abnormal orientation of SMA and SMV

98
Q

Malrotation with volvulus

A

Ladd’s procedure

99
Q

Jejunal/ ileal atresia

A

Usually caused by vascular insufficiency in utero
Presents within 24hours of birth
AXR will show air-fluid levels

100
Q

Jejunal/ ileal atresia mx

A

Laparotomy with primary resection and anastomosis

101
Q

Meconium ileus

A

Higher in CF
Presents 24-48 hours
Abdominal distension and bilious vomiting
IX: air-fluid levels on AXR, sweat test for confirm CF

102
Q

Meconium ileus mx

A

Surgical decompression

Damage may require surgical resection

103
Q

Necrotising enterocolitis

A

Risks increased in prematurity and inter-current illness
Presents in second week of life
Dilated bowel loops on AXR
Pneumatosis and portal venous air

104
Q

Management of necrotising enterocolitis

A

Conservative and supportive for non-perforated cases

Laparotomy and resection in cases of perforation of ongoing clinical deterioration

105
Q

Causes of paralytic ileus

A 
Chest infections
MI
Stroke 
AKI
Electrolytes: K, Mg, PO4
Surgeries 
Replace electrolytes IV
106
Q

Embryology of paediatric umbilical disorders

A

Umbilicus has two umbilical arteries and one umbilical vein
Arteries continuous with internal iliac arteries
Vein continuous with falciform ligament (ductus venosus)
After birth, cord dessicates and separates and umbilical ring closes on

107
Q

Umbilical hernia

A

Up to 20% of neonates may have an umbilical hernia, it is more common in premature infants. The majority of these hernias will close spontaneously (may take between 12 months and three years). Strangulation is rare.

108
Q

Paraumbilical hernia

A

These are due to defects in the linea alba that are in close proximity to the umbilicus.
The edges of a paraumbilical hernia are more clearly defined than those of an umbilical hernia.
They are less likely to resolve spontaneously than an umbilical hernia.

109
Q

Omphalitis

A

This condition consists of an infection of the umbilicus.
Infection with Staphylococcus aureus is the commonest cause.
The condition is potentially serious as infection may spread rapidly through the umbilical vessels in neonates with a risk of portal pyaemia, and portal vein thrombosis.
Treatment is usually with a combination of topical and systemic antibiotics.

110
Q

Umbilical granuloma

A

These consist of cherry red lesions surrounding the umbilicus, they may bleed on contact and be a site of seropurulent discharge.
Infection is unusual and they will often respond favourably to chemical cautery with topically applied silver nitrate.

111
Q

Persistent urachus

A

This is characterised by urinary discharge from the umbilicus. It is caused by persistence of the urachus which attaches to the bladder. They are associated with other urogenital abnormalities.

112
Q

Persistent Vitello-intestinal duct

A

This will typically present as an umbilical discharge that discharges small bowel content.
Complete persistence of the duct is a rare condition. Much more common is the persistence of part of the duct (Meckel’s diverticulum).
Persistent vitello-intestinal ducts are best imaged using a contrast study to delineate the anatomy and are managed by laparotomy and surgical closure.

113
Q

Umbilical hernia associations

A

Afro-caribe a
Down’s syndrome
Mucopolysaccharide storage disease

114
Q

Inguinal hernias

A

Common in children

Commoner in male

115
Q

Inguinal hernia pathophysiology

A

They are commoner in males as the testis migrates from its location on the posterior abdominal wall, down through the inguinal canal. A patent processus vaginalis may persist and be the site of subsequent hernia development.

116
Q

Management of inguinal hernia

A

Children presenting in the first few months of life are at the highest risk of strangulation and the hernia should be repaired urgently.
Children over 1 year of age are at lower risk and surgery may be performed electively.
For paediatric hernias a herniotomy without implantation of mesh is sufficient.
Most cases are performed as day cases, neonates and premature infants are kept in hospital overnight as there is a recognised increased risk of post operative apnoea.

117
Q

Malrotation

A

High caecum at midline
Feature in exophthalmos, congenital diaphragmatic hernia, intrinsic duodenal atresia
Volvulus may develop

118
Q

Pathophysiology of Meckel’s diverticulum

A

normally, in the foetus, there is an attachment between the vitellointestinal duct and the yolk sac. This disappears at 6 weeks gestation
the tip is free in the majority of cases
associated with enterocystomas, umbilical sinuses, and omphaloileal fistulas.
arterial supply: omphalomesenteric artery.
typically lined by ileal mucosa but ectopic gastric mucosa can occur, with the risk of peptic ulceration. Pancreatic and jejunal mucosa can also occur.

119
Q

Management of Meckel’s diverticulum

A

removal if narrow neck or symptomatic. Options are between wedge excision or formal small bowel resection and anastomosis.

120
Q

Presentation of Meckel’s

A

abdominal pain mimicking appendicitis
rectal bleeding
Meckel’s diverticulum is the most common cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years
intestinal obstruction secondary to an omphalomesenteric band (most commonly), volvulus and intussusception

121
Q

Meckel’s diverticulum

A

Meckel’s diverticulum is a congenital diverticulum of the small intestine. It is a remnant of the omphalomesenteric duct (also called the vitellointestinal duct) and contains ectopic ileal, gastric or pancreatic mucosa

122
Q

Meckel’s 2s

A

occurs in 2% of the population
is 2 feet from the ileocaecal valve
is 2 inches long

Child Health (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions