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
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
3
Q
Risks factors for appendicitis
A
FH
Ethnicity: Caucasians more common, but ethnic minorities greater risk of perforation
Environmental
4
Q
Symptoms of appendicitis
A
Abdominal pain: periumbilical (dull, poorly localised) —> RIF (localised and sharp) Vomiting Anorexia Nausea Diarrhoea Constipation
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
6
Q
Rovsings sign
A
RIF fossa pain on palpation of LIF
7
Q
Psoas sign
A
RIF pain with extension of right hip
Inflamed appendi abutting psoas major muscle in a retrocaecal position
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
9
Q
DD of appendicitis
A
Ectopic pregnancy Ovarian cysts Meckel’s diverticulum Mesenteric adenitis Constipation Gastroenteritis Intussusception UTI
10
Q
Ectopic pregnancy
A
Gynaecological emergency
Serum/urine bHCG to exclude
11
Q
Ovarian cysts
A
Pelvic and iliac fossa pain
Especially with rupture or torsion
12
Q
Meckel’s diverticulum
A
Malformation of distal ileum
2% of population
Can bleed, become inflamed or cause volvulus/ intussusception
Often removed prophylactically
13
Q
Mesenteric adenitis
A
Inflamed abdominal lymph nodes
Abdominal pain, usually in younger children
Associated with tonsillitis or URTI
No treatment required
14
Q
Laboratory tests for appendicitis
A
Urinalysis Pregnancy test FBC, CRP Serum b-HCG USS if inconclusive CT
15
Q
Risk stratification score appendicitis
A
Shera score
16
Q
Management of appenditicits
A
Emergency admission to hospital under surgical team
Laparoscopic appendicectomy
Send appendix to histopathology
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
18
Q
Pyloric stenosis pathophysiology
A
Progressive hypertrophy of pylorus
Gastric outlet obstruction
Food ejected into oesophagus
Projective vomiting
19
Q
Risk factors for pyloric stenosis
A
Male gender
FH
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
21
Q
Blood gas analysis of pyloric stenosis
A
Hypochloric metabolic alkalosis
Baby vomiting HCl
Hypokalaemia as kidneys exchange potassium to retain protons
22
Q
DD of pyloric stenosis
A
Gastroenteritis GORD Over-feeding Sepsis UTI Food allergy Malrotation
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
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
25
Operative management of pyloric stenosis
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
26
Complications of pyloric stenosis
Pre-op:
Hypovolaemia
Apnoea; hypoventilation from metabolic acidosis
```
Post-op:
Wound dehiscence
Infection
Bleeding
Perforation
Incomplete myotomy
```
27
Hirschsprung’s disease
Congenital aganglionic mega colon disease
Ganglionic cells fail to develop in the large intestine
Delayed or failed passage of meconium around birth
28
Hirschsprung disease epidemiology
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
29
Subtypes of Hirschsprung’s disease
Short-segment:
Long-segment:
Total colonic aganglionosis disease;
30
Short-segment Hirschsprung’s
Aganglionosis is restricted to rectosigmoid portion of colon
31
Long-segment Hirschsprung’s
Aganglionosis extends past rectosigmoid portion of the colon to the splenic flexure
32
Total colonic aganglionosis
Entire colon affected
33
Pathophysiology of Hirschsprung’s
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
34
Pathophysiology of Hirschsprung’s enterocolitis
```
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
```
35
Enteric nervous system
Vagal segment of neural crest cells which migrate along vagus nerve to enter foregut mesenchymal in cranial-> caudal direction
Myenteric (Auerbach’s plexus)
36
Risk factors
Males
Chromosomal abnormalities: Down’s syndrome
Neurofibromatosis
Waardenburg syndrome
MEN TY2
FH: due to mutations in RETproto-oncogene on chromosome 10q11
37
Clinical features
```
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
```
38
Triad of Hirschsprung’s
Failure to pass meconium
Abdominal distension
Bilious vomiting
39
Hirschsprung’s-associated enterocolitis
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
40
Hirschsprung’s-associated enterocolitis mx
Ax
Fluid resuscitation
Decompression of obstructed bowel
Stool culture
AXR
41
DD of Hirschsprung’s disease
```
Meconium ileus
Intestinal atresia
Intestinal malrotation
Anorectal malformation
Constipation
Meconium plug syndrome
```
42
Meconium plus syndrome
Symptoms pass after passage of plus
| Can be differentiated by barium enema or water-soluble contrast enema
43
Meconium ileus
Distal small bowel impacted by meconium
Abdominal distension and failure to pass meconium
Can be differentiated by radiograph, barium enema, water-soluble contrast enema
44
Intestinal atresia
Congenital malformation
Complete obstruction
Usually involve abdominal distension and failure to pass meconium
45
Intestinal malrotation
Congenital anomaly in the rotation of the midgut during embryological development
Midgut volvulus: bilious vomiting and abdominal distension
46
Anorectal malformation
Anal stenosis
Imperforate anus
Failure to pass meconium and abdominal distension
Can be differentiated by physical examination of rectum that reveals malformation
47
Investigations of Hirschsprung’s
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
48
Contrast enema findings Hirschsprung’s
Short transition zone between proximal end of colon and narrow distal end of colon
49
Rectal suction biopsy
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
Rectal suction biopsy should be avoided unless the following clinical features are present
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
Mx of Hirschsprung’s
IV ax
NG tube insertion
Bowel decompression
Surgery as definitive treatment
52
Surgery for Hirschsprung’s
Pull-through procedures:
Swenson
Soave
Duhamel
Resect aganglionic section of bowel
Connect unaffected bowel to dentate line
53
Complications of Hirschsprung’s
Hirschsprung’s associated enterocolitis: C.dif, staph aureus, anaerobes
Enterocolitis
```
Surgery complications:
Constipation
Enterocolitis
Perianal abscess
Faecal soiling
Adhesions
```
54
Intussusception
Telescoping of one part of the bowel into another
Proximal segment: intussusception
Distal segment: intussucipiens
55
Epidemiology of intussusception
5-7 months of age
| Boys: girls 2:1
56
Pathophysiology of intussusception
Intestinal obstruction
90% cases are ileo-colic type
Distal ileum passes into caecum through ileo-caecal valve
57
Risk factors for intussusception
```
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
History of intussusception
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
Examination of intussusception
```
Distension
Palpable sausage-shaped abdominal mass in RUQ
Signs of peritonism
Bowel sound
Check for dehydration/ shock
```
60
DD of intussusception
```
Colic
Testicular torsion
Appendicitis
Gastroenteritis
Volvulus
```
61
Diagnosis of intussusception
Abdominal US
AXR not recommended due to low sensitivity
Contrast enema
62
AXR intussusception
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
Abdominal US
Doughnut/ target sign on a transverse plane
| Pseudo kidney sign on a longitudinal plane
64
Management of intussusception
Fluid resuscitation
NG tube to decompress obstructed bowel
Non-operative reduction
Surgical reduction
65
Non-operative reduction
Air or contrast enema
Performed by radiologist or paediatric surgeon at time of diagnosis with USS
Contraindications:
Perforation
Peritonitis
Uncorrected shock
66
Surgical reduction
If contraindications to enema or enema intervention is unsuccessful
Surgery required to manually reduce intussusception
Resection of areas of necrotic bowel
67
Complications of intussusception
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
Biliary atresia
Section of bile duct is narrowed or absent
Cholestasis
Conjugated bilirubin excreted
69
Pathogenesis of biliary atresia
Infectious agents
Congenital malformations
Retained toxins within bile
70
Epidemiology of biliary atresia
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
TY1 biliary atresia
Proximal ducts patent but common duct obliterated
72
TY2 biliary atresia
Atresia of cystic duct and cystic structures are found in portal hepatic
73
TY3 biliary atresia
Atresia of left and right ducts to the level of the porta hepatic
Occurs in 90% of cases of biliary atresia
74
Presentation of biliary atresia
Presents in first few days of life
Jaundice extending beyond physiological 2 weeks
Dark urine and pale stools
Appetite and growth disturbance
75
Signs of biliary atresia
Jaundice
Hepatomegaly with splenomegaly
Abnormal growth
Cardiac murmurs if associated cardiac abnormalities present
76
Investigations biliary atresia
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
Management of biliary atresia
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
Complications of biliary atresia
Unsuccessful anastomosis formation
Progressive liver disease
Cirrhosis with eventual hepatocellular carcinoma
79
Prognosis of biliary atresia
Good prognosis if surgery successful
| Liver transplant may be required in first 2 years of life
80
Abdominal mass
```
AAA
Benign tumour
Bowel obstruction
Cancer
Cholecystitis
Congenital anomaly
Diverticulitis
Enlarged organ
Hydronephrosis
Infection
Ovarian cysts
Traumatic injury
Uterine fibroids
```
81
Adrenal causes of abdominal mass
```
Adrenal carcinoma
Nueroblastomas
Phaeochromocytoma
Adrenal adenoma
Adrenal haemorrhage
```
82
Gallbladder causes of abdominal mass
Leiomyosarcoma
Choledochal cyst
Gall-bladder obstruction
Hydrops
83
GI causes of abdominal mass
```
Leiomyosarcoma
Non-Hodgkin lymphoma
Appendiceal abscess
Intestinal duplication
Faecal impaction
Meckel’s diverticulum
```
84
Kidney causes of abdominal mass
```
Lymphomatous nephromegaly
Renal cell carcinoma
Renal neuroblastoma
Wilms tumour
Hydronephrosis
Multicystic kidney
Polycystic kidney
Mesoblastic nephorma
Renal vein thrombosis
Hamartoma
```
85
Liver causes of abdominal mass
```
Hepatoblastoma
Hepatocellular carcinoma
Embryonal sarcoma
Liver metastases
Mesenchymoma
Focal nodular hyperplasia
Hepatitis
Liver abscess
Storage disease
```
86
Lower genitourinary tract causes of addo mass
```
Ovarian germ cell tumour
Rhabdomyosarcoma of bladder
Rhabdomyosarcoma of prostate
Bladder obstruction
Ovarian cysts
Hydrocolpos
```
87
Spleen causes of abdominal mass
```
Acute or chronic leukaemia
Histiocyte sis
Hodgkin lymphoma
Non-Hodgkin lymphoma
Congestive splenomegaly
Histiocytosis
Mononucleosis
Portal HTN
Storage disease
```
88
Miscellaneous causes of abdo mass
```
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
Intestinal obstruction
```
Physical obstruction
Prevents flow of faeces through the intestines
Back pressure through GI system
Vomiting
Absolute constipation
```
90
Causes of intestinal obstruction
```
Meconium ileus
Hirschsprung’s disease
Oesophageal atresia
Duodenal atresia
Intussusception
Imperforate anus
Malrotation of intestines with a volvulus
Strangulated hernia
```
91
Causes of bilious vomiting in neonates
```
Duodenal atresia
Malrotation with volvulus
Jejunum/ ileal atresia
Meconium ileus
Necrotising enterocolitis
```
92
Presentation of intestinal obstruction
```
Persistent vomiting
Bilious
Abdominal pain and distension
Failure to pass stools or wind
Abnormal bowel sounds: high-pitched and tinkling
```
93
Diagnosis of intestinal obstruction
AXR
Dilated loops of bowel proximal to obstruction
Collapsed loops of bowel distal to obstruction
Absence of air in rectum
94
Management of intestinal obstruction
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
Duodenal atresia
Higher rate in Down’s syndrome
Presents few hours after birth
AXR: double bubble sign
96
Duodenal atresia mx
Duodenoduodenostomy
97
Malrotation with volvulus
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
Malrotation with volvulus
Ladd’s procedure
99
Jejunal/ ileal atresia
Usually caused by vascular insufficiency in utero
Presents within 24hours of birth
AXR will show air-fluid levels
100
Jejunal/ ileal atresia mx
Laparotomy with primary resection and anastomosis
101
Meconium ileus
Higher in CF
Presents 24-48 hours
Abdominal distension and bilious vomiting
IX: air-fluid levels on AXR, sweat test for confirm CF
102
Meconium ileus mx
Surgical decompression
| Damage may require surgical resection
103
Necrotising enterocolitis
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
Management of necrotising enterocolitis
Conservative and supportive for non-perforated cases
| Laparotomy and resection in cases of perforation of ongoing clinical deterioration
105
Causes of paralytic ileus
```
Chest infections
MI
Stroke
AKI
Electrolytes: K, Mg, PO4
Surgeries
Replace electrolytes IV
```
106
Embryology of paediatric umbilical disorders
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
Umbilical hernia
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
Paraumbilical hernia
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
Omphalitis
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
Umbilical granuloma
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
Persistent urachus
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
Persistent Vitello-intestinal duct
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
Umbilical hernia associations
Afro-caribe a
Down’s syndrome
Mucopolysaccharide storage disease
114
Inguinal hernias
Common in children
| Commoner in male
115
Inguinal hernia pathophysiology
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
Management of inguinal hernia
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
Malrotation
High caecum at midline
Feature in exophthalmos, congenital diaphragmatic hernia, intrinsic duodenal atresia
Volvulus may develop
118
Pathophysiology of Meckel’s diverticulum
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
Management of Meckel’s diverticulum
removal if narrow neck or symptomatic. Options are between wedge excision or formal small bowel resection and anastomosis.
120
Presentation of Meckel’s
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
Meckel’s diverticulum
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
Meckel’s 2s
occurs in 2% of the population
is 2 feet from the ileocaecal valve
is 2 inches long
