GI Surgery Flashcards
Appendicitis
Inflammation of appendix Gangrene and rupture Releases faecal contents and infective material into abdomen Peritonitis Peak age 10-20
Pathophysiology of appendicitis
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
Risks factors for appendicitis
FH
Ethnicity: Caucasians more common, but ethnic minorities greater risk of perforation
Environmental
Symptoms of appendicitis
Abdominal pain: periumbilical (dull, poorly localised) —> RIF (localised and sharp) Vomiting Anorexia Nausea Diarrhoea Constipation
Signs of appendicitis
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
Rovsings sign
RIF fossa pain on palpation of LIF
Psoas sign
RIF pain with extension of right hip
Inflamed appendi abutting psoas major muscle in a retrocaecal position
Acute appendicitis in children
Atypical presentations
Check all systems
Genital examination in boys
<6 years and >48hours of symptoms likely to be perforated
DD of appendicitis
Ectopic pregnancy Ovarian cysts Meckel’s diverticulum Mesenteric adenitis Constipation Gastroenteritis Intussusception UTI
Ectopic pregnancy
Gynaecological emergency
Serum/urine bHCG to exclude
Ovarian cysts
Pelvic and iliac fossa pain
Especially with rupture or torsion
Meckel’s diverticulum
Malformation of distal ileum
2% of population
Can bleed, become inflamed or cause volvulus/ intussusception
Often removed prophylactically
Mesenteric adenitis
Inflamed abdominal lymph nodes
Abdominal pain, usually in younger children
Associated with tonsillitis or URTI
No treatment required
Laboratory tests for appendicitis
Urinalysis Pregnancy test FBC, CRP Serum b-HCG USS if inconclusive CT
Risk stratification score appendicitis
Shera score
Management of appenditicits
Emergency admission to hospital under surgical team
Laparoscopic appendicectomy
Send appendix to histopathology
Complications of appendicectomy
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
Pyloric stenosis pathophysiology
Progressive hypertrophy of pylorus
Gastric outlet obstruction
Food ejected into oesophagus
Projective vomiting
Risk factors for pyloric stenosis
Male gender
FH
Clinical features of pyloric stenosis
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
Blood gas analysis of pyloric stenosis
Hypochloric metabolic alkalosis
Baby vomiting HCl
Hypokalaemia as kidneys exchange potassium to retain protons
DD of pyloric stenosis
Gastroenteritis GORD Over-feeding Sepsis UTI Food allergy Malrotation
Investigations for pyloric stenosis
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
Management of pyloric stenosis
Peri-operative
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
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
Complications of pyloric stenosis
Pre-op:
Hypovolaemia
Apnoea; hypoventilation from metabolic acidosis
Post-op: Wound dehiscence Infection Bleeding Perforation Incomplete myotomy
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
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
Subtypes of Hirschsprung’s disease
Short-segment:
Long-segment:
Total colonic aganglionosis disease;
Short-segment Hirschsprung’s
Aganglionosis is restricted to rectosigmoid portion of colon
Long-segment Hirschsprung’s
Aganglionosis extends past rectosigmoid portion of the colon to the splenic flexure
Total colonic aganglionosis
Entire colon affected
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
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
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)
Risk factors
Males
Chromosomal abnormalities: Down’s syndrome
Neurofibromatosis
Waardenburg syndrome
MEN TY2
FH: due to mutations in RETproto-oncogene on chromosome 10q11
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
Triad of Hirschsprung’s
Failure to pass meconium
Abdominal distension
Bilious vomiting
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
Hirschsprung’s-associated enterocolitis mx
Ax
Fluid resuscitation
Decompression of obstructed bowel
Stool culture
AXR
DD of Hirschsprung’s disease
Meconium ileus Intestinal atresia Intestinal malrotation Anorectal malformation Constipation Meconium plug syndrome
Meconium plus syndrome
Symptoms pass after passage of plus
Can be differentiated by barium enema or water-soluble contrast enema
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
Intestinal atresia
Congenital malformation
Complete obstruction
Usually involve abdominal distension and failure to pass meconium
Intestinal malrotation
Congenital anomaly in the rotation of the midgut during embryological development
Midgut volvulus: bilious vomiting and abdominal distension
Anorectal malformation
Anal stenosis
Imperforate anus
Failure to pass meconium and abdominal distension
Can be differentiated by physical examination of rectum that reveals malformation
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
Contrast enema findings Hirschsprung’s
Short transition zone between proximal end of colon and narrow distal end of colon
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
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
Mx of Hirschsprung’s
IV ax
NG tube insertion
Bowel decompression
Surgery as definitive treatment
Surgery for Hirschsprung’s
Pull-through procedures:
Swenson
Soave
Duhamel
Resect aganglionic section of bowel
Connect unaffected bowel to dentate line
Complications of Hirschsprung’s
Hirschsprung’s associated enterocolitis: C.dif, staph aureus, anaerobes
Enterocolitis
Surgery complications: Constipation Enterocolitis Perianal abscess Faecal soiling Adhesions
Intussusception
Telescoping of one part of the bowel into another
Proximal segment: intussusception
Distal segment: intussucipiens
Epidemiology of intussusception
5-7 months of age
Boys: girls 2:1
Pathophysiology of intussusception
Intestinal obstruction
90% cases are ileo-colic type
Distal ileum passes into caecum through ileo-caecal valve
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
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
Examination of intussusception
Distension Palpable sausage-shaped abdominal mass in RUQ Signs of peritonism Bowel sound Check for dehydration/ shock
DD of intussusception
Colic Testicular torsion Appendicitis Gastroenteritis Volvulus
Diagnosis of intussusception
Abdominal US
AXR not recommended due to low sensitivity
Contrast enema
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
Abdominal US
Doughnut/ target sign on a transverse plane
Pseudo kidney sign on a longitudinal plane
Management of intussusception
Fluid resuscitation
NG tube to decompress obstructed bowel
Non-operative reduction
Surgical reduction
Non-operative reduction
Air or contrast enema
Performed by radiologist or paediatric surgeon at time of diagnosis with USS
Contraindications:
Perforation
Peritonitis
Uncorrected shock
Surgical reduction
If contraindications to enema or enema intervention is unsuccessful
Surgery required to manually reduce intussusception
Resection of areas of necrotic bowel
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
Biliary atresia
Section of bile duct is narrowed or absent
Cholestasis
Conjugated bilirubin excreted
Pathogenesis of biliary atresia
Infectious agents
Congenital malformations
Retained toxins within bile
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
TY1 biliary atresia
Proximal ducts patent but common duct obliterated
TY2 biliary atresia
Atresia of cystic duct and cystic structures are found in portal hepatic
TY3 biliary atresia
Atresia of left and right ducts to the level of the porta hepatic
Occurs in 90% of cases of biliary atresia
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
Signs of biliary atresia
Jaundice
Hepatomegaly with splenomegaly
Abnormal growth
Cardiac murmurs if associated cardiac abnormalities present
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
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
Complications of biliary atresia
Unsuccessful anastomosis formation
Progressive liver disease
Cirrhosis with eventual hepatocellular carcinoma
Prognosis of biliary atresia
Good prognosis if surgery successful
Liver transplant may be required in first 2 years of life
Abdominal mass
AAA Benign tumour Bowel obstruction Cancer Cholecystitis Congenital anomaly Diverticulitis Enlarged organ Hydronephrosis Infection Ovarian cysts Traumatic injury Uterine fibroids
Adrenal causes of abdominal mass
Adrenal carcinoma Nueroblastomas Phaeochromocytoma Adrenal adenoma Adrenal haemorrhage
Gallbladder causes of abdominal mass
Leiomyosarcoma
Choledochal cyst
Gall-bladder obstruction
Hydrops
GI causes of abdominal mass
Leiomyosarcoma Non-Hodgkin lymphoma Appendiceal abscess Intestinal duplication Faecal impaction Meckel’s diverticulum
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
Liver causes of abdominal mass
Hepatoblastoma Hepatocellular carcinoma Embryonal sarcoma Liver metastases Mesenchymoma Focal nodular hyperplasia Hepatitis Liver abscess Storage disease
Lower genitourinary tract causes of addo mass
Ovarian germ cell tumour Rhabdomyosarcoma of bladder Rhabdomyosarcoma of prostate Bladder obstruction Ovarian cysts Hydrocolpos
Spleen causes of abdominal mass
Acute or chronic leukaemia Histiocyte sis Hodgkin lymphoma Non-Hodgkin lymphoma Congestive splenomegaly Histiocytosis Mononucleosis Portal HTN Storage disease
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
Intestinal obstruction
Physical obstruction Prevents flow of faeces through the intestines Back pressure through GI system Vomiting Absolute constipation
Causes of intestinal obstruction
Meconium ileus Hirschsprung’s disease Oesophageal atresia Duodenal atresia Intussusception Imperforate anus Malrotation of intestines with a volvulus Strangulated hernia
Causes of bilious vomiting in neonates
Duodenal atresia Malrotation with volvulus Jejunum/ ileal atresia Meconium ileus Necrotising enterocolitis
Presentation of intestinal obstruction
Persistent vomiting Bilious Abdominal pain and distension Failure to pass stools or wind Abnormal bowel sounds: high-pitched and tinkling
Diagnosis of intestinal obstruction
AXR
Dilated loops of bowel proximal to obstruction
Collapsed loops of bowel distal to obstruction
Absence of air in rectum
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
Duodenal atresia
Higher rate in Down’s syndrome
Presents few hours after birth
AXR: double bubble sign
Duodenal atresia mx
Duodenoduodenostomy
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
Malrotation with volvulus
Ladd’s procedure
Jejunal/ ileal atresia
Usually caused by vascular insufficiency in utero
Presents within 24hours of birth
AXR will show air-fluid levels
Jejunal/ ileal atresia mx
Laparotomy with primary resection and anastomosis
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
Meconium ileus mx
Surgical decompression
Damage may require surgical resection
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
Management of necrotising enterocolitis
Conservative and supportive for non-perforated cases
Laparotomy and resection in cases of perforation of ongoing clinical deterioration
Causes of paralytic ileus
Chest infections MI Stroke AKI Electrolytes: K, Mg, PO4 Surgeries Replace electrolytes IV
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
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.
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.
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.
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.
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.
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.
Umbilical hernia associations
Afro-caribe a
Down’s syndrome
Mucopolysaccharide storage disease
Inguinal hernias
Common in children
Commoner in male
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.
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.
Malrotation
High caecum at midline
Feature in exophthalmos, congenital diaphragmatic hernia, intrinsic duodenal atresia
Volvulus may develop
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.
Management of Meckel’s diverticulum
removal if narrow neck or symptomatic. Options are between wedge excision or formal small bowel resection and anastomosis.
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
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
Meckel’s 2s
occurs in 2% of the population
is 2 feet from the ileocaecal valve
is 2 inches long
