Surgery Flashcards
Appendicitis
Inflammation of the appendix
Appendicitis pathophysiology
- typically caused by direct luminal obstruction, usually either secondary to a faecolith or lymphoid hyperplasia
- when obstructed, commensal bacteria in the appendix can multiply → acute inflammation
- reduced venous drainage & localised inflammation → increased pressure with appendix → ischaemia within the appendiceal wall
- if left untreated → necrosis → perforation
Appendicitis risk factors
- family history
- ethnicity
- environmental - summer
Appendicitis clinical features
- dull peri-umbilical pain that is poorly localised but later migrates to the right iliac fossa becoming localised & sharp
- vomiting
- anorexia
- nausea
- diarrhoea
- sepsis
- on examination:
- rebound tenderness & percussion tenderness over McBurney’s point → can progress to guarding
- right lower abdomen mass
- Rovsing’s sign
- Psoas sign
Appendicitis ix
- urinalysis
- pregnancy test
- routine bloods
- clinical assessment alone can be sufficient
Appendicitis mx
laparoscopic appendicectomy
Appendicitis complications
- perforation
- surgical site infection
- appendiceal mass
- abscess formation
Biliary atresia
Progressive fibrosis and obliteration of the extrahepatic and intrahepatic biliary tree
Without intervention, chronic liver failure develops and death occurs
Biliary atresia clinical features
- mild jaundice
- pale stools (colour may fluctuate but becomes increasingly pale as the disease progresses)
- normal birthweight followed by faltering growth
- hepatomegaly is often present initially
- splenomegaly develops due to portal hypertension
Biliary atresia ix
- raised conjugated bilirubin
- abnormal LFTs
- fasting abdominal ultrasound may demonstrate a contracted/absent gallbladder
- diagnosis confirmed with cholangiogram → fails to outline a normal biliary tree
- liver biopsy → initially demonstrates neonatal hepatitis with features of extrahepatic biliary obstruction developing with time
Biliary atresia mx
- palliative surgery with a Kasai hepatoportoenterostomy
- bypasses the fibrotic ducts and facilitates drainage of bile from any remaining patent ductules
- early surgery increases success rate
- disease progresses in most children → develop cholangitis & cirrhosis with portal hypertension
- nutrition & fat-soluble vitamin supplementation is essential
- liver transplantation can be considered
Epididymitis pathophysiology
- usually caused by local extension of infection from the lower urinary tract
- in males aged <35 years old, the most likely mechanism is sexual transmission
- most common organisms are N. gonorrhoeae and C. trachomatis
- often secondary to bladder outflow obstruction from prostatic enlargement, leading to retrograde ascent of the pathogen
- most common organisms are N. gonorrhoeae and C. trachomatis
Mumps orchitis
- orchitis can occur as a common complication of a mumps viral infection, occurring in up to 40% of post-pubertal boys with mumps infection
- presents as unilateral or bilateral orchitis, typically accompanied with a fever, around 4-8 days after the onset of mumps parotitis
- can lead to complications such as testicular atrophy & infertility
- if mumps is suspected → mumps IgM/IgG serology should be measured, notifiable disease
Epididymitis RFs
- men who have sex with men
- multiple sexual partners
- a known contact of gonorrhoea
Epididymitis clinical features
- unilateral scrotal pain with associated swelling
- fever
- rigors
- associated symptoms → dysuria, storage LUTS, urethral discharge
- examination
- affected side will be red and swollen
- tender on palpation
- may be associated hydrocele
- Prehn’s sign → pain is relieved by elevation of the scrotum
Epididymitis ix
- urine dipstick
- first-void urine should be collected and sent for NAAT
- routine bloods
- ultrasound imaging of the testes via an US Doppler can be useful to confirm the diagnosis
Epididymitis mx
- appropriate abx therapy
- sufficient analgesia
- abstain from sexual activity, barrier contraception counselling
Epididymitis complications
- reactive hydrocele formation
- abscess formation
- testicular infarction
Diaphragmatic hernias
left-sided herniation of abdominal contents through the posterolateral foramen of the diaphragm
Diaphragmatic hernias clinical features
- apex beat & heart sounds will then be displaced to the right side of the chest
- poor air entry in the left chest
- pneumothorax due to vigorous resuscitation
Diaphragmatic hernias ix & mx
- diagnosis confirmed via x-ray of chest and abdomen
- NGT is passed and suction is applied to prevent distension of the intrathoracic bowel
- after stable → surgical repair
- most infants have pulmonary hypoplasia → compression by the herniated viscera throughout pregnancy has prevented development of lung → mortality is high
Inguinal hernias
Protrusion of viscus through a defect of the walls of its containing cavity
Inguinal hernias pathophysiology
- indirect inguinal hernias (most common in children)
- abdominal contents protrude through the deep inguinal ring into the inguinal canal & through the superficial inguinal ring into the groin
- due to incomplete closure of the processus vaginalis after the descent of testes in utero
Inguinal hernias RFs
- prematurity
- male sex
- family history
Inguinal hernias clinical features
- groin swelling
- N&V, constipation, abdominal pain/discomfort = obstruction or strangulation
- on examination
- inguinal mass that you cannot ‘get above’, reducible when lying flat, does not transilluminate & positive cough reflex
Inguinal hernias ix
- clinical diagnosis, only if uncertain/more information is required
- USS
- CT scan
- MRI scan - rarely used
Inguinal hernias mx
- definitive management is achieved through surgical repair of the hernia (herniotomy)
- emergency surgery may be required in the case of an irreducible to prevent bowel and testicular ischaemia
Inguinal hernias complications
- recurrence
- strangulation
- incarceration
- bowel obstruction
Hirschsprung disease
A congenital disease in which ganglionic cells fail to develop in the large intestine
Commonly presents as delayed or failed passage of meconium around birth
Hirschsprung disease pathophysiology
- ganglionic cells of the myenteric and submucosal plexuses in the bowel aren’t present proximally from the anus to a variable length along LI
- arrest of the neuroblast, derived from the neural crest cell migration in fetal development
- aganglionic segment remains in a tonic state leading to failure in peristalsis & bowel movements
- accumulation of faeces in the rectosigmoid region is responsible for the functional obstruction → proximal bowel dilatation → abdominal distension
- stasis can lead to bacterial proliferation & subsequent complication = Hirschsprung’s enterocolitis
Hirschsprung disease risk factors
- males
- chromosomal abnormalities
- family history
Hirschsprung disease clinical features
- failure to pass meconium within 48 hours of birth
- abdominal distension
- bilious vomiting
- faecal mass in left lower abdomen
Hirschsprung disease ix
- plain abdominal radiograph
- contrast enema - contraindication would be presence of perforation
- classical finding - short transition zone between the proximal end of the colon & narrow distal end of colon
- gold standard - rectal suction biopsy
- bedside investigation
- biopsy stained for acetylcholinesterase → confirm aganglionosis
Hirschsprung disease mx
- IV antibiotics
- nasogastric tube insertion
- bowel decompression
- only definitive treatment is surgery
- Swenson
- Soave
- Duhamel pull-through procedures
- all involve resecting the aganglionic section of bowel and connecting the unaffected bowel to the dentate line
Hirschsprung disease complications
- Hirschsprung associated enterocolitis - main cause of mortality
- stasis of faeces leads to bacterial overgrowth within the colon
- fever, vomiting, diarrhoea, abdominal tenderness & sepsis
- treatment: fluid resuscitation, bowel decompression & broad-spectrum IV antibiotics
- constipation
- enterocolitis
- perianal abscess
- faecal soiling
- adhesions
Intestinal obstruction and ileus
Physical obstruction prevent the flow of faeces through the intestines
Blockage will lead to a back-pressure through the GI system
Small bowel obstruction causes
- atresia or stenosis of the duodenum (1/3 Down’s syndrome)
- atresia or stenosis of the jejunum or ileum → there may be multiple atretic segments of bowel
- malrotation with volvulus (may lead to infarction of the entire midgut)
- meconium ileus → thick, inspissated meconium (puttylike consistency) becomes impacted in the lower ileum (almost all have CF)
- meconium plug
Large bowel obstruction causes
- Hirschsprung’s disease → absence of the myenteric nerve plexus in the rectum, more common in boys & in infants with Down’s syndrome
- often does not pass meconium within 48 hours of birth & subsequently the abdomen distends
- rectal atresia → absence of the anus at the normal site
- treatment is surgical
Intestinal obstruction and ileus clinical features
- persistent vomiting, which is bilious stained unless the obstruction is above the ampulla of Vater
- abdominal pain and distension
- failure to pass stools or wind
- abnormal bowel sounds
- high pitched and ‘tinkling’ early in the obstruction & absent later
Intestinal obstruction and ileus ix
- initial investigation is an abdominal x-ray
- may show dilated loops of bowel proximal to the obstruction & collapsed loops of bowel distal to the obstruction
- absence of air in the rectum
Intestinal obstruction and ileus mx
- referral to paediatric surgical unit as an emergency
- initial management - NBM & NGT to help drain the stomach and stop vomiting, require IV fluids to correct any dehydration & electrolyte imbalances
Intussusception
The movement or ‘telescoping’ of one part of the bowel into another
Intussusception epidemiology
- peak incidence is between 5-7 months of age
- boys are 2x more likely to be affected than girls
Intussusception risk factors
- Meckel diverticulum
- polyps
- henoch-schonlein purpura
- lymphoma and other tumours
- post-operative
Intussusception clinical features
- sudden onset of inconsolable crying episodes
- pallor
- child may draw up their knees to their chest
- in between episodes → child returns to normal self
- red-current consistency of stools → blood & mucus
- older children → vomiting & abdo pain
- examination
- distension
- palpable ‘sausage-shaped’ abdominal mass which can be found in the RUQ
- signs of peritonism
- presence of bowel sounds
Intussusception ix
- diagnosis is confirmed radiologically:
- AXR may confirm the diagnosis but not recommended
- distended small bowel loops
- curvilinear outline of the intussusception
- absence of bowel gas in colon distal to intussusception site
- perforation → Rigler’s sign
- abdominal ultrasound: ultrasound is the preferred method of diagnosis
- doughnut/target sign of a transverse plane
- pseudokidney sign on longitudinal plane
- contrast enema: can reveal a diagnosis
- contraindicated if evidence of peritonitis/perforation
- AXR may confirm the diagnosis but not recommended
Intussusception mx
- 1) nonoperative reduction: involves the use of an air/contrast enema to reduce the intussuscepted bowel
- usually performed by a radiology
- contraindications are perforation, peritonitis or uncorrected shock
- 2) surgical reduction: manually reduce the intussusception
Intussusception complications
- obstruction
- one of the most common causes of bowel obstruction & important surgical emergency in children
- perforation
- dehydration and shock
Spontaneous bacterial peritonitis
Infection of existing ascites, without an obvious intra-abdominal source
Secondary peritonitis
Peritonitis stemming from another condition, commonly a defect in an abdominal viscus
Pyloric stenosis
Hypertrophy of the pyloric muscle causing gastric outlet obstruction
Pyloric stenosis risk factors
- male gender
- family history of pyloric stenosis
- firstborn
Pyloric stenosis clinical features
- presents at 2-8 weeks of age
- non-bilious vomiting after every feed
- vomiting, which increases in frequency & forcefulness over time → projectile
- continue to feed hungrily
- weight loss & dehydration
- on examination:
- visible peristalsis
- palpable olive-sized pyloric mass, best felt during a feed
Pyloric stenosis ix
- test feed should be performed with an NG tube in situ & stomach aspirated
- examiner should palpate for a pyloric mass and observe for visible peristalsis
- ultrasound of abdomen - hypertrophy of the pyloric muscle
- blood gas
- hypochloraemic metabolic alkalosis with a low plasma sodium and potassium = result of vomiting stomach contents
Pyloric stenosis mx
- peri-operatively - correct any underlying metabolic abnormalities
- oral feeding should be stopped & NG tube passed and aspirated at 4 hourly intervals
- blood gases + U&Es should be checked regularly & acted upon accordingly
- surgically managed = Ramstedt’s pyloromyotomy
- can be performed laprascopically/through a supra-umbilical incision and muscle is divided along down to the mucosa
- babies can resume feeding after 6 hours
- post-op vomiting is common after surgery, due to gastric distension and dysmotility
Pyloric stenosis complications
- pre-operative:
- hypovolaemia
- apnoea (hypoventilation associated with metabolic acidosis)
- post-operative:
- wound dehiscence
- infection
- bleeding
- perforation
- incomplete myotomy
Testicular torsion
Occurs when the spermatic cord and its contents twists within the tunica vaginalis, compromising the blood supply to the testicle
Peak incidence is in neonates and adolescents between the ages of 12-25 years
Testicular torsion pathophysiology
- torsion occurs when a mobile testis rotates on the spermatic cord
- leads to reduced arterial blood flow, impaired venous return, venous congestion, resultant oedema & infarction of the testis
- males with a horizontal lie → more prone to developing testicular torsion
- neonatal testicular torsion
- the attachment between the scrotum and tunica vaginalis is not fully formed
- entire testis and tunica vaginalis can tort → extra-vaginal torsion
Testicular torsion risk factors
- age
- previous testicular torsion
- family history of testicular torsion
- undescended testes
Testicular torsion clinical features
- sudden onset severe unilateral testicular pain
- N&V
- referred abdominal pain
- examination
- testis will have a high position with a horizontal lie
- swollen
- extremely tender
- cremasteric reflex is absent
- negative Prehn’s sign
Testicular torsion ix
- clinical diagnosis → suspected cases should be taken straight to theatre for scrotal exploration
- sufficient doubt → doppler ultrasound can be used to investigate potential compromised blood flow to the testis
- urine dipstick
Testicular torsion mx
- surgical emergency with a 4-6 hours window
- urgent surgical exploration
- strong analgesia and anti-emetics
- bilateral orchidopexy → both testicles fixed to the scrotum
- if testis not viable → orchidectomy may be warranted
Testicular torsion complications
- testicular infarction
- atrophy
- chronic pain
- palpable suture
- risk to future fertility
- risk of future torsion
Undescended testis complications
Infertility
Torsion
Testicular cancer
Psychological
Undescended testis mx
Unilateral undescended testis - referral should be considered from around 3 months of age; baby ideally seeing urological surgeon < 6 months
- orchidopexy - around 1 year of age
Bilateral undescended testes - reviewed by senior paediatrician within 24 hours as child may need urgent endocrine/genetic investigation
Malrotation
Congenital anomaly in which the midgut undergoes abnormal rotation and fixation during embryogenesis
Misplacement of the gut makes it susceptible to volvulus → life-threatening condition characterised by bowel twisting & duodenal compression by peritoneal bands (Ladd bands)
Malrotation clinical features
Bilious vomiting
- often occurring within the first day of life
Malrotation ix
Upper GI contrast study - gold standard ix
- reveals the obstruction point as no contrast can pass distally from this location
- corkscrew appearance → proximal bowel
USS
Malrotation mx
Urgent surgery → relieve the obstruction and correct the anatomical abnormality
Volvulus → Ladd’s procedure
