15.4.1 Neonatal Bowel Obstruction Flashcards
Define:
Neonate
Antenatal or prenatal
Perinatal
Postnatal
Gestational age
Atresia
Neonate: Babies between 0 and 28 days old
Antenatal or prenatal: before birth/during pregnancy
Perinatal: the period surrounding the birth of a baby (just before and just after birth)
Postnatal: after the baby is born
Gestational age: the age of a pregnancy (usually from the mom’s last menstrual period)
Atresia: failure of complete development of a part of the body/ a condition in which an orifice or passage in the body is closed or absent
• Can be divided into:
➢ Complete (atresia) or Incomplete (stenosis)
➢ Anatomically according to the part involved (e.g., oesophageal, duodenal)
Bowel obstruction
Def
Reasons
- Bowel obstruction: Something is preventing food, fluid and/or gas from moving from the oesophagus through the stomach and small intestine to the large intestine, as it normally would.
Reasons
- Midgut volvulus
- Congenital: Atresia/Stenosis
- Incarcerated or strangulated hernia
- Distal bowel obstruction (ARM/HD)
Malrotation vs Volvulus vs Midgut Volvulus
Malrotation:
- Intestine lies in an abnormal position/rotation
- Not a volvulus but has a high change to develop a midgut volvulus
Volvulus:
- An obstruction caused by twisting of the stomach or intestine
Midgut Volvulus:
- An obstruction caused by twisting of the midgut
Bile-stained vomiting
- green/ yellow vomiting
Midgut volvulus
Epidemiology
Embryology
REMEMBER: Any child with sudden onset of bile-stain vomiting = midgut volvulus until proven otherwise
Epidemiology
- 1 in 6000 live births
- 3% of the population has malrotation of the intestines, predisposing them to midgut volvulus (NB malrotation is not the same as a volvulus)
- 75% of patients with midgut volvulus are symptomatic within the first month of life (neonatal period)
Embryology
The normal development of the midgut includes:
1. Herniation (the midgut herniates through umbilical opening)
2. Rotation (midgut rotates 270o anticlockwise)
3. Retraction (midgut moves back into the abdominal cavity)
4. Fixation (midgut fixes into its normal position with a wide-open mesentery)
- Intestinal obstruction may result in a patient with malrotation in three possible ways:
1. Obstruction of the duodenum may result from congenital peritoneal bands (Ladd’s bands) which run over the duodenum from the caecum which is in the right upper quadrant (NOT its normal position in right iliac fossa)
2. Midgut volvulus: ABSOLUTE EMERGENCY
• The entire midgut may twist on its mesentery (supplied by the superior mesenteric artery) due to non-fixation of the mesenteric root during development.
• Ischaemia and strangulation of the bowel may result if uncorrected.
3. Internal hernia in the mesentery
Midgut volvulus
Presenting symptoms and signs
Associated abnormalities for Malrotation (not volvulus)
Morbidity and mortality
Presenting symptoms and signs:
Total bowel necrosis may develop within 6 hours of cut-off of blood supply by twisted mesentery, thus rapid referral and transfer is essential. This is every paediatric surgeon’s nightmare!
Early signs: (NB! Make diagnosis ASAP)
- 75% of patients with midgut volvulus are symptomatic within the first month of life.
- The sudden onset of bile-stained vomiting in a previously well child must be regarded as a midgut volvulus until proved otherwise.
- Non-tender not distended abdomen.
Late signs: (NB! Intervention needed ASAP)
- Blood may be passed per rectum.
- Abdominal distension (big abdomen) may result from intestinal obstruction.
- Peritonitis (tender abdomen) may result secondary to ischaemic bowel.
Malrotation (NOT volvulus):
Occasionally, older children may present with:
- Failure to thrive.
- +/- chronic bilious/ non-bilious vomiting
- This is usually due to partial or intermittent volvulus (vomiting when volvulus happens and normal in between)
Associated abnormalities for MALROTATION (not volvulus):
- Congenital diaphragmatic hernia
- Exomphalos
- Gastroschisis
- Situs inversus
Morbidity and mortality:
- Survival is excellent if condition is recognized early, and child has surgery before any ischaemia or loss of bowel.
- HOWEVER: survival is poor with devastating loss of the midgut as it is not compatible with long term life.
Oesophageal atresia
Epidemiology
Embryology
Classification
OA = oesophageal atresia (born without a complete oesophagus)
TOF = trachea-oesophageal fistula (A connection between the oesophagus and the trachea)
Epidemiology:
- Incidence of OA with or without TOF is 1 in 2500-3000 live births.
- Slightly more common in males when compared to females.
Embryology:
- Normally the foregut starts to divide during the 4th week of gestation into a respiratory and oesophageal part.
- This separation is usually complete during 6-7th week of gestation.
- OA with or without a TOF occurs when something goes wrong.
➢ There is incomplete separation of the respiratory tree and oesophageal part.
➢ Leading to any one of the different types of OA/TOF.
Classification
- 5 Main types (Pure OA + one involving other structures)
- Most common type is Oesophageal Atresia with a distal Trachea-oesophageal fistula.
Oesophageal atresia
Associated Abnormalities
Morbidity and mortality
Associated Abnormalities:
- 50 % of OA with/or without TOF will present with associated abnormalities.
- This can include:
➢ Any of the VACTERL anomalies:
o Vertebralabnormalities:abnormalspineorvertebra
o Anorectal abnormalities: born without an anus or with anus in abnormal
place.
o Cardiac abnormalities (Most common associated abnormality): Heart
abnormalities
o Trachea-oEsophagealfistula
o Renalabnormalities:kidneys,ureter,orbladder o Limb abnormalities (Radial dysplasia)
➢ Chromosomal anomalies e.g., Trisomy 18 or 21
Morbidity and mortality:
- Survival >90% for most babies
- Morbidity (complications) and mortality (death) is usually due to:
o Prematurebirth
o Associated abnormalities
Oesophageal atresia
Signs and symptoms
Antenatal history:
- Mother presents with polyhydramnios (too much amniotic fluid)
- Absent/small stomach bubble (not very sensitive)
Postnatal:
- Prematurity is common.
- Symptoms in the first few hours after birth include:
▪ excessive drooling/ frothing of saliva from the mouth
▪ respiratory distress especially after feeds (e.g., cough, cyanosis, tachypnoea, aspiration pneumonia); stridor (from tracheomalacia)
▪ Unable to pass a naso-gastric tube (NGT)
▪ NB! Head to toe examination of the baby is very important.
Intestinal atresia
Two types
Epidemiology
Embryology
Classification (don’t have to remember)
Duodenal atresia: abnormality of any part of the duodenum
Intestinal atresia: abnormality of the jejunum, ileum or colon
Epidemiology
DA
- 1 in 5000 – 10 000 live births
- Males > Females
IA
- Jejunal/Ileal:
- 1 in 5000 live births
- Males=Females
- Colonic: 1 in 20 000 live births
Embryology
- Disruption of normal configuration of the duodenum (genetic/developmental abn)
- Something happens early during development
- Duodenum does not develop normally
Classification
DA - Types 1-3
IA - Types 1-4
Intestinal atresia
Associated abnormalities
Signs and symptoms
Morbidity and mortality
Associated abnormalities
DA
- Common (45-65 % of casses)
- Most common abnormalities:
➢ Trisomy 21
➢ Cardiacabnormalities
➢ Malrotation
➢ VACTERL esp: ARM and OA
IA
- Less common
- Associated with other atresia’s (if you find one, you have to look for others)
- Colonic atresia: can be associated with Hirschprung’s disease
Signs and Symptoms
DA
- Polyhydramnios
- Vomiting feeds (later bile-stained) from the FIRST feed
- Epigastric distention
- No/small amount of meconium passed
- Dehydration
- +/- Jaundice
IA
- Polyhydramnios later in pregnancy
- Vomiting feeds (later bile-stained) from the FIRST feed
- Abdominal distention
- No/small amount of meconium passed
- Dehydration
- +/- Jaundice
Morbidity and mortality
- DA: Early post-operative survival of > 90 %
- Type 3 B intestinal atresia with loss of small bowel is associated with a poor prognosis due to loss of small bowel.
Define pyloric stenosis
Pyloric stenosis is a narrowing of the opening from the stomach to the first part of the small intestine (the pylorus).
Hypertrophic pyloric stenosis
Epidemiology
Risk Factors NB
Anatomy
Epidemiology
- IHPS is one of the most common surgical causes of non-bilious vomiting.
- Incidence: 1 – 4 per 1000 live births
Risk factors
- Gender (4 times more common in males) o Caucasian population
- Familyhistory
- Young maternal age
- First born child
- Feeding (Formula feeds)
Anatomy
- Pyloris muscle become hypertrophic
Hypertrophic pyloric stenosis
Signs and Symptoms
Signs and symptoms:
Classic presentation: Non-bilious, projectile vomiting in a term neonate who is between 2 – 8 weeks old.
History (from mother):
- Vomiting:
- Usually starts two to three weeks after birth
- NOT bile-stained
- Associated with feeds
- Becoming more and more forceful with each feed until eventually vomiting all the feeds
Signs and symptoms:
- Continuous vomiting of stomach contents (non-bile stained) is the most important clinical feature.
- Baby is hungry and cries a lot, feeding eagerly.
- Vomiting becomes progressively more forceful and may be projectile.
- +/- May have haematemesis (“coffee-ground” vomits)
- Dehydration and metabolic derangements.
- Abdomen:
o Large, distended stomach (full epigastrium) may be visualised in cases that present late:
o Soft abdomen
o Peristalsis may be visible on the abdominal wall and may run from left to right during a test feed.
o An“Olive”or“tumour”mightbepalpablein 70 % of patients.
- Additional signs and symptoms that may be present:
o Malnourished (late presentation) with possible anaemia
o Jaundiced (due to increased unconjugated bilirubin reabsorption from unused small bowel and impaired glucoronyl transferase activity)
o Little urine is passed (oliguria)
o Small hard stools (hunger stools)
