Oesophageal & Duodenal Atresia Flashcards
Outline the primary care of oesophageal atresia with TOF
Suction proximal oesophageal ouch with 8F nasal tube every 15min or continuous using double lumen replogle tube
Keep nil per os
Prevent aspiration by positioning in lateral head up position at 30 degrees
Peroxide oxygen to prevent hypoxia
Broad spectrum antibiotics
Avoid ETT due to risk of air going down and causing distension of abdo.
10% dextrose to prevent hypoglycemia
Maintain warmth in an incubator
Refer urgently to tertiary
Standard tx of TOA
Repaired through a right lateral thoracotomy
• Division and closure of the TOF and end to end anastomosis of the
oesophageal ends.
Complications of surgical anastomosis of TOF
GERD
Anastomotic structures
Tracheomalacia which presents with barking cough and frequent chest infections
Clinical presentation of oesophageal atresia and TOF
Drooling
Coughing or Resp distress after feeds, tachypnoea (aspiration protection)
Milk vomits
Stridor
Duodenal stenosis vs duodenal atresia
Stenosis is incomplete obstruction and atresia is complete obstruction/obliteration (so it’s on its own)
Clinical presentation of duodenal atresia
Antenatal
-Polyhydramnions
Growth retardation
Postnatal
-vomiting -bile stained
-abdo distension (epigastric distension)
-failure to pass normal meconium (white stool)
-dehydration and biochemical deraingments (hypochloremic, Hyponatremiatremic metabolic alkalosis + jaundiced)
Special investigations in duodenal atresia
AXR
Contrast meal follow through
Which congenital abnormality is associated
Trisomy 21
Management of duodenal atresia preoperatively
ETT on free drainage
Aspiration prevention: nil by mouth
Replacements: IV fluid (resusc, mainainance and replacement of fluid lossses)
Broad spectrum
Dextrose , maintain and monitor serum glucose levels
Resp support
Keep warm
Monitor cardio, Resp and metabolic status.
Differentials for biliary atresia
Midgut vulvulus
GERD
Jejune-ioeal atresia
What comorbidities are associated with jejune-ileum atresia
Prematurity
Cystic fibrosis
Gastroschisis
Contraindications to anastomosis in colon obstruction / atresia
Hirschprung disease
Longer distance between proximal dilated colon and distal unused narrow bowel
When does intessusception occur
3 months (peak) to 3 years
Complications of Hirschsprung’s disease
Infection- (enterocolitis)
Small bowel
Risk factors for Hirschsprung’s disease
Family hx
Male
Trisomy 21, CHD
Clinical presentation of intesusception
• Sudden onset of colicky abdominal pain associated with vomiting.
• Pain is severe enough to wake the child. The classic feature is one of pulling the
legs up to the abdomen during the pain. The pain is colicky and intermittent and
may then go away only to return every half hour or so, lasting 20 to 30 seconds.
The child lies very still in between attacks.
• Vomiting may initially be milk feeds but becomes bilious, and later faeculent
• Passage of blood and mucus per rectum (“RED CURRANT JELLY” stools)
• Progressive abdominal distension.
Contraindications of air reduction of intessusception
Pure small bowel intessusception
Shock or incomplete Descuss
Signs of peritonitis or dead bowel
Where do most neoplasms in children occur
More than 90% neoplasms in children occur in the parotid glands
Features of a non benign lesion (non-benign radula)
Firm, fixed lesions that are often non tender
Special investigations for a mass in sublingual suggestive of a ranula
Ultrasonography
CT
MRI
Tissue specimen to conform dx by needle aspiration, truculent biopsy or excision biopsy
What is sialadenitis
Inflammation of salivary glands
Discuss management of ranula
Tx or ranula varies from simple marsupialisation (small incision to make continuos surface-imbobo) to complete excision of the gland.
Non benign are treated according to oncological principles and pleomorphic. Are treated with small excision.
Sialadenitis (inflammation) and in case an abscess has formed, careful incision and drainage of ductal orifice. Rarely entire gland needs to be excised.
Sialadenitis can be classified into viral (CMV,EBV,HIV,Mumps),
bacterial(Staph,Strep)or chronic (obstructive from stones or non-obstructive
associated with systemic conditions such as sarcoidosis, tuberculosis or Sjorgen’s
syndrome)
What’s the normal size of lymph nosed in children
Less than 1cm
1-2cm, firm and fixed nodes warrant investigation, also, persistent lymphadenopathy (more than 4-6 weeks)
What conditions can cause lymphadenopathy and hence can be our differentials
- TB (firm, fixed, non tende)
- EBV
- CMV
- Bacterial lymphadenitis (inflamed)
- Malignancy (firm, fixed, non tender)
neoplasticism conditions include lymphoma, leukaemia or distal metastasis
Special investigations in lymphadenitis
Bloods: FBC,smear and LDH, Infectious markers
TB investigation
Tissue sample by needle aspirate or incision/excision
Tx of lymphadenitis
Depends on condition diagnosed
Malignancy: chemo and radiotherapy often
Incision and drainage in case of an abscess
Presentation of thyroglsal cysts
Midline mass neck that moves upwards when protruding tongue
If cysts is infected, drainage sinus is seen
Cysts mat communicate with oral cavity, foul taste reported by patient in their mouth
Differentials for thyroglobulin cyst
Thyroid nodule
Goitre
Thyroditis
Dermoid cysts (if small, firm and mobile central neck mass been present at birth)
Tx of duodenal atresia
Resp and stabilise
NG tube
Fluid bolus normal saline
Maintenance fluid and electrolytes
-KCL and 5% dextrose
Keep warm
(Risk of pontine demyelination if sodium is raised quickly)
When ph<7.5, sodium<100, normal potassium and chloride
Ramstedt pyeloromyopathy
-laparoscopic and open
What condition gives you ‘double bubble’ on radiological investigations
Duodenal atresia
In which part of the duodenum do you get bile stained vomiting
And in which part do you get milky vomits
Bile stained: distal to ampulla of Vater (most common)
Milky: proximal to ampulla of vater
What metabolic deraingments do you get with duodenal atresia
Hypochloremic Hyponatremic hypokalemic aklalosis
What is the average time to full feed in an uncomplicated oesophageal atresia post op
10days
What is the pathophysiology of jejuno-ileal atresia
-Mesenteric vascular insult in intrauterine life disrupts focal development of section of intestinal wall
-Causes of vascular insult: Micro-emboli or antenatal volvulus, gastroschisis as well.
Vascukar insipult results in proximal and distal blind ending bowel lumen on either side of the necrotic portion of bowel (bowel ihlukana phakathi)
Main complication of jejune-ileal atresia
Short bowel syndrome
Classify the different types of Jejunal-ileal atresia
Stenosis
Type 1 atresia
Type 2 atresia
Type 3A
Type 3B
Type 4
Stenosis, Type 1&2 don’t result in loss of bowel length.
Type 3 and 4 is associated with short bowel syndrome
When do intestines return to pleuroperitoneal folds
Week 10-14
When does diaphragm develop
Week 7-10
2 most common sites of diaphragm hernia
Parasternal (Morgagni) hernia
Posterolateral (Bochdalek) hernia
Complications of diaphragmatic hernia
• Lung hypoplasia – there are fewer alveoli than normal
• Mediastinal shift- heart is shifted to contralateral side
• Thickened pulmonary arteries – there is more muscle in the arterioles and less
surfactant in the lungs
• Pulmonary arterial hypertension – resulting in a left to right shunt, persistent
foetal circulation, hypoxia and hypercarbia
GORD post op, Chronic lung disease and failure to thrive too
Symptoms of diaphragmatic hernia
• Respiratory distress, cyanosis – both to a variable degree
• Asymmetric chest development and movements
• Absent breath sounds on the affected side
• Heart sounds on the right
• Bowel sounds in the chest
• Scaphoid abdomen
