8 week old Nicholas Schueet, presents with his mother Michelle, to the emergency department. She is very concerned because Nicholas has started to vomit with every feed; it started out as just small possets but has now become much more forceful. She recently changed his formula because she was concerned that it may be the cause.
General observations:
Abdomen:
Other:
SURGICAL cause likely if:
| Physiological: | Pathological |
|---|---|
| Vomiting/ regurgitation often appears effortless may be mild distress. May be provoked by lying down or sudden movements | Severe irritability, Sleep disturbance |
| Feeding well | Feeding difficulties : feed refusal, severe irritability during or between meals, posturing after meals Haematemesis/iron deficiency (oesophagitis) |
| Normal weight gain | Failure to thrive Apneic or cyanotic episodes in young infants, especially occurring with position change after feeding Cough, stridor, wheeze Unexplained recurrent pneumonia ( aspiration) |
| Usually settles with simple management; posturing upright during feeds and sleep, feed thickeners. | Does not settle with simple management. Posturing upright for feeds and sleep, feed thickeners |
| Resolves over time usually by 12 months | Often continues beyond 12 months |
The physiologic and anatomic factors that prevent the reflux of gastric juice from the stomach into the esophagus include the following:
Normal factors promoting reflux in infants are their small stomach capacity, frequent large-volume feedings, short esophageal length, supine positioning, and slow swallowing response to the flow of refluxed material up the esophagus. Infants' individual responses to the stimulus of reflux, particularly the maturity of their self-settling skills, are important factors determining the severity of reflux-related symptoms.
Diagnostic Algorithm for GOR Management:
General Management Steps:
CLINICAL FEATURES:
Pyloric stenosis most often occurs in neonates and infants aged 1-10 weeks (mean, 5 wks.), with a range of 5 days to 5 months
Projectile vomiting typically occurs and is always non-bilious but may have brown discoloration or a coffee-ground appearance from associated gastritis, particularly if emesis has persisted for several days. The vomiting occurs within 30-60 minutes after feeding. The infant remains hungry and usually attempts to feed immediately after vomiting. Weight loss and evidence of dehydration (e.g. decreased tearing and urinary output, with poor skin turgor) are present if vomiting is allowed to continue for more than a few days.
Careful examination may reveal an oblong, smooth, hard mass that is 1-2 cm in length (hypertrophied pylorus: commonly referred to as an olive or pyloric tumour,) in the epigastrium just above the umbilicus, either in the midline or just to the right.
Observation of the abdomen of the infant with pyloric stenosis after feeding often reveals visible gastric contractions occurring in a wavelike manner from left to right across the abdomen.
ANATOMY and PATHOPHYSIOLOGY
Pyloric stenosis involves hypertrophy of the circular muscle of the pylorus, resulting in narrowing and obstruction. Grossly, the pylorus is enlarged, resembling a tumour approximating the size and shape of an olive (i.e. 2 cm long, 1 cm diameter). Microscopically, the circular muscle hypertrophies, with increased connective tissue in the septa between the muscle bundles. Gastric fluid loss is associated with the loss of H+ and Cl-. This fluid loss is unlike that in conditions caused by vomiting with an open pylorus, which involves losses of gastric, pancreatic, biliary, and intestinal fluid. Hypochloremic, hypokalemic metabolic alkalosis is the characteristic biochemical disturbance observed in pyloric stenosis. Urinary Na+ and HCO3 - losses, which compensate for Cl- losses, perpetuate this alkalosis
CLINICAL FEATURES:
Can occur at any age but is most likely in the infant between 3 and 18 months who suddenly develops screaming attacks of pain with vomiting. During each episode of pain the infant becomes pale and may draw up the legs.
The spasms of pain tend to last 2-3 minutes and occur at intervals of about 10-20 minutes, although after a while the pain becomes more persistent. Vomiting is an early symptom. The passage of a few loose stools early on represents evacuation of the bowel distal to the obstruction. The small volume and limited duration of loose stools in intussusception helps differentiate it from acute gastroenteritis. Congestion of the intussusceptum may lead to the passage of bloodstained or 'redcurrant' stools. Many infants with intussusception present with little more than pallor, lethargy and vomiting and may have little evidence of abdominal pain. Should these symptoms be ignored, the infant may progress to develop signs of septicaemia or shock.
The infant with intussusception looks pale, lethargic, anxious and unwell. A vague mass may be felt in the right or left upper quadrants of the abdomen but, once abdominal distension has developed, the mass becomes obscure and difficult to palpate. The apex of the intussusceptum may be palpable on rectal examination in a few, and the examining glove may be bloodstained. A plain X-ray of the abdomen will often be normal but may show an unusual bowel gas distribution or features of bowel obstruction
ANATOMY AND PATHOPHYSIOLOGY:
In intussusception, the distal ileum (the intussusceptum) telescopes into adjoining distal bowel (the intussuscipiens), resulting in intestinal obstruction. Vascular compromise and subsequent bowel necrosis are the primary concerns with intussusception Intussusception is most often (80%) ileocolic but it may be ileoileal, colocolic, or ileoileocolic.
Most infants and toddlers (95%) do not have an identifiable specific lead point. In these idiopathic cases, careful examination may reveal hypertrophied mural lymphoid tissues (Peyer patches), which are due to adenovirus or rotavirus.
Specific lead points are more commonly found in children older than 3 years. Meckel diverticulum is the most common lead point, followed by polyps and duplications. Other lead points described include lymphomas, submucosal hemorrhage with Henoch-Schönlein purpura, hemangiomas, and lymphosarcomas. Children with cystic fibrosis (CF) may present with intussusception due to inspissated meconium in the terminal ileum. While generally observed as a complication in older children with CF, neonatal intussusception with meconium plug syndrome associated with CF has been reported.
CLINICAL FEATURES:
In the first month of life, the most typical presentation is of bilious vomiting and sudden onset of abdominal pain. Bilious vomiting is observed 77-100% of the time. In infants of this age, consider such a presentation diagnostic of malrotation with midgut volvulus until proven otherwise. In older children, symptoms can be vague and may include chronic intermittent vomiting and abdominal cramping, failure to thrive, constipation, bloody diarrhoea, and hematemesis
ANATOMY and PATHOPHYSIOLOGY
Volvulus is defined as a complete twisting of a loop of intestine around its mesenteric attachment site. Such twisting can occur at various sites of the GI tract, including the stomach, small intestine, cecum, transverse colon, and sigmoid colon. Midgut volvulus refers to twisting of the entire midgut around the axis of the superior mesenteric artery. It is the most common type of volvulus.
Numerous rotational abnormalities have been described that correlate with abnormal embryologic development of the midgut and cause the small bowel and its vascular supply to become suspended from a narrow pedicle, like a bell clapper, which predisposes to midgut volvulus and infarction.