Neonatal GI Emergencies
Curry J. Bordelon, PNP-AC, MBA
Piedmont Healthcare
Objectives
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Overview of basic GI anatomy
Overview of GI function
Discussion of open abdominal wall defects and their treatment
Discussion of closed abdominal wall defects and their treatment
1) Overview of basic anatomy and function of each part of the GI tract
a) Stomach
i)
bean-shaped hollow muscular organ of the gastrointestinal tract involved in the second
phase of digestion, following mastication.
ii) highly acidic environment due to gastric acid production and secretion
iii) pH range usually between 1 and 4 depending on the species, food intake, time of the day,
drug use, and other factors.
iv) Combined with digestive enzymes, such an environment is able to break down large
molecules (such as from food) to smaller ones so that they can eventually be absorbed from
the small intestine.
v) produce and secrete about 2 to 3 liters of gastric acid per day with basal secretion levels
being typically highest in the evening.
vi) Absorption of vitamin B12 from the small intestine is dependent on conjugation to a
glycoprotein called intrinsic factor which is produced by parietal cells of the stomach.
b) Deuodenal
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i)
hollow jointed tube about 25-30 cm long connecting the stomach to the jejunum.
ii) first and shortest part of the small intestine and it is where most chemical digestion takes
place.
iii) begins with the duodenal bulb and ends at the ligament of Treitz.
iv) Largely responsible for the breakdown of food in the small intestine.
v) Brunner's glands, which secrete mucus, are found in the duodenum.
vi) Regulates the rate of emptying of the stomach via hormonal pathways.
vii) Secretin and cholecystokinin are released from cells in the duodenal epithelium in response
to acidic and fatty stimuli present there when the pyloris opens and releases gastric chyme
into the duodenum for further digestion. These cause the liver and gall bladder to release
bile, and the pancreas to release bicarbonate and digestive enzymes such as trypsin, lipase
and amylase into the duodenum as they are needed.
c) Jejunal
i)
The central of the three divisions of the small intestine and lies between the duodenum and
the ileum.
ii) The change from the duodenum to the jejunum is usually defined as the ligament of Treitz.
In adult humans, the small intestine is usually between 5.5-6m long, 2.5m of which is the
jejunum.
iii) The pH in the jejunum is usually between 7 and 8 (neutral or slightly alkaline).
iv) The jejunum and the ileum are suspended by mesentery which gives the bowel great
mobility within the abdomen
v)
It has a lining which is specialized in the absorption of carbohydrates and proteins. The
proteins have been broken down in the stomach by enzymes called pepsin and acid into
amino acids. The carbohydrates are broken down in the duodenum by enzymes from the
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pancreas and liver into sugars. Fats are broken down in the duodenum by "lipase" from the
pancreas into fatty acids. Amino acid, sugar, fatty acid particles, vitamins, minerals,
electrolytes and water are small enough to soak into the villi of the jejunum and drop into
the blood stream.
d)
ileum
i)
Last portion of the small intestine, and it is responsible for absorption of fats, and bile salts
which are a component of bile.
ii) Pores in the ileum are slightly bigger than those in the jejunum and allow vitamin B12,
vitamins dissolved in fatty liquids, electrolytes, bile salts and water to be reabsorbed.
iii) Where the ileum joins the large intestine is a valve, called the ileocecal valve, which
prevents the back flow of materials into the small intestine. By the time material reaches
this point, it has a rather pasty consistency.
e) Colon.
i)
Its function is to move the waste from the small intestine on to the rectum.
ii) Material first passes through the ascending colon and then through the transverse colon.
iii) Throughout this process, it absorbs more water and potassium.
iv) The sigmoid colon is designed to slow down this movement of the waste until it is ready to
be eliminated.
f)
Rectum.
i)
It stores wastes in adults.
2) Types of emergencies
a) open abd wall-all or some of the abdominal contents noted outside the infant
b) closed abd wall-normal appearance outside the infant
3) Open abd wall
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a) Gastroschisis
i)
Full-thickness defect of the abd wall exposing intestinal contents.
ii) Generally a small defect (3-6 cm) and right lateral to the umbilicus.
iii) 1 in 40,000 births. Male> female
iv) Infants are generally preterm or SGA
v) Malrotation affects all infants
vi) Generally always seen on US
vii) Survival rate is higher than omphalocele, 95%
viii) Treatment involves
(1) Gastric decompression
(2) Gut rest
(3) Antibiotics
(4) Silo suspension (sealed plastic device surgically attached to infant and suspended above
infant.
(a) This allows the bowel to return to normal size.
(b) Infants commonly have underdeveloped abd capacity thus not allowing for primary
closure.
(c) Daily decompression allows for stretching of the abd tissue and minimizes intestinal
damage.
(5) Primary closure- generally for small defects or those term infants with adequate abd
tissue.
b) omphalocele
i)
Failure of the intestines to return from the umbilical cord into the abd cavity resulting in a
transparent membrane that encapsulates intestinal tissue.
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ii) 1 in 5,500 births. Male > female
iii) Frequently associated (50% - 77%) with other syndromes such as trisomies, CHD, CDH
iv) Ranges from 2-15 cm on average. Smaller defects may be overlooked
v) Larger defects may include spleen and liver also
vi) Most are clearly visible on US prenatally
vii) Survival rates are high (75% - 95%).
viii) Due to associative chromosomal issues, surgery is the second choice of treatment. First line
treatment involves abdominal wrapping or painting the defect with silver nitrate or silvadine
to promote eschar formation and epitheal tissue growth.
ix) Abd decompression and delayed feedings are important to allow the inflamed intestinal
lumen to return to normal size. Antibiotics may also be used.
x) Surgical repair is generally reserved for the most severe cases and involves using gortex
flaps to cover the transparent sack.
xi) An unfortunate result of non-surgical closure is malrotation.
4) Closed abd wall
a) Atresia
i)
Biliary atresia-complete obstruction of the bile duct.
(1) 1 in 10,000 births, females > males
(2) Impairment of fat metabolism and absorption
(3) > 73% survival rate.
(4) Commonly associated with other atresias, trisomies and heart defects
(5) Normal at birth with slow increase of direct bili and transition of stools to clay-colored.
(6) Survival if untreated is < 2yrs of age.
(7) Can be identified in late pregnancy US
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(8) Treatment involves hepatic portoentostomy (removal of the atresia area and resection
to the more distal portion of the duodenum.
ii) Duodenal atresia-result of incomplete recanalization of the lumen.
(1) 1 in 6,000 to 10,000 births
(2) ¼ are associated with trisomy 21. Other associated anomalies are TE fistulas,
malrotation, VATERs, VACTERL and renal anomalies.
(3) Polyhydramnios is the # 1 identifying risk factor. Too much unswallowed fluid.
(4) 70% of infants do not pass meconium.
(5) Proximal atresias/obstruction generally results in vomiting within the first few hours of
life.
(6) Distal atresias/obstruction results in emesis longer after delivery.
(7) Classic double bubble on xray. Gasless pattern after the atresias
(8) 65%-84% survival rate with early intervention.
(9) Treatment involves decompression of the stomach by continuous suctioning followed by
surgical removal of the atresia area with a side to side anastomosis.
iii) Jejunoileal atresia-atresia or obstruction of the distal segment of the small intestine.
(1) Most commonly near the ileo-cecal valve
(2) 1 in 20,000 births
(3) Polyhydramnios is not as common of a risk factor (only ¼ of the presenting infants).
(4) Classic “triple bubble” and microcolon on xray
(5) 84%-95% survival rate.
(6) Treatment involves decompression of the stomach by continuous suctioning followed by
surgical removal of the atresia area with a side to side or end to end anastomosis
b) Stenosis
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i)
Far less common than atresias/obstructions.
ii) Generally from excessively narrow areas of the small intestine (duodenum or the ileo-cecal
valve).
iii) Most common cause is by webbed areas of the inner lumen.
iv) Occurs most often following other GI surgeries.
c) TE fistula and/or EA
i)
Failure of the trachea to differentiate from the esophagus
ii) There are different types of disorder
(1) 85% have EA and a TE fistula
(2) 8% have EA without any connection to the trachea
(3) 1% have esophageal fistula and no connection to the stomach
(4) 4% are an H type fistula
iii) 1 in 4,500 births
iv) VATER and VACERL association is common
v) 20%-30% are preterm
vi) Signs are excessive oral secretions (from an inability to swallow), inability to pass OG/NG
tubes, aspiration, chronic pneumonias.
vii) 97% survival rates
viii) Mortality is associated with associative disorders
ix) Surgery depends on the type of disorder.
d) NEC- Necrotizing enterocolitis.
i)
Necrosis of the mucosal and submucosal layer of the intestinal lining
ii) Any portion of the GI tract can be affected.
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iii) Causes are still a debate. The three most common causes are selective bowel ischemia,
delayed or lack of proper bacterial establishment and the effects of feedings.
iv) The osmolarity of certain formulas and the lack of feeding EBM play large roles in increasing
the risk of NEC. Early feeding of EBM decreases the risk of NEC by 65% in the preterm
infant.
v) Most common disease affecting hospitalized infants, 8% of all inpatient infants.
vi) 65%-92% of infants affected with NEC are preterm infants.
vii) Most commonly seen in infants 3-21 days post delivery.
viii) Xray shows tiny lucent bubbles.
ix) Generally infants present with abd distention, increased emesis, bloody stools or feeding
intolerance.
x) Treatment involves 3 basic principles:
(1) Bowel rest—NPO for 10-14 days
(2) Prevention of progressive injury—NPO, Fluid management, antibiotics
(3) Placement of abd drains.
e) Perforation
i)
Spontaneous rupture of the intestine/colon allowing for leakage of air into the abd cavity,
pneumoperitoneum
ii) Most commonly associated with NEC and ischemic bowel
iii) Most common risk factors are NEC, sepsis, mechanical ventilation, prematurity, long term
steroid usage and postoperative abd complications.
iv) Survival is directly related to how quickly the staff is able to identify clinical changes.
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v) Pneumoperitoneum (free air in the abd cavity) is the most common radiographic sign of
perforation. Generally a football of sail sigh in the right most lateral abd aspect on a left
lateral decub xray.
vi) INTESTINAL PERFORATION IS AN EMERGENCY!!!!
vii) Surgical removal of the damaged and perforated area is almost always required.
viii) Treatment also involves:
(1) Bowel rest—NPO for 10-14 days
(2) Gastric decompression
(3) Prevention of progressive injury—NPO, Fluid management, antibiotics
(4) Placement of abd drains may not be needed.
f)
Diaphragmatic hernia
i)
Herniation of intestinal contents into the thoracic cavity resulting in underdeveloped lung
tissue leading to respiratory distress.
ii)
1 in 4,000 births
iii) Usually present with cyanosis, respiratory distress and scaphoid abd.
iv) Usually seen during routine prenatal US.
v) Post delivery xray reveals intestinal loops in the chest cavity
vi) Immediate intubation and gastric decompression is essential to higher survival rates.
vii) Treatment also involves surgical placement of abd tissue back into abd cavity once the
infant has become stable in regards to both respiratory and hemodynamic status.
g) Hirshsprungs
i)
Also known as megacolon or aganglionic colon
ii) Congenital absence aganglionic cells of the distal colon and rectum.
iii) Failure of the neural crest cells to migrate properly to the caudal region.
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iv) Local failure of the colon to relax thus causing a restrictive, narrowed area.
v) The zone between the ganglionic and the tapered aganglionic area of the distal colon is
called the transitional zone.
vi) The rectum is always involved.
vii) 1 in 5,000 births. Males > females
viii) Most infants are chromosomally normal
ix) Primary symptoms are bilious vomiting, failure to pass stools and abdominal distention.
x) A significantly dilated colon proximal to the transitional zone on xray.
xi) Survival rates are high at 80%-95% with early intervention
xii) Diagnosis is only definitive by performing a rectal biopsy
xiii) Treatment involves a standard rectal “pull trough” which involves a complete removal of the
affected aganglionic zone, allowing for 7-10 days of bowel rest and slow reintroduction of
feeds.
h) Analrectal agenesis/imperforate anus
i)
The abnormal or incomplete partitioning of the cloacae resulting in anal stenosis or atresia.
ii) Rectourethral and rectovaginal fistulas are common.
iii) Cause is unknown
iv) 1 in 5,000 births
v) 20% - 75% have associated anomalies.
vi) VATER and VACTERAL syndromes are common
vii) ½ has spinal anomalies
viii) Atresias are the most obvious types.
ix) Stenosis is less obvious and usually present as stooling from the penis/vagina or meconium
stained urine.
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x) Overall mortality (20%) depends on the type if defect and the associated anomalies.
xi) Treatment for stenotic anal openings involves daily progressive dilation of the anus.
xii) For more involved complete atresia, surgical opening and pull through is essential.
i)
Meconium plug syndrome
i)
Intestinal obstruction of the lower distal colon and rectum
ii) Most commonly associated with decreased colonic motility and hyptonicity.
iii) Different from hirschprungs. There is no aganglionic cell regions.
iv) Risk factors include prematurity, diabetic mothers, neurologically devastated infants and
mothers treated with magnesium sulfate.
v) Primary symptoms are bilious vomiting, failure to pass stools and abdominal distention.
vi) Mortality is very low once the stool is passed.
vii) Surgical intervention is rare.
viii) Small saline enemas are the preferred treatment.
j)
Meconium ileus
i)
Obstruction of the distal colon due to abnormally thick meconium
ii) Generally due to pancreatic insufficiency.
iii) 95% of the infants with meconium ileus have CF.
iv) 1 in 2,000 births
v) Primary symptoms are progressive abdominal distention within the first 12-24 hours of life
followed by bilious vomiting and a failure to pass stools.
vi) On xray the infant will have dilation proximal to the obstruction and a soap-bubble
appearance at the point of obstruction (due to the trapped air in the dense meconium).
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vii) Non operative therapy is generally successful in 15%-25% of infants and involves regular
hyperosmolar enemas to evacuate the thickened stool. Medication therapy also should be
implemented.
viii) A temporary ostomy to decompress the obstructed area may be necessary until fluid status
is stabilized.
k) Small left colon syndrome
i)
Functional immaturity of the distal portion of the colon from the rectum to the splenic
flexure of the colon.
ii) The proximal portion if the colon is dilated and filled with meconium.
iii) 40% of the infants are from diabetic mothers.
iv) Primary symptoms are bilious vomiting, failure to pass stools and abdominal distention.
v) Management is conservative and non-surgical. Generally the colon will enlarge and become
fully functional with time.
References:
Cloherty, J. P., et al. (2004). Manual of Neonatal Care. (6th Ed). Lippincott, Williams and Wilkins.
Gomella, T. L., et al. (2004). Neonatology: Management, procedures, on-call problems, diseases and
drugs. (5th Ed). Lange Medical Books/McGraw-Hill.
Merenstein, G. B., et al. (2002). Handbook of Neonatal Intensive Care. (5th Ed). Mosby.
Health Leadership Associates. (2006). Acute Care Pediatric Nurse Practitioner Certification Review
Course. (2nd Ed.)
Kenner, C. and Lott, J. W. (2003). Comprehensive neonatal Nursing: A Physiologic Perspective. (3rd Ed.).
Saunders: Philadelphia.
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