Neonatal Problems - Part 2

Gastroesophageal Reflux and Vomiting 

Regurgitation of small amounts of milk or formula is common in neonates due to reduced lower esophageal sphincter pressure. Parents often confuse regurgitation with vomiting. Adequate weight gain in a baby with GER is reassuring but those who fail to thrive or have respiratory symptoms related to feeding should be investigated for anatomic causes of regurgitation. Reflux can be reduced with  thick feeds and feeding in upright position. Regurgitation with stridor and cough should be evaluated for anatomical defects. Potential causes of vomiting include tracheoesophageal fistula with esophageal atresia, GI obstruction or midgut malrotation, intussusception, necrotising enterocolitis  It may also be a symptom of sepsis, raised ICP, inborn errors of metabolism, incarcerated hernia. 

Diarrhea and Dehydration 

Neonates are susceptible to dehydration and electrolyte abnormalities associated with severe diarrhoea. Bloody diarrhoea may be a symptom of volvulus, intussusception, or necrotising enterocolitis. Abdominal distention may also occur in association with diarrhoea, bowel obstruction, constipation, necrotizing enterocolitis, or ileus due to sepsis. Obtain serum electrolytes, glucose, stool testing and a urine sample in the setting of fever to evaluate for UTI.

Blood in Diaper 

Potential causes include blood from genital tract in girls, anal fissure, swallowed maternal blood, coagulopathies, necrotizing enterocolitis, allergic or infectious colitis, congenital defects or idiopathic. A newborn with a single event of hematochezia and no concerning findings may be observed as an outpatient. Persistent symptoms or concerning exam findings should be further evaluated. 

Constipation 

Infrequent bowel movements in neonates do not necessarily mean that the infant is constipated. Infants occasionally may go without a bowel movement for 5 to 7 days and then pass a normal stool. However, if the neonate has never passed stools, especially if there has not been a stool in the first 48 hours of life, consider intestinal stenosis, Hirschsprung’s disease, or meconium ileus associated with cystic fibrosis. Neonates with constipation should have a careful evaluation of thyroid function and lumbosacral spine for evidence of occult neural tube defects. The diagnosis of Hirschsprung’s disease is supported by absence of feces on rectal examination, a tonic or tight sphincter tone, and an abrupt change in bowel luminal size on barium enema, and is confirmed by a rectal biopsy demonstrating absence of ganglion cells. 

Neonatal Jaundice

Jaundice signifies hyperbilirubinemia and can represent normal new-born physiology or a pathologic process. 

Physiologic jaundice is characterized by a slow rise in bilirubin (<5 milligrams/dL per 24 hours), with a peak of 5 to 6 milligrams/dL during the second to the fourth days of life and a decrease to <2 milligrams/dL by 5 to 7 days. Decreased neonatal hepatic glucuronyl transferase activity, a shortened life span of neonatal red blood cells and relative polycythemia, and decreased intestinal bacterial colonization all lead to an increase in enterohepatic circulation that produces the normal rise in bilirubin seen in physiologic jaundice. 

Breast milk jaundice occurs be due to the presence of substances that inhibit glucuronyl transferase in the breast milk; it may start as early as the third to fourth day and reaches a peak of 10 to 27 milligrams/dL by the third week of life. Cessation of breastfeeding is not routinely recommended. It is unlikely to cause kernicterus and usually can be treated with phototherapy, when necessary. 

Breast feeding (starvation) jaundice occurs when a newborn is exclusively breastfed and the mother’s milk supply is still inadequate. Poor oral intake leads to reduced bowel movement and less bilirubin excretion through the GI tract. Treatment is optimizing the neonate’s feeding pattern with supplementations or donated breast milk. Severe hyperbilirubinemia may require treatment.

Excessive hyperbilirubinemia can lead to permanent brain injury (kernicterus). 

Distinguishing between physiologic and pathologic neonatal jaundice is important, and the timing of the onset of jaundice in the newborn provides useful clues. 

Timing:
<24hrs - Congenital or Acquired  infections, ABO/Rh incompatibility, Hematoma (Cephal/IM)
2-3 days - Physiologic
3-7days - Congenital or Acquired  infections, CN Syndrome, Giblert's Syndrome
>7 days -  Acquired infection, Breast milk jaundice, Congenital or acquired hepatitis, Biliary Atresia, RBS membrane of enzyme defects, Metabolic (galactosemia, fructosemia)

Key questions to evaluate jaundice:

• Day of onset
• Blood group and Rh status
• Maternal infections during pregnancy
• Maternal blood type and RhoGAM® administration
• Color of stool 
• Fever
• Family history of hemolytic anaemia 
• Conjugate or Unconjugate Hyperbilirubinemia

Scleral icterus is typically noted with serum bilirubin >5 mg/dL. 

Unconjugated hyperbilirubinemia is much more common, presents earlier in the neonatal period, and is related to the normal or abnormal breakdown of hemoglobin, although inherited enzyme deficiencies or infection may be pathologic causes. Conjugated hyperbilirubinemia results from the inability to excrete bilirubin into the bile and intestines and is usually the result of primary hepatic or biliary disease such as biliary atresia or hepatitis. Conjugated hyperbilirubinemia is always pathologic and often presents later in the neonatal period with jaundice, acholic stools, and dark urine.

The treatment of hyperbilirubinemia depends on the cause, but for most cases of unconjugated hyperbilirubinemia, phototherapy is sufficient. For severe cases, exchange transfusion may be required. 

References;

Tintinalli's Emergency Medicine 8th edition

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic