How Long Do Late Preterm Infants Need Supplemental Feedings?

Patient Presentation
A 19 day old, former 35 1/7 week late preterm male infant came to clinic for his first appointment after he was discharged from the neonatal intensive care unit. He was breastfeeding every 2-2.5 hours for 10 minutes and then parents would syringe feed him breastmilk that was fortified to 24 kcal/ounce with premature infant powdered formula. He would take about 10 ml after most feeds. His weight gain had been averaging 15-20 grams/day before discharge, and since he had been home for the last 4 days it had been 10-15 grams/day . His mother noted that he still seemed quite sleepy but would appropriately arouse, eat and then fall back to sleep. “Since we’ve been home though, its probably closer to every 2.5 hours feeding than the 2 hours we were doing in the hospital,” she said. The past medical history showed a neonatal intensive care course where he received antibiotics for 48 hours as his mother was Group B streptococcus positive and had not been adequately treated with antibiotics before delivery. His laboratory values and cultures were negative and his antibiotics were then stopped. He had mild respiratory distress initially that was treated by nasal canula for 3 days. He also had poor feeding so he received parenteral nutrition for 6 days, transitioned to gavage feedings and then to full oral feeds.

The pertinent physical exam showed a small infant with normal vital signs. His birth weight had been 2.230 kg (10-50% on Fenton premature infant growth chart) and now was 2.544 kg (10%). His length was 48 cm (10%) and his head circumference was 34 cm (50%). He had an open, flat fontanelle without overriding sutures. He had some subcutaneous fat but was still somewhat thin. His examination was otherwise unremarkable. The diagnosis of a late preterm infant who was now feeding and growing was made. The pediatrician recommended that the family continue the current feeding regimen but to also try to feed the infant closer to every 2 hours. “We don’t want to tire him out, but if he eats closer to every 2 hours then he’ll get another 1-2 feedings a day and that is huge for him and his growth. I also would not limit the amount he takes by syringe. If he seems hungier you can give him more, but I would try to give him at least 10 ml,” he recommended.

The patient’s clinical course the following week showed him to be gaining 20 g/day. “We’ve been feeding him closer to every 2 hours, plus he seems to be eating better at the breast. He’s only taking about 5 mls after feedings,” described his mother. “He’s obviously growing and doing better. I’m glad to hear that he is breastfeeding better. He’s still not full-term yet so I’d continue to offer the fortified supplement,” said the pediatrician. Over the next 2 weeks, the infant started to breastfeed more vigorously and stopped taking the supplements. At 41 weeks adjusted age, he was 3.432 kg (10-50%), and was not taking any supplementation.

Discussion
Premature infants have many problems to overcome because they just aren’t ready to live outside the uterine environment.
Late premature infants are defined as birth between 34 0/7 weeks and 36 6/7 weeks gestation. In the U.S. this gestational age accounts for ~70% of all preterm births or ~300,000 births/year. Late preterm infants can have delayed oral feeding skills and failure to thrive along with increased hospital readmissions. Breastfeeding can be difficult as infants can have poor coordination and poor tone, along with decreased lactation in the mother.

Learning Point
Weight gain lags behind intrauterine weight gain in premature infants including late preterm infants. The intrauterine growth is ~15 g/day at this age and in one study only 2% of preterm infants achieved this weight gain. Late preterm infants have increased energy, protein, calcium and phosphorous needs as this is the time that the fetus would be storing fat and minerals. It is also a time when brain growth and volume are markedly increased. Late preterm infants need additional nutritional supplementation. Therefore it is recommended that late preterm infants be breastfed with fortified human milk until at least 40 weeks postconceptional age. Human milk fortifier or special preterm discharge formula are recommended for use as the supplements as they contain additional calories, protein and minerals compared to standard infant formula. Preterm infants that are born earlier and weigh less, not surprisingly need supplemental nutrition for longer. For infants 25 grams/day) and reaches term weight (~3.25 kg). For formula fed infants, fortified formula with a premature infant formula at 22 kcal/ounce should be offered until the infant is 40 weeks postconceptional age and term weight. Then the infant can be transitioned to term formula at 20 kcal/ounce.

Questions for Further Discussion
1. What are indications for enteral or parenteral nutrition in preterm infants?
2. By what age should preterm infants be “caught-up” and following term infant growth patterns?
3. What nutritional supplementation do low birth weight or extremely low birth weight infants need?
4. What are some advantages of human donor breastmilk? They can be reviewed here

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for these topics: Premature Babies and Child Nutrition.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Carlson SK, Segar JL. Nutritional Needs of the Late Preterm Infant.
The Iowa Perinatal Letter. 2014;32(2).

Gianni ML, Roggero P, Piemontese P, et.al. Is nutritional support needed in late preterm infants? BMC Pediatr. 2015 Nov 23;15:194.

Raaijmakers A, Allegaert K. Catch-Up Growth in Former Preterm Neonates: No Time to Waste. Nutrients. 2016 Dec 17;8(12). pii: E817.

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

What Causes White Nails?

Patient Presentation
A 15-month-old male came to clinic for his health supervision examination. He was well but the mother was concerned about white spots on his fingernails. His previous doctor had told the mother that they were not a problem but the infant should take a multivitamin which she says he took every day. She was concerned because they were not going away. The past medical history was non-contributory. The pertinent physical exam showed a healthy toddler with normal vital signs and growth parameters in the 5-15%. He had normal appearing toenails. On 3 fingers he had small whitish grouped spots. The groupings were at the same location on each finger and did not change with pressure. There was no ridging of the nails and the nail folds appeared normal.

The diagnosis of leukonychia was made. The parent was educated that the spots were common problems encountered by children often because of trauma. That they were grouped at the same location on each hand indicated that they all probably occurred at the same time. The parent was told that the multivitamin could be continued but it would not make any difference in the nails and that the spots would grow out over time.

Discussion
The nail matrix covers the area of the nail plate, and extends proximally in a crescent moon shape with the edges of the crescent extending proximally and inferiorly toward the underlying bone. The nail matrix is a multilayered epithelium that physiologically produces keratinization and gives rise to the nail plate. The distal matrix forms the lower 2/3s of the nail plate and the proximal matrix forms the upper 1/3 of the nail plate. the thickness of the nail plate is proportion to the matrix’s thickness. The nail plate’s free edge contour follows the shape of the nail’s lunula. Melanocytes occur in the nail matrix but are 1/6 as numerous as those in the skin epidermis. In the distal matrix about 50% are activable and 50% are dormant. In the proximal matrix almost 100% are dormant. If activated, the melanocytes produce pigment, which is transferred to the keratin and a colored area of the nail plate occurs.

Regrowth of fingernails takes about 6 months and toenails can be 12-18 months. It usually takes 4-8 weeks for any incident to even begin to show up on the nails.

Learning Point
Leukonychia means white nail. It occurs when the normally translucent color is gone and the nail plate looks totally or partially white.

  • True leukonychia has abnormal keratinization of the nail plate so that the nail plate appears white because of changes in the light diffraction. The coloring does not change with pressure, and the opacity changes with nail growth.
  • Apparent leukonychia has an abnormal nail bed vasculature so that the nail plate appears white. The coloring changes with pressure and the opacity does not change with nail growth.
  • Pseudoleukonychia when there the cause is not the mail matrix nor vasculature but is a surface problem such as superficial onychomycosis or keratin granulations.

If a patient has extensive changes to the nail plate then more evaluation or referral is needed including complete blood count, metabolic panel and heavy metal screening and possible dermatology referral.
Treatment is eliminating the underlying cause particularly gentle (instead of rough) manipulation of the digits and less frequent use of irritating products such as artifical nails or nail polish remover.

Different forms of leukonychia include:

  • Punctate leukonychia
    • True leukonychia
    • Usually least severe form of leukonychia
    • Solitary or grouped spots usually on the fingernails
    • Causes
      • Trauma***
      • Idiopathic childhood
      • Psoriasis
  • Transverse leukonychia
    • True leukonychia
    • Parallel to the nail bed or lunula and usually spans the across the entire nail bed
    • Transverse leukonychia is often referred to as Mee’s lines after Mee’s who reported it in arsenic poisoning
    • It is often an incidental finding in children because of unnoticed trauma
    • They can be found on young infant’s fingernails about 8-12 weeks after birth also.
    • Causes
      • Trauma***
      • Heavy metal poisoning – arsenic, thallium
      • Drug therapy including chemotherapy, radiation
      • Systemic disease
        • Cancer
        • Heart failure
        • Infection – measles, tuberculosis, HIV, parasites
        • Renal failure
        • Systemic lupus erythematosus
        • Ulcerative colitis
      • Hypoalbuminemia
        • Muehrcke lines are paired transverse lines that are associated with periods when the body is not able to synthesize proteins as well, such as malnutrition, liver disease, etc.
        • Chemotherapy
        • HIV
        • Liver disease
        • Malnutrition
        • Organ transplant
  • Longitudinal leukonychia
    • True, apparent or pseudo- leukonychia depending on location of origin
    • Occurs perpendicular to the nail bed or lunula, running along the axis of the digit itself. Causes “stripes”
    • Causes
      • Darier disease – “candy-cane” appearance with alternating red and white streaks
      • Hailey-Hailey disease – multiple white stripes
      • Half and Half nails
        • White and red/brown band alternating
        • Kidney transplant but not hemodialysis
        • Behcet’s disease
        • Crohn’s disease
        • Chemotherapy
        • Liver failure
        • Kawasaki disease
        • Pellegra
        • Zinc deficiency
      • Onchopapilloma
      • Onchomycosis
  • Partial or total leukonychia
    • True leukonychia that is uncommon
    • Causes
      • Congenital
      • Terry nails
        • Ground glass appearance that affects about 75% of the nail. lunula is not seen.
        • Liver failure
        • Diabetes
        • Heart failure
        • Peripheral vascular disease
        • Reactive arthritis
        • Tuberculosis

** – Trauma is the most common cause including manipulation of the digits, artifical nails, irritants such as nail polish remover, nail glue, etc.

Questions for Further Discussion
1. What are Beau’s lines and what are their cause?
2. What causes brown lines and what are their cause?
3. What are signs of potential malignant melanoma of the nails?
4. What causes nail pitting?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for this topic: Nail Diseases.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Howard SR, Siegfried EC. A case of leukonychia. J Pediatr. 2013 Sep;163(3):914-5.

Richert B, Caucanas M, Andre J. Diagnosis using nail matrix. Dermatol Clin. 2015 Apr;33(2):243-55.

Lipner SR, Scher RK. Evaluation of nail lines: Color and shape hold clues. Cleve Clin J Med. 2016 May;83(5):385-91.

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

What Causes Hypernatremia?

Patient Presentation
A 7-month-old male came to the emergency room with a 3 day history of watery diarrhea. The mother has tried some commercial electrolyte oral rehydration solution but the infant has refused the fluid for the last 1-2 days. She also tried his formula but he had refused that too. She said that she couldn’t tell when he last urinated because the diarrhea is so profuse. She denies any blood or mucous in his stool, and it currently is only brown water. He has been having increased sleepiness over the past 18 hours. She denies any fever but there was some emesis initially of the fluids she gave him. There is no one currently ill at home, but there is diarrhea in his daycare. There is no travel history nor exposures to pets other than the family dog. The past medical history shows a nasolacrimal duct obstruction as a neonate.

The pertinent physical exam showed that he was 8.640kg (75%) at his 6 month check and his current weight is 7.960 kg. Based on 75% for his age he should be ~9.00 kg. Therefore he is estimated to be 11.6% dehydrated. His blood pressure is 58/40, heart rate is 168 beats/minute, his respirations are 40/minute, and temperature is 37.8°C. He is lethargic but will awaken when stimulated and cry. His capillary refill is 4+ seconds on his trunk and longer in his extremities which are cold. He has poor skin turgor with mild tenting and his mucous membranes are dry. The rest of his HEENT, heart and lung exams are normal. His abdomen is relatively soft but he cries when examining him. His bowel sounds are hyperactive but there are no masses or organomegaly.

The diagnosis of severe dehydration with hemodynamic compromise due to enteritis was made and the patient was given 20 ml/kg of normal saline bolus. He continued to have low blood pressure and another bolus was given. The laboratory evaluation showed a serum sodium of 153 mEq/L, chloride of 116 mEq/L and potassium of 6.8 mEq/L.

The patient’s clinical course was that he was taken to the pediatric intensive care unit for fluid management. He was given additional fluid and then started on 0.2 normal saline to correct his hypernatremia over 48 hours. Ongoing diarrhea losses were also replaced by intravenous fluids. KCl was given after urination was established. He became more alert over this time and on day 3 began to take sips of fluid. The diarrhea also improved and he was sent to the floor on Day 4 of hospitalization. The cause of the diarrhea was Rotavirus.

Discussion
Hypernatremia is a serum sodium of > 150 mEq/L. Basic causes are too much sodium or too little free water.

If body weight is normal or increased, there is an increase in total body sodium without an appropriate increase in total body water. Normally when the serum sodium is increased there is transient hypertonicity of the plasma which causes the thirst center to be stimulated and antidiuretic hormone (ADH) to be released. The thirst center tells the person to drink more water and ADH causes the kidney to retain free water. This normally will allow the plasma tonicity to go back to normal. Treatment is by treating the underlying cause and appropriate free water administration.

If the body weight is decreased, there is a lower amount of free water with a relative increase in total body salt. This occurs usually when there is hypovolemic dehydration such as diarrhea and inadequate free water intake. Normally ADH is produced to increase the free water but without adequate access to free water, the hypernatremia continues to be maintained. Treatment is by treating the underlying causes and appropriate free water administration.

Severe diarrhea is one of the most common reasons for hypernatremia. Patients with hypernatremic dehydration have both lower total body sodium and free water, but there is relatively more free water loss than sodium loss. Patients then develop hypernatremia. Because the hypernatremic plasma is hypertonic, intracellular free water passes into the extracellular environment which helps to maintain body’s hemodynamics. Therefore patients with hypernatremic dehydration usually are 3-5% more dehydrated than estimates based on clinical signs.

Patients who have had a prolonged period of hypernatremia should have their hypernatremia progressively decreased over a prolonged period of time to minimize the risk of cerebral edema. During hypernatremia, other osmolytes are produced intracellularly to help to balance the electrolytes extracellularly. These additional intracellular osmolytes are not created nor dissipated quickly. Therefore if additional free water is added too quickly to the extracellular environment to correct the hypernatremia, then as the serum sodium decreases, the extra free water can enter cells where the additional osmolytes are and this can lead to cellular edema.

While patients are given normal saline (sodium and fluid to expand the intravascular circulation immediately) if they are hemodynamically compromised, patients are often given Dextrose 5% (or 10%) + 0.2% normal saline (smaller amount of sodium and more free water) to correct the hypernatremia over 48 or more hours. Potassium and chloride are also replaced appropriately after the patient is voiding and it is obvious there is not a component of intrinsic renal disease. Patients should be monitored frequently (every 4-6 hours) and changes to the intravenous fluids made promptly. If the serum sodium decreases too quickly and cerebral edema and seizures occur, patients are usually given 3% saline to increase the serum sodium and the seizures usually stop after 4 ml/kg of 3% saline. Slower correction of the hypernatremia can then begin again.

Learning Point
Causes of hypernatremia include:

If body weight is normal or increased, there is an increase in total body sodium without an appropriate increase in total body water.

  • Urine sodium is high and urine osmolality is high
    • Salt poisoning
    • Excessive salt administration, such as salt tablets or medications such as sodium bicarbonate, hypertonic intravenous fluids, salt-water ingestion, excessive use of soy sauce, inappropriate mixing of infant formula, inappropriate use of salt instead of sugar
    • Cellular lysis such as tumors, rhabdomyolysis, crush injury
  • Urine sodium is variable and urine osmolality is low
    • Central hypodipsia
    • Reset osmostate – usually because of brain trauma
    • Hyperaldosteronism – infrequent
    • Cushing syndrome – infrequent
  • If the body weight is decreased, there is a lower amount of free water with a relative increase in total body salt
    • Urine sodium is low and urine osmolality is high
      • Diarrhea
      • Insensible water loss – fever, tachypnea, radiant warming of premature infants, burns
      • Excessive sweating
      • Lack of access to free water
    • Urine sodium is high and urine osmolality is isotonic to high
      • Diuretic
      • Glycosuria
      • Post urinary tract obstruction diuresis
      • Acute tubular necrosis, diuretic phase
      • Acute tubular necrosis, non-oliguric
    • Urine sodium is high and urine osmolality is isotonic to high
      • Diabetes insipidus
        • Central (non production of ADH)
        • Nephrogenic (non response to ADH)

    Questions for Further Discussion
    1. What causes hyponatremia?
    2. What causes hypokalemia? THE differential diagnosis is available here

    Related Cases

    To Learn More
    To view pediatric review articles on this topic from the past year check PubMed.

    Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

    Information prescriptions for patients can be found at MedlinePlus for these topics: Sodium and Dehydration.

    To view current news articles on this topic check Google News.

    To view images related to this topic check Google Images.

    To view videos related to this topic check YouTube Videos.

    Rudolph CD, et.al. Rudolph’s Pediatrics. 21st edit. McGraw-Hill, New York, NY. 2003:1651-2.

    Moritz ML, Ayus JC. Intravenous fluid management for the acutely ill child. Curr Opin Pediatr. 2011 Apr;23(2):186-93.

    Powers KS. Dehydration: Isonatremic, Hyponatremic, and Hypernatremic Recognition and Management. Pediatr Rev. 2015 Jul;36(7):274-83.

    Author
    Donna M. D’Alessandro, MD
    Professor of Pediatrics, University of Iowa