Lactobezoar
in the
Low-Birth-Weight
Infant
Allen Erenberg, M.D., Robert D. Shaw, M.D., and David Yousefzadeh, M.D.
Ironi thC l)epartnlents of Pediatrics and Radiology, University of Iowa Hospitals and Clinics, Iowa City
ABSTRACT. Lactobezoar is an unusual complication
asso-ciated with infant feeding. Seven low-birth-weight infants developed lactol)ezOars, including one whose case was
colllplicated l)y gastric perforation. Six of these infants were
fed formulas specifically designed for the low-birth-weight infant. Al)(lonhinal (listefltioll or regurgitation ‘ere the most frequent sylnptoms. The diagnosis was confirmed or made prospectively on supine or cross table lateral chest roentgen-ograiiis that included the upper abdomen. Treatment consisted of withholding feeding for 24 hours. There was no
recurrence of symptoms following resumption of feedings.
Pediatrics 63:642-646, 1979, lw’tol’:oar, lolL-birth-Weight
infant. infant feeding.
Lactobezoar is an unusual coniplication
asso-ciated with infant feeding,1 with only one case
reported in a low-birth-weight infant.T We wish
to report seven cases of lactobezoar in
low-birth-weight infants, including one case complicated by
gastric perforation. Six of these observations were
made during a 12-month period following the
introduction of tWo forni silas specifically designed
for feeding the low-birth-weight infant.
METHODS
The gestational age was determined by a
modification of the method of Dubowitz et al.’
From October 1977 to September 1978, all
infants weighing less than 2,000 gin were fed
either Similac 24 LBW or Mead Johnson
Prema-ture Formula. Since October 1978, the
low-birth-weight infants have been fed Similac 24
without iron (24 cal/oz). The decision to start
enteric feedings was made by the attending
physician based on the infant’s clinical condition.
Prior to feeding, a 3.5 or 5 Fr polyvinyl chloride
feeding tube was passed through the nares into
the stomach, the tube’s position confirmed by
auscultation, and the stomach aspirated to check
for gastric residual. Most infants received an
infusion of formula for three hours. One hour
later, if the gastric residual was less than 20% of
the total volume given over the previous
three-hour period, the infusion was repeated. Infants
receiving bolus feedings were fed through a
nasogastric tul)e by gravity, and the stomach was
aspirated for residual formula before the next
feeding. All infants were fed in the supine
posi-tion on an overhead radiant heater bed or in an
incubator, and received intravenous dextrose and
water with electrolytes.
PATIENT POPULATION
The sex, birth weight, gestational age, and
perinatal complications of the seven patients with
lactobezoar are shown in Table I. There were
three male and four female infants with birth
weights ranging from 960 to 1,800 gm. The
gestational ages ranged from 29 to 34 weeks; four
infants were appropriate size for their gestational
age and three were small for their gestational age.
Five of the seven infants were asphyxiated at
birth, and three developed idiopathic respiratory
distress syndrome. Umbilical arterial catheters
were used in four infants; in three cases, the
catheters were removed at least ten days prior to
the identification of the lactobezoar. Four infants
became icteric and required phototherapy, which
was discontinued three to eight days prior to the
onset of symptoms. One infant was receiving
supplemental oxygen via nasal continuous
posi-tive airway pressure. All but one infant received
antibiotics for presumed sepsis. None of the
cultures was positive for bacterial pathogens.
The feeding history and symptoms of the seven
patients with lactobezoars are presented in Table
II. Four of the infants were fed Similac 24 LBW, two were fed Enfamil Premature formula, and
Accepted for publication January 18, 1979.
TABLE I
PROFILE OF SEVEN PATIENTS WITH LACTOBEZOARS
Patient Sex Birth Weight Gesta tional Age Perinatal Complications
(gill)
(wk) (Growth)’
it F 960 28 SGA Prolonged rupture of melnbranes Asphyxia
Idiopathic respiratory distress syndrome Hyperbilirubinemia
2 F 1,040 32 SGA Asphyxia
Hyperbilinibinemia
:3 M 1,410 30 AGA Prolonged rupture of membranes
Asphyxia
41: F 1,480 34 SGA Prolonged rupture of membranes Hyperbilirubinemia
Cesarean section
5 M 1,640 32 AGA Amnionitis Asphyxia
Idiopathic respiratory distress syndrome Hyperbilirubinemia
6 M 1,800 33 AGA Cesarean section Hypoglycemia Polycythemia 7 F 1,420 30 AGA Cesarean section
Asphyxia
Idiopathic respiratory distress syndrome
Bronchopulmonar dsplasia Patent ductus arteriosus
#{176}SGA= small for gestational age; AGA = appropriate for gestational age. tFirstborn of triplets.
Firstborn of twins.
TABLE II
FEEDING HISTORY AND S’MPTosls OF SEVEN PATIENTS WITH LACTOBEZOARS
Patient I’or,nula Age at Method of Volume of Age at Symptoms
(
24 cal/ox) Onset ofFeeding (days)
Feeding Formula Fed
at Time of
Diagnosis
Diagnosis (days)
1 Enfamil 2 Nasogastric 9 1111/hr 14 Abdominal distention
Preniature infusion Regurgitation
2 Siniilac 24 2 Nasogastric 10 ml/hr 11 Abdominal distention
LBW infusion Gastric retention
Abdominal mass in left up-per quadrant
Free air in abdomen
3 Similac 24 1 Nasogastric 11 mI/hr 6 Regurgitation
LBW infusion Apnea
Bradycardia
4 Siniilac 24 8 Nasogastric 13 nil/hr 11 Regurgitation
LBW infusion Gastric retention
Abdominal distention 5 Similac 24 3 Nasogastric 15 nil/hr 6 Asymptomatic
LB\V infusion
6 Enfalllil 1 Bolus via 40 mi/feeding 5 Regurgitation
Premature flasogastric
tube every
three hours
7 Similac 2 Bolus via 45 mi/feeding 34 Neutropenia without iron nasogastric
tube every three hours
patient 2.
one was fed Similac 24 without iron (24 cal/oz).
Feedings were begun with half-strength formula
in two infants and full-strength formula in five
infants. Five infants were fed by nasogastric
infusion, and two received bolus feedings every
three hours. Enteric feedings were initiated three
to 30 days prior to the onset of symptoms. Two
patients (No. 6 and 7) were given a vitalnin
mixture by mouth. Abdominal distention and
regurgitation were the most frequent symptoms.
One infant was asmptomatic, and the diagnosis
was made froni the chest roentgenogram.
Patient 2 developed a left upper quadrant
abdominal mass and was found to have free air in
the abdomen 12 hours later. At surgery, the infant
had a perforation in the posterior aspect of the
greater curvature of the stomach and a 90-gm
curd-like mass was removed from the stomach
(
Fig 1). There was no evidence of pneumnatosis gastrica or intestinalis. Following d#{233}bridement of the necrotic area and closure of the perforation,the patient has done well.
Patient 7 was feeding well until one day prior to the diagnosis of lactobezoar when she devel-oped signs and symptoms of sepsis. All cultures
were negative. The lactobezoar was not suspected
clinically, and was identified on chest
roentgeno-gram obtained as part of the workup for sepsis.
Except for patient 2, the roentgenographic
diagnosis of lactobezoar was confirmed or made
prospectively on conventional supine or cross
table lateral chest roentgenograms that routinely
include the upper abdomen (Fig 2 and 3). Opaque
contrast media were not used in any of the
studies. The lactobezoar cast resolved
roentgeno-graphically five to 15 days after the initial
diag-nosis was made.
Five infants became asymptomatic after
feed-ings were withheld for 24 hours. In one patient,
the lactobezoar resolved without cessation of
feeding. There was no recurrence of symptoms
following resumption of feedings.
DISCUSSION
In previously reported cases, the formation of
the lactobezoar was thought to be caused by
improper dilution of powdered milk or forinula14
or by dehydration. The previously reported
pre-term infant with a lactobezoar associated with gastric perforation had pneumatosis of the hindus of the stomach with multiple ulcerations,
consis-tent with necrotizing enterocolitis. Neither
improper formula preparation nor necrotizing
enterocolitis was associated with the formation of
lactobezoars in our patients.
The signs and symptoms associated with the
formation of a lactobezoar are nonspecific. The
lactobezoar, consisting of a well-formed
intralu-ininal cast surrounded by air (Fig 2 and 3), can be
seen on conventional supine or cross table lateral
chest roentgenograms that include the upper
abdomen. If the stomach is gasless or distended by
fluid retained because of outlet obstruction,
decompression by gentle aspiration followed by
introduction of a small amount of air will portray
the diagnostic image. Additional abdominal
stud-ies using contrast media are not necessary.
There are several factors that may have contributed to the formation of the lactobezoars. Milk curds are created by the interaction of formula with gastric secretions. In the term
infant, gastric acidity increases during the first
two days of life with concolnitantly elevated
serum gastrin levels.1’ Little is known about
gastric secretion and curd formation in the
low-birth-weight infant. It is possible that retention of
formula because of delayed gastric emptying
allowed for greater curd formation in our
patients.
Factors that influence gastric emptying in the
neonate have been recently reviewed.12 The rate
of gastric emptying is similar in healthy term,
preterni, and infants small for their gestational
age but delayed in infants with respiratory
distress syndrome or those fed in the supine
position.’’4 When the infant is supine, air may
accumulate in the ventral pyloric antrum,
preventing the passage of formula from the hindus into the duodenum.’5
Medium-chain triglycerides have been shown
to improve absorption of fat in the
low-birth-weight infant.’6 The two formulas designed for the low-birth-weight infant can provide 40% to 50% of their fat content as medium-chain triglyc-erides, the remainder coming from coconut and
soy or corn oil. In adults, medium-chain
triglycer-ides have been shown to stimulate duodenal chemoreceptors, which elicit a neurogenic and/ or hormonal response resulting in delayed gastric emptying.’7 The hormonal response to feeding
may differ in the low-birth-weight and term
infant.
An increase in gastric volume enhances the rate of gastric emptying.’2 Compared to an
intermit-tant bolits feeding, a constant nasogastric feeding
is assumed to decrease gastric distention and
therefore may delay gastric emptying; however,
there are no studies comparing the effect of these
two feeding techniques on the rate of gastric
emptying. Constant nasogastric feedings have
been shown to be an effective method of
provid-ing calories in the low-birth-weight infant with few complications. Vomiting and abdominal
distention were noted in four of 66
tubes, it may be difficult to aspirate the thick
curd.s froni infants with lactobezoars.
Jack Gold, M.D., of Ross Laboratories (oral
communication, December 1978) reported nine
other cases of lactobezoar formation associated
with the use of formulas designed for the
low-birth-weight infant. Until the causative factors
are identified, these formulas should be used with
caution. If a lactobezoar is identified, treatment
should consist of withholding feeding for 24 hours
or until the infant becomiies asmptomatic.
SUMMARY
Of seven low-birth-weight infants who devel-oped lactobezoars following enteric feeding, six were fed with formulas specifically designed for the low-birth-weight infant. Infants fed these formulas should be monitored for gastric reten-tion, regurgitation, and formation of a lactobe-zoar. The diagnosis can be made prospectively or confirmed by supine or cross table lateral chest
roentgenogram that includes the upper
abdo-men.
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ACKNOWLEDGMENTS
This investigation was supported in part by Research Career Development Award No. 1 K04 HD00155 to Dr.
Erenberg from the National Institute of Child Health and
Human Development.
