Reprint requests to (R.I.C.) Department of Pediatrics, Mt Zion Medical Center, San Francisco, CA 94115.
PEDIATRICS (ISSN 0031 4005). Copyright © 1980 by the
American Academy of Pediatrics.
EXPERIENCE AND REASON 117
particularly to the apparent high risk during
in-fancy.
L. REBECCA CAMPBELL, MD
ARNOLD J. ZEDD, MD
RICHARD H. MICHAELS, MD
Department
of
PediatricsUniversity of Pittsburgh School of Medicine
Children’s Hospital of Pittsburgh
Pittsburgh
REFERENCES
1. Tejani A, Dobias B, Nangia BS, et a!: Intrafamily spread of
Haemophilus type b infections. Am J Dis Child 131:778, 1977
2. Fiice GA, Andrews JS Jr, Hudgins MP, et a!: Spread of Haemophilus influenzae: Secondary illness in household contacts ofpatients with H. influenzae meningitis. Am JDiS
Child 132:757, 1978
3. Ward JI, Fraser DW, Baraff U, et al: Haemophilus influ. enzae meningitis: A national study of secondary spread in household contacts. N EngI JMed 301:122, 1979
4. Glode MP, Daum RS, Goldman DA, et al: Haemophilus influenzae type B meningitis: A contagious disease of chil-dren. Br Med J 1:899, 1980
5. Granoff DM, Basden M: Haemophiius influenzae infections in Fresno County, California: A prospective study of the effects of age, race, and contact with a case on incidence of
disease. J Infect Dis 141:40, 1980
6. Michaels RH, Norden CW: Pharyngeal colonization with
Haemophilus influenzae type b: A longitudinal study of
familjes with a child with meningitis or epiglottitis due to H
influenzae type b. J Infect Dis 136:222, 1977
7. Coulter D, Whisnant JK, Marks MI: Hemophilus influenzae
b meningitis in identical twins of a triplet sibship. Pediatrics 54:502, 1974
8. Whisnant JK, Rogentine GN, Gralmck MA, et a!: Host
factors and antibody response in Haemophilus influenzae
type b meningitis and epiglottitis. J Infect Dis 133:448, 1976 9. Yogev R, Lander HB, Davis AT: Effect of rifampin on
nasopharyngeal carriage of Haemophilus influenzae type b.
J Pediatr 94:840, 1979
10. Sinclair SE: H. influenzae type b in acute laryngitis with bacteremia. JAMA 117:170, 1941
11. Good PG, Fousek MD, Grossman MF, et al: A study of the
familial spread of H influenzae type b. Yale J Biol Med 15: 913, 1943
12. Addy MG, Ellis PDM, Turk DC: Haemophilus epiglottitis: Nine cases in Oxford. Br Med J 1:40, 1972
Control
of Oxygenation
during
the Transport
of Sick
Neonates
A safe neonatal transport system is an essential
component in the regionalization of perinatal care.
Despite efforts to provide continuous intensive care
to sick infants during transport,’5 several studies
have revealed an increased morbidity and mortality
among
infants
transported to newborn intensivecare units (NICU) compared with those infants
born at the NICU.6’7 There is little information
available
about
the
adequacy
of monitoring
and
maintaining oxygenation and
acid-base
statusdur-ing infant transport. In a preliminary study we
examined the ability of a neonatal transport team
to maintain an infant’s Pao2 (46 to 100 torr), pH
(7.25 to 7.55), and Paco2 (20 to 50 torr) in the
“physiologic” range during transport. We compared
the umbilical artery blood gases taken at departure
from the referring hospital and those taken on
arrival at the NICU in 58 infants. Of the newborns
85% (49) had blood gases that were in the
physio-logic
range
for
pH and Paco2 at these two timesduring transport. However, 66% (38) were either
hyperoxic (> 100 torr) or hypoxic (< 46 torr) at the
times
the arterial
gases
were measured. The presentstudy is an attempt to examine in a prospective
manner the effectiveness of using a transcutaneous
TcPo2 monitor to maintain normoxia during the
transport
of sick newborns.
METHODS
Thirty-six newborn infants with respiratory
dis-tress
were transported
to
Mount Zion MedicalCen-ter by fixed winged aircraft (pressurized to sea
bevel), or ambulance (equipped with Veriflow meter,
oxygen, and compressed air, and FIO2 analyzer).
Experienced neonatal fellows and NICU nurses
were used. All infants had umbilical artery catheters
inserted at the referring hospital and positioned at
L3-L4 for medical management. Arterial
blood
gases were drawn into heparinized glass syringes
and placed on ice during the transport until they
were analyzed.
Samples
of 0.3 ml were obtained atdeparture from the referring hospital and at
30-minute intervals during the transport. These were
analyzed on a Corning 165
blood
gas analyzer at theNICU within
three
hours
of collection.In a preliminary study we found that the Pao2 of
blood gas samples handled in this manner was
within 5% of the Pao2 obtained when samples were
analyzed within 5 minutes following collection. An
infant was considered to have drifted out of the
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* Groups compared using
x2
analysis, P < .01.Corrective change
No change made
Change not
cor-recting Pao2
118 PEDIATRICS Vol. 66 No. 1 July 1980
TABLE 1. Characteristics of 32 Infants Who Required Changes in Ventilatory
Manage-ment to Maintain Pao2 in the Physiologic Range
Infant Transports
TcPo2 TcPo2
Not Monitored (%) Monitored (%)
(n=21) (n=11)
Birth weight (gm ± SEM) 1,750 ± 180 1,890 ± 226
Ventilatory Support:
Respirator 12 (57%) 4 (37%)
Continuous distending pressure 2 (10%) 2 (18%)
Hood 02 (FIO2 > 0.5) 2 (10%) 2 (18%)
Hood 02 (FIO2 < 0.5) 5 (23%) 3(27%)
Respiratory disease
IRDS 14 (67%) 8 (73%)
Other (meconium aspiration, bacte- 7 (33%) 3 (27%)
rial pneumonia, TTNB)
Transport time (mm) 108 ± 10 79 ± 14
No. of air transports 13 (62%) 5 (46%)
No. of blood samples for Pao2 per trans- 3.4 ± 0.2 3.4 ± 0.5
port
TABLE 2. Blood with Pao2 <46 or >
Gases During Transport of Infant’s
100 Torr
No. of Gases out of TcPo, Not Moni- TcPo, Monitored Physiologic Range tored (%) (n = 21) (%)* (n = 11)
:1 6 (30) 9 (80)
2 6 (30) 2 (20)
3 9 (40) 0 (0)
physiologic range during transport if the Pao2 of
any individual blood sample was less than 46 torr
or greater than 100 torr. A Litton transcutaneous
oxymonitor (TcPo2) (electrode placed on the
in-fant’s abdomen) was used during eleven transports;
its use during transport depended on its availability,
ie, whether it was being used on another sick infant
at the NICU. The correlation of TcPo2 with
simul-taneous arterial Pao2 has been previously
re-ported.8’9 Data were evaluated by a
x2
analysis orunpaired
t-test.
RESULTS AND DISCUSSION
Of the 36 infants, 35 left the referring hospital
with the Pao2 in the physiologic range. Only four of
the 36 infants maintained their Pao2 in the
physio-logic range as determined by intermittent sampling
of arterial blood. These four infants required no
changes in ventilatory support (FIO2 or assisted
ventilation) during transport. Of the 32 infants who
required
alterations
in
ventilatory support tomain-tam
their Pao2 in the physiologic range, there wereno significant differences between infants who were
transported with or without the transcutaneous
monitor
in
birth weight, frequency of idiopathicrespiratory distress syndrome, type of ventilatory
support during transport, mean transport time, or
TABLE 3. Management Decisions for 32 Infants Who
Required Ventilatory Changes During Transport*
Management No. of Infant Transports
TcPo2 not Moni- TcPo Monitored
tored (%) (n = 21) (%) (n = 11)
4 (19) 8 (73)
12 (57) 1 (9)
5 (24) 2 (18)
* The group using the transcutaneous monitor had
sig-nificantly more corrective changes (changes in ventilatory
support that returned Pao2 to the physiologic range) than
did the group that did not have the monitor where either
no change or a change that did not bring the Pao2 into
the physiologic range was more likely to be made (P <
.01,
x2
analysis).the frequency of air transports (Table 1). Table 2
demonstrates that the 1 1 infants who were
mom-tored with a transcutaneous oxygen monitor spent
less time (as determined by the number of arterial
blood samples) with their Pao2 out of the
physio-logic range. In addition, during transports in which
the transcutaneous monitor was used, physicians
were more likely to make changes in ventilatory
management that brought the infant’s Pao2 into the
physiologic range (Table 3).
Despite the fact that 35/36 infants left the
refer-ring
hospital
with
a
Pao2 in the physiologic range,and that transports were conducted by skilled
neo-natal fellows with NICU nurses, 32 of the 36 infants
required alterations in ventilatory support to
main-tain their Pao2 in the physiologic range during
transport. The use of a portable transcutaneous
oxygen monitor enabled the physicians to limit the
periods of hyperoxia or hypoxia that occurred
dur-ing transport to the NICU.
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Reprint requests to (J.S.) Department of Pediatrics, Post Office Box 3967, Duke University Medical Center, Durham, NC 27710.
PEDIATRICS (ISSN 0031 4005). Copyright © 1980 by the
American Academy of Pediatrics.
ACKNOWLEDGMENT REFERENCES
EXPERIENCE AND REASON 119
We would like to thank Ms Susan Axeirod for her help
in the preparation of this manuscript.
CAROL MILLER, MD
RONALD I. CLYMAN, MD
ROBERT S. ROTH, MD
SUSAN H. SNIDERMAN, MD
ROBERTA A. BALLARD, MD
DOUGLAS HENNING, MD
PHILIP RIEDEL, MD
ALAN ROSEN, MD
LiNDA BURDEN, MD
Department
of
PediatricsMount Zion Hospital and Medical Center
San Francisco
1. Chance GW, O’Brien MJ, Swyer PR: Transportation of sick
neonates. Can Med Assoc J 109:847, 1973
2. Gunn T, Outerbridge EW: Effectiveness of neonatal tram-port.Can Med Assoc J 1 18:646, 1978
3. Hackel A: A medical transport system for the neonate.
Anesthesiology 43:258, 1975
4. Pettett G, Merenstein GB, Batt.agLia FC, et al: An analysis of air transport results in the sick newborn infant. I. The
transport team. Pediatrics 55:774, 1975
5. Cunningham MD, Smith FR Stabilization and transport of severely ill infants. Pediatr Clin North Am 20:359, 1973 6. Hirata T: Increased handicaps in transported very low
birth-weight infants. Clin Res 27:125A, 1979
7. Clark C, Lane B, Clyman R, et al: Decreased risk of intra-ventricular hemorrhage (P/H) for infants born in a perinatal center. C/in Res 27:123A, 1979
8. Huch R, Huch A, Albani M, et al: Transcutaneous Po, monitoring in routine management of infants and children with cardiorespiratory problems. Pediatrics 57:681, 1976 9. Huch R, Lubbers DW, Huch A: Reliability of transcutaneous
monitoring of arterial P0, in newborn infants. Arch Dis
Child 49:213, 1974
Infantile
Water
Intoxication
at
Home
Water intoxication in infants living at home has
been considered an unusual entity.’ This paper
describes two infants who were seen because of
seizures. It appears that the metabolic
derange-ments were a consequence ofparental error. In view
of the similarity between these and previously
re-ported cases,’4 including the context of parental
poverty,
the problem
and population at risk may bemore common than previously recognized.
CASE REPORTS
Case I
T.W. is a 5-month-old boy with no previously known
health problems. After being irritable for most of the
afternoon, he developed generalized seizures in the
eve-fling. His temperature was 97 F rectally, blood pressure
70 mm Hg by palpation, pulse rate was 132 beats per
minute, and respirations 20/mm. Measurements included
length 63.5 cm (25th percentile), weight 60 kg (third
percentile), and head circumference 40 cm (35th
percen-tile). He was actively convulsing at presentation. The
anterior fontanel was soft and flat. Transifiumination of
the skull was unremarkable. The optic fundi were normal.
The neck was supple. The skin had good turgor, there
were no lesions or edema. The remainder of the physical
examination was normal.
Blood glucose was 90 mg/100 ml. CSF showed no cells,
glucose was 60 mg/100 ml, protein 10 mg/100 ml, and
Gram stain and culture were negative. There was a mild
hypochromic, microcytic anemia. The white blood cell
count was unremarkable. The erythrocyte sedimentation
rate was 2 mm/hr. The serum electrolytes were: sodium
11 1 mEq/liter, potassium 3.8 mEq/Iiter, chloride 85 mEq/
liter, CO, 17 mm/liter, BUN 7 mg/100 ml, calcium 8.0
mg/100 ml, phosphorus 3.7 mg/100 ml, magnesium 1.5
mg/100 ml. Plasma osmolality was 230 mOsm/kg; urine
osmolality was 155 mOsm/kg; urine sodium was 47 mEq/
liter. Arterial blood gases on FIO 0.40 showed pH of
7.186, Pco2 38.3 mm Hg, Po, 199 mm Hg, and HCO, of 14
mm Hg.
Upon requestioning about the infant’s diet, the mother
confided that she ran out of whole milk, his usual major
nutritional source, on the day before admission. Tap
water was used as a substitute. At least 64 oz of water
was consumed on the day of admission, in addition to ‘/4
jar of commerically prepared strained fruit and /4 jar of
commercially prepared vegetable with ham dinner.
His seizures were unresponsive to the usual
pharma-cobogic management. When the serum sodium
concentra-tion became known, he was given NaHCO, cakulated to
raise the serum sodium by 10 mEq/liter and to
treat
themetabolic acidosis. Serum sodium rose to 131 mEq/liter
within an hour, and his seizures abated.
Body weight decreased to 5.62 kg eight hours after
admission. Fluid output exceeded 670 ml. Serum electro-lytes were: sodium 138 mEq/liter, potassium 3.4 mEq/
liter, chloride 101 mEq/liter, and CO2 22 mm/liter. Fluid
restriction was discontinued at this time.
Case 2
RL is a 6-month-old (corrected for birth at 36 weeks
of gestation) boy who had a convulsion while awaiting a
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1980;66;117
Pediatrics
Douglas Henning, Philip Riedel, Alan Rosen and Linda Burden
Carol Miller, Ronald I. Clyman, Robert S. Roth, Susan H. Sniderman, Roberta A. Ballard,
Control of Oxygenation during the Transport of Sick Neonates
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1980;66;117
Pediatrics
Douglas Henning, Philip Riedel, Alan Rosen and Linda Burden
Carol Miller, Ronald I. Clyman, Robert S. Roth, Susan H. Sniderman, Roberta A. Ballard,
Control of Oxygenation during the Transport of Sick Neonates
http://pediatrics.aappublications.org/content/66/1/117
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