Refractory Hypoglycemia Associated with a Malpositioned Umbilical Artery Catheter

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ABSTRACT. An infant with unexplainedhypoglycemia

who responded poorly to medical management had the

tip of his umbilical artery catheter

positioned near the

major arteries supplying the pancreas. Catheter reposi tioning resulted in immediate normoglycemia. A â€œ¿reac tiveâ€• response to the direct infusion of glucose is postu lated on the basis of the clinical response and a decrease in serum insulin/blood glucose ratio. Pediatrics 64:315â€” 317, 1979; umbilical artery catheter, hypoglycemia.

Complications previously associated with umbil ical artery catheterization have included infection, thrombosis with embolization, the development of

renovascular

hypertension,

vasculitis

with

aneu

rysm formation, hemorrhage, extravascular place ment with perforation, arrhythmias, neurologic def icits, and the occurrence of necrotizing enterocoli tis.'@9 To our knowledge, hypoglycemia responsive to catheter repositioning has not been reported.

CASE REPORT

A white male infant, who weighed 2,637 gm after a 36-week gestation by Dubowitz score, was referred to the

Florida Regional Perinatal Intensive Care Center at Pen

sacola at 12 hours of age for evaluation and treatment of

progressive respiratory distress. Maternal and family his

tories were unremarkable. Spontaneous rupture of mem branes occurred shortly before vaginal delivery. Apgar scores were not recorded but only bulb suctioning was required in the immediate postpartum period. On admis sion to the hospital, the respiratory rate was 55/mm and the infant was requiring 40% inspired oxygen by hood. A Dextrostix test (Ames Company, Elkhart, IN) indicated 80 mg/lOO ml. A No. 5.0 French umbilical artery catheter (Sherwood Medical, St Louis, MI) was inserted with the end hole above the diaphragm at the level of the 11th

Received for publication Nov 10, 1978; accepted Feb 23, 1979. Reprint requests to (@J.W.N.) Sacred Heart Children's Hospital of Pensacola, 5151 North 9th Aye, Pensacola, FL 32504.

thoracic vertebra on x-ray examination. Since the chest films were compatible with respiratory distress syndrome, continuous distending airway pressure was delivered through nasal prongs in addition to the oxygen.

By the second day of life, lOOc inspired oxygen and 6 cm of water pressure were required. By the fourth day, however, he had improved considerably and only 27@ inspired oxygen and 2 cm of distending pressure were necessary.

At 88 hours of age while receiving a 5@?idextrose and electrolyte solution through the umbilical catheter at 17.5 ml/hr, the infant experienced several profound episodes of apnea and vigorous resuscitation was required. Arterial blood gases and serum electrolytes were normal. The infant was already receiving supplemental calcium glu conate for hypocalcemia diagnosed on the second day of life, and parenteral antibiotics pending the results of a blood culture drawn at the time of hospital admission (subsequently negative). The clinical and laboratory

events from this point are summarized in the Table. Two

Dextrostix

determinations

failed

to show

any color

change and an immediate microglucose (true glucose method) was reported at 13 mg/lOO ml with an immediate repeat value of 9 mg/100 ml. The infant was given 2.5 ml

of 25% dextrose solution by arterial catheter, and the

dextrose content of the fluid given through the same

catheter

by infusion was increased

to 10%. A repeat

Dextrostix determination

with a reflectance colorimetric

method (Eyetone/Dextrostix System, Ames Company, Elkhart, IN) was 78 mg/100 ml. This method was used

for all further Dextrostix determinations

which were per

formed on capillary blood samples. Within 50 minutes,

the Dextrostix value fell to 25 mg/ 100 ml and the dextrose

content of the parenteral infusion was increased to 15%. A repeat determination in another 50 minutes showed a blood glucose of 10 mg/100 ml with microglucose confir

mation. Hydrocortisone,

12.5 mg, was given through the

catheter and a transient

rise in blood glucose to 45 mg/

100 ml was observed. Repeated values in the range 10 to

20 mg/100 ml over the next hour, however, resulted in catheter administration of 5 ml of 25% dextrose solution as a bolus over 5 minutes and constant infusion of the

same solution at 17.5 mI/hr. Epinephrine

aqueous sus

pension 1:200 (Sus-Phrine, Cooper Laboratories, Parsip

PEDIATRICS Vol. 64 No. 3 September

1979

315

Refractory Hypoglycemia Associated with a

Malpositioned Umbilical Artery Catheter

Jon W. Nagel, MD, J. Stephen Sims, MD, Charles E. Aplin II, MD,

and Edward R. Westmark,

MD

From the Florida Regional Perinatal Intensive Care Center at Pensacola, Pensacola, Florida

at Viet Nam:AAP Sponsored on September 7, 2020

www.aappublications.org/news

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TimeDextrose

Infusion

(mg/kg/mm)Other

TherapyBlood

Glucose

(mg/100

ml)Remarks@â€”-08005.60900-09305.60-1310005.6D25W,

2.5

ml@UAC*102011.278111011.225113016.8122016.810122916.8Hydrocortisone,

12.5

mg-UAC125516.845140016.810141216.8D25W,

5 ml-UAC151528.060Trace

urine reduc ing

substance163528.0Aqueous

epinephrine

0.06 ml subcutane

ously170028.090Serum

insulin 20.2

mCi/mi181028.02101+

urine reducing substance200016.8120Arterial

catheter re positioned200516.822020301

1.22+ urine reducing

substance213011.225021405.622205.61251+

urine reducing substance14005.658Serum

insulin 7.4 mCi/ml

TABLE.

Clinical and Laboratory Data

* UAC, umbilical artery catheter.

pany, NJ), 0.06 ml, was administered subcutaneously. Urine examination revealed only trace reducing sub

stance. A serum insulin was drawn through the arterial

catheter

and later reported to be 20.2 @U/mlwith a â€˜¿@â€˜I

radioimmunoassay method (Pharmacia, Piscataway, NJ),

while a simultaneous

blood glucose of 90 mg/100 ml was

recorded

to give an insulin to glucose ratio of 0.22. A

roentgenogram of the chest obtained for verification of catheter position showed that the tip had become repo sitioned at the level of the 12th thoracic vertebra since admission. The catheter was withdrawn to the level of the fourth lumbar vertebra as confirmed by repeat film of the abdomen. Dextrostix determinations done imme diately before and after withdrawal were 120 mg/100 ml and 220 mg/100 ml, respectively. Despite the absence of

further therapeutic

intervention,

rapid reduction in par

enteral fluid glucose content to 5% over the ensuing two

hours was accomplished. Serial Dextrostix and microglu cose levels remained between 125 and 250 mg/100 ml. A

repeat serum insulin obtained through the umbilical ar

tery catheter 19 hours after repositioning was 7.4 @U/ml

with a simultaneous

microglucose of 58 mg/100 ml (in

sulin to glucose ratio of 0.12). The infant continued to

recover uneventfully

and was discharged

on the 1lth

hospital day. At 7 months of age, he continues to develop

normally without recurrence of symptoms.

DISCUSSION

Conditions

predisposing

neonates

to hypoglyce

mia are diverse and include intrauterine growth retardation, multiple gestation, maternal diabetes

mellitus,

Rh isoimmunization,

intracranial

injury,

birth asphyxia, Beckwith-Wiedemann syndrome, insulinoma, hypothermia, and sudden cessation of an intravenous infusion of glucose.'Â° None of these

conditions

was or has become

apparent

in the infant

reported here.

Lilien et al' â€˜¿

have demonstrated

that

a constant

intravenous

infusion

of glucose

at a rate of 8 mg/

kg/mm

in 22 hypoglycemic

infants

resulted

in nor

moglycernia within 30 minutes except in the case of

one severely

growth

retarded

baby.

More

impor

tantly,

all

appropriately

grown

infants

attained

blood glucose values of 30 mg/100 ml or greater within ten minutes and 40 mg/100 ml or greater

(3)

within

20 minutes.

Sustained

determinations

greater

than 40 mg/100

ml in our patient

were not

attained until an infusion rate of 28 mg/kg/mm was

reached.

He was also being

treated

with

cortico

steroids and catecholamines.

The pancreas

is situated

between

the celiac trunk

and superior mesenteric artery and receives its blood supply from four pancreaticoduodenal arter ies, a dorsal pancreatic artery, and multiple other branches of the splenic arteries.'2 In a radiographic study of 15 infants, Phelps et alâ€•showed the origin of the celiac axis to be within one vertebral body of the top of the 12th thoracic vertebra, and the su

perior

mesenteric

artery

to be within

one vertebral

body below in all cases. If one assumes a cardiac output of 200 ml/kg/min and a 1% distribution of

flow to these

two

major

arteries'4

the

constant

infusion

of 10% and 15% dextrose

solutions

at a rate

of 17.5 ml/hr via a catheter positioned near their origins would have resulted in blood glucose con centrations of 560 and 840 mg/100 ml, respectively,

within

the pancreas.

Direct

infusion

into the pan

creas would explain the severe hypoglycemia which was so poorly responsive to aggressive therapy and otherwise unexplained in the patient reported here. Studies with the isolated perfused dog pancreas have shown 100-fold increases in insulin secretion with an increase in glucose concentration in a con stant infusate from 25 mg to 300 mg/100 ml.'5 Since the venous drainage of the pancreas is through the

portal

12 a â€œ¿reactiveâ€•

hyperinsulinemic

re

sponse from pancreatic beta cells could have re sulted in rapid clearance of infused glucose by the liver with contributions from other insulin sensitive tissues as well. Such an exaggerated response would account for the extremely low values for peripheral

blood glucose

which

were observed.

The rapid

re

turn of levels to normoglycemic

values, decrease

in

serum insulin/blood glucose ratio, and subsequently

benign

course

after the arterial

catheter

was repo

sitioned away from the celiac and superior mesen teric origins support such a sequence of events.

Although

the peak insulin level of 20.2 @.tU/mlmight

appear

to be only a modest

elevation,

Salle

and

Ruitton-Uglienco

â€˜¿@

noted

significantly

higher

insu

lin responses

measured

in the portal

vein of appro

priately

grown infants

when compared

with simul

taneous values obtained through aortic catheters

after a glucose

challenge.

Mean

peak aortic

values

obtained

in several

of the infants

studied

by them

were of the same magnitude

as the response

which

we recorded.

Unfortunately,

portal

vein insulin val

ues were not obtained in our own patient.

We suggest that reactive

hypoglycemia

be consid

ered

in any infant

with

unexplained

or unusually

severe hypoglycemia in the presence of an umbilical

artery

catheter.

Catheter

position

should

be con

firmed

by roentgenogram;

if the

tip is near

the

origins

of the vessels

supplying

the pancreas

(11th

thoracic

to first

lumbar

vertebrae),

it should

be

withdrawn

to the

level

of the

aortic

bifurcation

(fourth

lumbar

vertebra)

while monitoring

the level

of blood glucose.

REFERENCES

1. Lim MO, Gresham EL, Franken EA, et al: Osteomye litis as a complication of umbilical artery catheteri

zation.Am J Dis Child 131:142,1977

2. White EA, Crelin ES, McIntosh S: Septic arthritis of the hip joint secondary to umbilical artery catheteri zation associated with transient femoral and sciatic neuropathy. Clin Orthop 100:190, 1974

3. Egan EA, Eitzman DV: Umbilical vessel catheteriza tion. Am J Dis Child 121:213, 1971

4. Plumer LB, Kaplan GW, Mendoza SA: Hypertension in infantsâ€”a complication of umbilical arterial cath eterization. J Pediatr 89:802, 1976

5. Rajs J, Finnstrom 0, Wesstrom G: Aortic aneurysm

developing after umbilical artery catheterization. Acta Paediatr Scand 65:495, 1976

6. Van Leeuwen G, Patney M: Complications of umbil ical vessel catheterization: Peritoneal perforation. Pe diatrics 44:1028, 1969

7. Hoekstra RE, Semba T, Fangman JJ, et al: Intestinal

perforation following withdrawal of umbilical artery

catheter. J Pediatr 90:290, 1977

8. Aziz EM, Robertson AF: Paraplegia: A complication

of umbilical artery catheterization. J Pediatr 82:1051,

1973

9. Lehmiler DJ, Kanto WP: Relationships of mesen teric thromboembolism, oral feeding, and necrotizing

enterocolitis.J Pediatr 92:96,1978

10. Avery GB: Neonatologyâ€”Pathophysiology and Management of the Newborn. Philadelphia, JB Lip

pincott, 1975, p 423

11. Liien LD, Grajwer LA, Pildes RS: Treatment of neonatal hypoglycemia with continuous intravenous glucose infusion. J Pediatr 91:779, 1977

12. Woodburne RT: Essentials ofHuman Anatomy. New

York, Oxford University Press, 1969, p 405

13. Phelps DL, Lachman RS, Leake RD, et al: The radiologic localization of the major aortic tributaries in the newborn infant. J Pediatr 81:336, 1972 14. Smith CA, Nelson NM: The Physiology of the New

born Infant, ed 4. Springfield, Charles C Thomas,

1976,p 117

15. â€˜¿ppE, Dobbs RE, Arimura A, et al: Release of im munoreactive somatostatin from the pancreas in re sponse to glucose, amino acids, pancreozymin-chole cystokinin, and tolbutamide. J Clin Invest 60:760, 1977

16. Salle B, Ruitton-Uglienco A: Glucose disappearance rate, insulin response and growth hormone response in the small for gestational age and premature infant of very low birth weight. Biol Neonate 29:1, 1976

ARTICLES

317

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1979;64;315

Pediatrics

Jon W. Nagel, J. Stephen Sims, Charles E. Aplin II and Edward R. Westmark

Refractory Hypoglycemia Associated with a Malpositioned Umbilical Artery Catheter

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