Postprandial Hypoglycemia Resulting From Nasogastric Tube Malposition

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582 PEDIATRICS Vol. 81 No. 4 April 1988 natal intubations and differential diagnosis of res-piratory distress.

ACKNOWLEDGMENT

This work was supported, in part, by grant MCT 952

from the Public Health Service of the US Department

of Health and Human Services.

REFERENCES

DI0N ROBERTS, MD

TIM MCQUINN, MD

ROBERT C. BECKERMAN, MD Department of Pediatrics Section of Pulmonary Diseases

Constance Kaufman Center for the

Study of Breathing Disorders in

In-fants and Children

Tulane University School of Medicine

New Orleans

1. Schultz-Coulon HJ: Luxation des arytaenoidknorpels als intubationsschaden. HNO 1974;22:242-245

2. Quick CA, Merwin GE: Arytenoid dislocation. Arch

Oto-laryngol 1978;104:267-270

3. Prasertwanitch Y, Schwarz JH, Vandam LD: Arytenoid

cartilage dislocation following prolonged endotracheal in-tubation. Anesthesiology 1974;41:516-517

4. Dudley JP, Mancuso AA, Fonkalsrud EW: Arytenoid dis-location and computed tomography. Arch Otolaryngol

1984;110:483-484

5. Kormon RM, Smith CP, Erwin JR: Acute laryngeal injury

with short-term endotracheal anesthesia. Laryngoscope

1973;83:683-690

6. Rudert H: Uber seltene intubationsbedingte innere

kehlk-opftraumen. HNO 1984;32:393-398

7. Kambi V, Radel Z: Intubation lesions of the larynx. Br J Anesth 1978;50:587-590

8. Chatteiji S, Gupta NR, Mishra TR: Valvular glottic

ob-struction following extubation. Anaesthesia

1984;39:246-247

Postprandial

Hypoglycemia

Resulting

From Nasogastric

Tube

Malposition

Recurrent, severe hypoglycemia in infants and

children usually reflects an immature or defective

Received for publication April 24, 1987; accepted June 2, 1987. Reprint requests to (D.B.A.) Department of Pediatrics, Uni-versity of Wisconsin Hospital, 600 Highland Aye, H4/442, Madison, WI 53792.

adaptation to fasting (postabsorptive

hypoglyce-mia). Rarely, however, symptoms of

hypoglyce-mia occur predominantly in the postprandial

pe-nod (less than four hours after a meal). Recent

studies have focused attention on postprandial

hypoglycemia as a manifestation of the late

post-prandial dumping syndrome in children following

gastric surgery.”2 In this setting, hypoglycemia is attributed to reactive hyperinsuhinemia

follow-ing a rapid initial increase in blood glucose

con-centration.3 We report the finding of severe,

re-current hypoglycemia in a nonsurgical patient

receiving nasogastric feedings. In this patient,

in-advertent intubation of the proximal small bowel

simulated the altered gastrointestinal dynamics

associated with the late postprandial dumping

syndrome.

CASE REPORT

An 18-month-old Laotian girl was hospitalized for

ventilatory care and nutrition. She weighed 930 g at

birth after a 28-week gestation. She had a twin. At

birth the patient experienced severe respiratory

dis-tress syndrome with subsequent bronchopulmonary

dysplasia and subglottic stenosis. A tracheostomy was

created at 3 months ofage. Neonatal hypoglycemia was not noted. Prolonged hospitalization was necessitated

by a persistent need for intermittent ventilatory

as-sistance. Height and weight (corrected for gestational age) had increased consistently along the 25th and fifth

to tenth percentiles, respectively. Her feeding regimen

included oral intake as tolerated supplemented by 250 mL of Osmolite (Ross)/SMA (Wyeth) formula (1 : 1 mix-ture), given via nasogastric tube, four times per day.

One afternoon, two hours following oral ingestion of applejuice, the patient had a “staring spell” and rapidly

became obtunded. Serum glucose measured 29 mg/dL.

Administration of 10% dextrose led to rapid resolution

of her symptoms and an increase in serum glucose to

156 mg/dL. The frequency ofher supplemental feedings was increased. Within two days, however, hypoglyce-mia (serum glucose 27 mg/dL) associated with lethargy and weakness reoccurred two and one-half hours

fol-lowing a nasogastric feeding. A urine specimen

ob-tamed at that time revealed glycosuria but no ketones. An IV catheter was inserted and a fasting study was

begun. Throughout a 24-hour period of fasting, the

child remained euglycemic (serum glucose 60 to 90 mgI

dL). A challenge with 220 mL of OsmolytelSMA (1:1)

via nasogastric tube was then performed. At one hour postfeeding, the serum glucose concentration was 294

mgldL. At two hours postfeeding, the child rapidly

be-came unresponsive; serum glucose concentration was

13 mgldL. Concurrent laboratory values included:

serum insulin 96 1iU/mL (normal less than 20 pU/mL

during hypoglycemia), growth hormone 6.2 nglmL,

cor-tisol 18.8 p.gIdL, no serum ketones, lactate 1.2 mmoh/

L.

An abdominal radiograph revealed the nasogastric

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EXPERIENCE AND REASON 583 tube end to be positioned in the duodenum. Withdrawal

ofthis tube to a gastric location resulted in stabilization

ofthe serum glucose values (75 to 107 mgldL) following resumption offeedings. A repeat two-hour postprandial

insulin level was 20 pUImL (concurrent serum glucose

109 mgldL). Thirty-six hours later, the child

experi-enced a seizure. A blood glucose level (Chemstrip) was

20 mgldL, and prompt resolution of symptoms occurred

with glucose administration. A repeat abdominal film

revealed migration ofthe nasogastnic tube into the

duo-denum. Careful replacement and monitoring of

naso-gastric tube position eliminated further hypoglycemic

episodes.

DISCUSSION

Severe postprandial hypoglycemia is unusual

in children. Its occurrence has recently been

re-ported in young patients in whom dumping

syn-drome developed following gastric surgery for

gas-troesophageal reflux.”2 Well described in adults,

the dumping syndrome can have distinctive early

and late manifestations.3’4 Early symptoms are

dominated by gastrointestinal complaints,

dizzi-ness, weakness, and pallor. Rapid gastric

emp-tying of hypertonic fluids leading to jejunal

dis-tention, increased splanchnic blood flow, and

decrease in circulating blood volume are thought

to be responsible for these findings.57 The late

dumping syndrome, occurring one to four hours

following a meal, is characterized by diaphoresis,

weakness, lethargy, and mild or absent

gastroin-testinal symptoms frequently associated with

hy-poglycemia. A typical response to an oral glucose

challenge in children with the late dumping

syn-drome includes a rapid increase in blood glucose

concentration to supranormal levels followed by

a precipitous decline to hypoglycemic levels.’ This pattern appears to result from hypeninsulinemia

evoked by the exaggerated initial increase in

serum glucose concentrations.8’9

This patient’s clinical history is reminiscent of

the late dumping syndrome. Marked

hypergly-cemia occurred soon after nasogastnic tube

feed-ing and was followed by equally profound

hyper-insulinemia and symptomatic hypoglycemia one

hour later. The wide fluctuation in serum blood

glucose concentrations accounted for the

appar-ently paradoxical finding of simultaneous

glyco-suria and hypoglycemia. This constellation of

ab-normal findings returned to normal with

repositioning of the nasogastnic tube. The

unfor-tunate later reoccurrence of hypoglycemia

never-theless confirmed its association with a duodenal

position of the nasogastnic tube.

The likely pathogenesis of postprandial

hypo-glycemia in this child resembles that of the late

dumping syndrome. Inadvertent duodenal

intu-bation simulated accelerated gastric emptying

with rapid filling of the proximal small intestine.

Subsequent hyperglycemia, hypeninsulinemia,

and hypoglycemia may have been exaggerated by

the readily absorbed carbohydrate source (glucose

polymers) of Osmolite formula. On the other

hand, the absence of gastrointestinal and volume

depletion symptoms characteristic of early

dump-ing syndrome in this patient may have been due

to the relative isotonicity of the infant formulas (approximately 300 mosm/kg).

Displacement of nasogastnic feeding tubes into

the proximal small bowel is not a rare occurrence in pediatric patients. As such, it is surprising that

postprandial hypoglycemia in this setting has not

been reported. Studies of adults following

gas-trointestinal surgery have shown that rapid

gas-tnic emptying leads to dumping syndrome only in

a subset ofpatients who appear predisposed to this

disorder.7 Duodenal infusions of glucose in

non-surgical patients with comparable gastric

emp-tying rates produced hyperglycemia,

hypeninsu-linemia, and symptomatic hypoglycemia only in

patients with a prior history of postprandial

hy-poglycemia, suggesting a primary abnormality

that was intestinal in location.9 Pretreatment of

these patients with phenformin, which inhibits

intestinal transport ofglucose,’#{176} corrected the

hy-peninsulinemic response and prevented

hypogly-cemia.9 Therefore, the occurrence of severe

post-prandial hypoglycemia in tube-fed infants may

require the coincident displacement of a feeding

tube in a patient with enhanced intestinal glucose

absorption, thus accounting for its rarity.

Never-theless, this case illustrates that severe

postpran-dial hypoglycemia mimicking the dumping

syn-drome should be considered a potential

complica-tion of gastric tube feeding.

REFERENCES

DAVID B. ALLEN, MD

Department of Pediatrics University of Wisconsin School of Medicine Madison

1. Caulfield ME, Wyllie R, Firor HV, et al: Dumping

syn-drome in children. J Pediatr 1987;110:212-215

2. Meyer S, Deckelbaum RJ, Lax E, et al: Infant dumping syndrome after gastroeosphageal reflux surgery. JPediatr

1981;99:235-237

3. Woodward ER, Neustein CL: The late postprandial dump-ing syndrome. Major Probi Clin Surg 1976;20:28

4. Woodward ER, Neustein CL: The early postprandial dumping syndrome: Clinical manifestations and

patho-genesis. MajorProbi Clin Surg 1976;20:1

5. Lawaetz 0, Blackburn AM, Blood SR, et al: Gut hormone profile and gastric emptying in the dumping syndrome: A

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584 PEDIATRICS Vol. 81 No. 4 April 1988 hypothesis concerning pathogenesis. Scand J

Gastroen-terol 1983;18:73

6. Lawaetz 0, Aritas Y, Blackburn AM, et al: Gastric

emp-tying after peptic ulcer surgery: Some pathophysiological mechanisms ofthe dumping syndrome. ScandJ

Gastroen-terol 1982;17:1065

7. Moir IH: The role of altered gastric emptying in the

mi-tiation of clinical dumping. Scand J Gastroenterol

l979;14:463

8. Roth DA, Meade RC: Hyperinsulinism-hypoglycemia in

the postgastrectomy patient. Diabetes 1965;14:526

9. Permutt MA, Kelly J, Bernstein R, et al: Alimentary hy-poglycemia in the absence of gastrointestinal surgery. N

Engi J Med 1973;288:1206-1209

10. Hollobaugh SL, Rao MB, Kruger FA: Studies on the site and mechanism of action of phenformin: I. Evidence for significant “nonperipheral” effects of phenformin on glu-cose metabolism in normal subjects. Diabetes

1970;19:45-49

Inflammatory

Bowel

Disease

in

a Patient

With Nephropathic

Cystinosis

Cystinosis is an inherited metabolic disorder

characterized by the accumulation of free cystine

within lysosomes resulting in cystine crystal

de-position in multiple organs and tissues. Although

the most affected organ is the kidney and renal

failure develops at approximately 10 years of age,

other nonrenal manifestations have been

increas-ingly recognized.”2 As a result ofsuccessful renal

transplantation, patients are living beyond the

first decade and hypothyroidism, photophobia,

de-creased visual acuity, corneal ulcerations,

hepa-tomegaly, and splenomegaly are becoming more

prominent. We report a 6-year-old boy with

cys-tinosis in whom ulcerative colitis developed. This

is the first such report of the occurrence of these

two uncommon diseases in the same patient.

CASE REPORT

The patient’s diagnosis of cystinosis was made when

he was 2.5 years of age because of failure to thrive, a fair complexion, metabolic acidosis, rickets, and

evi-dence of renal tubular dysfunction including

glyco-sunia, aminoacidunia, proteinuria, and

hyperphospha-turia. A slitlamp examination disclosed homogenous

Received for publication April 20, 1987; accepted June 9, 1987. Reprint requests to (W.R.T.) Division of Pediatric GI and Nu-trition, The Hartford Hospital, 80 Seymour St, Hartford, CT 06115.

American Academy of Pediatrics.

refractile opacities in the cornea and conjunctiva.

Re-sults ofa renal biopsy was consistent with the diagnosis

of cystinosis with crystals seen in tubular epithelial

cells. The leukocyte-free cystine level was elevated at

7.7 nmol of /2 cystme per milligram of protein (normal

<0.2). Treatment included potassium and sodium

ci-trate, phosphate, chloride, calcium, and magnesium supplements, vitamin D, and intermittent cysteamine

for 3 years. Because of nausea, epigastric pain, and

vomiting, the cysteamine therapy was terminated 6

months prior to hospital admission.

At the age of6 years, he was admitted with a 3-month

history of diarrhea, a two-day history of vomiting, and

the acute onset of carpopedal spasms with a serum

cal-cium concentration of 4.3 mgldL, a magnesium level of

0.7 mgldL, sodium value of 131 mEqIL, and potassium

concentration of 3.0 mEq/L. His abdomen was

dis-tended, tympanitic, and diffusely tender. A flat plate

of the abdomen showed a dilated colon but no evidence

of free air or pneumotosis intestinalis. He had been

in-termittently treated with loperamide for his diarrhea but had not taken this drug for 1 week prior to admis-sion. Stool examinations were positive for both occult

blood and polymorphonuclear leukocytes but stool

cul-tures and examination for ova and parasites,

cryptos-poridium, Clostridia difficile toxin, and rotavirus were

all negative. His CBC showed a hemoglobin of 7.8 gI

dL, a WBC of 19.3 x iO L with 45 polymorphonuclear

leukocytes and ten band forms, and an ESR of 32 mml

h. Although his serum albumin was usually low (2.4 to

2.8 gIdL) due to chronic proteinuria, on this admission

it was further decreased to 1.6 gIdL. With bowel rest, calcium, magnesium, electrolyte supplements, and

al-bumin, his colonic dilation partially resolved but on the

eighth hospital day his diarrhea became grossly bloody

with mucous.

A full colonoscopy showed a confluent diffusely

fri-able edematous erythematous mucosa with scattered

small ulcerations and petecchiae. The rectum and

sig-moid were most involved with less severe changes seen

in the transverse and the right colon. Colon lavage

spec-imens were examined for bacterial, viral and parasitic

pathogens and the results were negative. A latex slide

agglutination test for C difficile toxin was negative

(Marion Scientific, Kansas City, MO). Representative

light microscopic and electron microscopic findings are shown in Figs 1 to 3. There was no evidence of

pseu-domembranes granulomas or viral inclusions. Results

of an upper gastrointestinal series with small bowel

follow-through were normal. There was no family

his-tory of ulcerative colitis or Crohn disease.

The patient was treated with bowel rest, N

alimen-tation, IV methylprednisolone, 2 mglkgld, and

metron-idazole, 20 mglkgld. He responded with decreased stool

frequency and decreased hematochezia. After ten days,

the metronidazole was discontinued and the

methyl-prednisolone switched to oral prednisone. A stool

spec-imen was positive for C difficile toxin but a second

spec-imen was negative. Because of the possibility of

pseudomembranous colitis, the patient was treated for

ten days with oral vancomycin, 40 mglkg/d. While

tak-ing oral prednisone and vancomycin, his stools became

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1988;81;582

Pediatrics

DAVID B. ALLEN