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adolescent.

Such results would indicate that phy- REFERENCES


sicians’ educational efforts in the office need to be 1. Greitzer L, Stapleton FB, Wright L, Wedgwood RJ. Tele-
refocused and intensified. Our present study mdi- phone assessment of illness by practicing pediatricians. J
Pediatr. 1976;88:880-882
cates that a concentrated educational effort focused
2. Perrin EC, Goodman HC. Telephone management of acute
on defined, topic-specific behavioral and develop- pediatric illnesses. N EngI J Med. 1978;298:130-135
mental issues in the 0 through 5 range would ad- 3. Fosarelli PD. The telephone in pediatric medicine, a review.
Clin Pediatr (Phila). 1983;22:293-296
dress areas of greatest concern.
4. Levy JC, Rosekrans J, Lamb GA, Friedman M, Kaplan D,
Parents and caretakers have many questions ne- Strasser P. Development and field testing of protocols for
ganding child health issues and new methods must the management of pediatric telephone calls: protocols for
pediatric telephone calls. Pediatrics. 1979;64:558-563
be developed to address these concerns. We, as
5. Strasser PH, Levy JC, Lamb GA, Rosekrans J. Controlled
physicians, should take note of these issues and use clinical trial of pediatric telephone protocols. Pediatrics.
this information to target anticipatory guidance 1979;64:553-557
6. Katz H, Pozen J, Mushlin A!. Quality assessment of a
efforts within the confines of our own practice
telephone care system utilizing non-physician personnel.
setting, as well as advocate the expansion of efforts Am J Pub/ic Health. 1978;68:31-37
to educate parents in the community at large. 7. Villarrel SF, Berman 5, Groothius JR, Strange V, Schmitt
BD. Telephone encounters in a university pediatric group.
C/in Pediatr (Phi/a). 1983;23:456-458
JAMES L. TROUTMAN, MD 8. Levy JC, Strasser PH, Lamb GA, et al. Survey of telephone
JEFFREY A. WRIGHT, MD encounters in three pediatric practice sites. Public Health
Rep. 1980;95:324-328
DONALD L. SHIFRIN, MD
9. Reisinger KS, Bires JA. Anticipatory guidance in pediatric
University of Washington practice. Pediatrics. 1980;66:889-892
Dept of Pediatrics 10. Fulginiti VA. Role of the pediatrician in patient education.
Pediatrics. 1984;74(suppl):914-916
Children’s Hospital and Medical Center
Seattle, WA

Captopril-Induced Reversible with hypertension due to coarctation of the aorta


who developed acute renal insufficiency while ne-
Acute Renal Failure in an ceiving captopnil. Functionally, renal hemodynamic
Infant With Coarctation of changes in this child may have been similar to those
postulated in patients with bilateral renal artery
the Aorta stenosis who have developed acute renal failure
when receiving ACE inhibitors.

Activation of the nenin-angiotensin system has


been implicated in the initiation of hypertension CASE REPORT
associated with coanctation of the aorta, with so- This patient was a 1.73-kg white female infant born at
dium and volume expansion playing a role in main- 33 weeks postconception. She was found to be clinically
tenance of the hypertension. Increase in total pe- hypertensive at birth with diminished pulses in the lower
niphenal resistance induced by the stenosis itself extremities. Four extremity blood pressures revealed an
also has received increasing attention in the etiol- upper extremity blood pressure of 150 mm Hg systolic
ogy of coanctation and renal vascular hyperten- and a lower extremity blood pressure of 55 mm Hg
systolic. Echocardiogram demonstrated a severe periduc-
sion.’5 To date, angiotensin-converting enzyme
tal coarctation, small left ventricle, bicuspid aortic valve,
(ACE) inhibitors have been used to lower acutely
and a hypoplastic aortic arch. She was treated medically
blood pressure in patients with coarctation, as well
with furosemide and digoxin; but, due to worsening
as in “paradoxical” postoperative treatment of hy- congestive heart failure, she underwent surgical repair of
pentension.2’6 We recently cared for a small infant the periductal coarctation. Severe hypertension, thought
to be secondary to the hypoplastic arch, persisted post-
operatively despite therapy with propranolol, hydrala-
zine, and furosemide. Doppler estimation of the remain-
Received for publication Oct 22, 1990; accepted Dec 5, 1990.
ing gradient contributed by the hypoplastic arch was 34
Reprint requests to (E. G. W.) Division of Pediatric Nephrology,
Cardinal Glennon Children’s Hospital, St. Louis University, to 100 mm Hg. Surgical arch repair was considered ex-
1465 S Grand Blvd, St. Louis, MO 63104. tremely risky in this 2-kg infant. Due to persisting hy-
PEDIATRICS (ISSN 0031 4005). Copyright © 1991 by the pertension and congestive heart failure despite continu-
American Academy of Pediatrics. ing therapy with furosemide, digoxin, propranolol, and

816 PEDIATRICS Vol. 88 No. 4 October 1991


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hydralazine, captopril was instituted 1 month after sun- artery stenosis affecting a single kidney.9”#{176}The case
gery at a dose of 0.5 mg/kg and increased to 1.1 mg/kg currently reported suggests that the same risk may
per dose every 6 hours. Hydralazine and propranolol exist in patients with suprarenal aortic coanctation.
subsequently were discontinued within 1 week of initia-
Autoregulation of glomerular filtration rate in
tion of captopril. During the next 2 weeks her blood
the presence of decreased renal arterial pressure
pressure improved, but it still remained elevated with
has been reported experimentally to depend on
upper extremity blood pressures of 130 to 140 mm Hg
angiotensin production producing an increase in
systolic. During this same time, despite a stable dose of
captopnil, her creatinine level slowly increased from 0.5 effenent arteniolar constriction, which along with
mg/dL to a high of 2.3 mg/dL, associated with oliguria, affenent arteniolar relaxation maintains filtration
weight gain of 500 g, and hyperkalemia (potassium, 8.2 fraction.”2 We postulate that the decreased gb-
mEq/dL). There was no evidence of eosinophilia, eosi- merubar filtration rate in our patient was due to the
nophiluria, or rash. During this interval, she received no inability to autonegulate gbomerular filtration rate
medications other than those previously described except as has been hypothesized in patients with bilateral
oral vitamins. There was no evidence to suggest a sec- renal artery stenosis after treatment with ACE
ondary etiology for the renal deterioration such as sepsis,
inhibitors. Sodium depletion caused by use of fu-
volume depletion, hypotension, or renal venous or arterial
nosemide may have accentuated the impaired au-
thrombosis. Captopril was discontinued, and the patient
tonegulation, as has been shown in animals with
was given propranolol, prazosin, furosemide, and Aldac-
tazide. Blood pressure control was achieved, however, decreased renal artery pressure and blockade of the
only after replacing the prazosin with minoxidil. Her renin-angiotensin system.’2 Whether these changes
creatinine level improved to a baseline of 0.6 mg/dL are related only to the decrease in the constrictor
within a week. Two months later, she died secondary to influence of angiotensin II on the efferent arteriole
metabolic acidosis, gastric aspiration, and respiratory on the combination of decreased angiotensin II and
arrest. At autopsy there was no evidence of renal artery increased blood and/on tissue levels of bradykinin,
stenosis or persistent periductal coarctation. Other ech- prostacyclin, and prostaglandin E2 induced by ACE
ocardiographic diagnoses were confirmed. inhibition is controversial.’3 The severity of me-
chanical obstruction in our patient with hypoplastic
aortic arch could have placed her at a higher risk
DISCUSSION than the more typical patient with uncomplicated
supnanenal coanctation.
Suprarenal aortic coanctation hypertension has
ACE inhibitors also have been reported to pro-
multiple interacting etiologies. Increased renin 1ev-
duce acute interstitial nephnitis associated with fe-
els have been demonstrated in the acute phase in
yen, eosinophibia, eosinophibunia, and rash.’4 Our
experimental coanctation. Sodium retention also
patient did not manifest signs of interstitial ne-
has been reported in patients and in animal models,
phnitis, and no evidence for this diagnosis was found
with “maintenance” of hypertension being volume-
at post mortem examination. In addition, there
dependent.’5 Similar mechanisms have been de-
were no hypotensive episodes, no decrease in body
scnibed in experimental renovasculan hypertension
weight to suggest volume depletion, or change in
using the one kidney-one clip Goldblatt model.
clinical status or other laboratory parameters to
After the acute phase, a decrease in volume induced
suggest septicemia or other overwhelming systemic
by diuretics or by sodium restriction can result in
illness as etiologies for the deterioration of renal
responsiveness of blood pressure to angiotensin II
function. No potentially nephrotoxic antibiotics
blockade.3’4’7 In addition, Anderson et al reported
were used for 1 month preceding on during captopnil
that the stenosis itself accounted for about one
therapy.
third of the increase in total peripheral resistance
In conclusion, ACE inhibitors have been found
occurring in the one-kidney Goldblatt model,
to be effective in the treatment of hypertension
whereas the remaining increase in peripheral re-
associated with coanctation of the aorta. In the child
sistance was due to vasoconstniction of other, non-
with coarctation receiving an ACE inhibitor, mon-
renal vascular beds, presumably from increased
itoring renal function is essential. ACE inhibitors
plasma levels of angiotensin 11.8 Similar observa-
should be considered in the etiology of any change
tions have been made in neonatally induced coarc-
in renal function. Careful attention to serum potas-
tation hypertension in pups.5 The increase in pe-
sium bevels is extremely important in these pa-
riphenal resistance from the stenosis itself may be
tients.
independent of the nenin-angiotensin system.5
ACE inhibitors have been used in the treatment
of coanctation-induced hypertension. These agents
have been associated, however, with development ACKNOWLEDGMENT
of acute renal failure in patients with bilateral renal We thank Darlene Laws for preparation of the manu-
artery stenosis as well as in individuals with renal script.

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EXPERIENCE AND REASON 817
ELLEN G. WooD, MD coarctation of the aorta. Clin Cardiol. 1982;5:551-553
7. Gavras H, Brunner HR, Vaughan ED Jr, Laragh JH. Angio-
TIMOTHY E. BUNCHMAN, MD tensin-sodium interaction in blood pressure maintenance of
ROBERT E. LYNCH, MD, PHD renal hypertensive and normotensive rats. Science.
Department of Pediatrics 1973;180:1369
8. Anderson WP, Korner P1, Angus JA, Johnston CI. Contri-
St. Louis University School of Medicine bution of stenosis resistance to the rise in total peripheral
resistance during experimental renal hypertension in con-
scious dogs. C/in Sci. 1981;61:663-670
REFERENCES 9. Curtis JJ, Luke RG, Whelchel JD, Diethelm AG, Jones P,
Dustan HP. Inhibition of angiotensin-converting enzyme in
1. Alpert BS, Bain HH, Balfe JW, Langford Kidd BS, Olley renal transplant recipients with hypertension. N EngI J
PM. Role of the renin-angiotensin-aldosterone system in Med. 1983;308:377-381
hypertensive children with coarctation of the aorta. Am J 10. Hricik DE, Browing PJ, Kopelman R, Goorno WE, Madias
Cardiol. 1979;43:828-834 NE, Dzau VJ. Captopril induced functional renal insuffi-
2. Fallo F, Maragno I, Merola P, Mantero F. Effect of Captopril ciency in patients with bilateral renal-artery stenosis or
on blood pressure and on the renin-angiotensin-aldosterone renal artery stenosis in a solitary kidney. N EngI J Med.
system in coarctation of the aorta. Clin Exp Hypertens. 1983;308:373-376
198:3;:321-328 11. Hall JE, Guyton AC, Cowley AW Jr. Dissociation of renal
:3. Whitlow KatholiPL, RE. Neurohumoral mechanisms in blood flow and filtration rate autoregulation by renin deple-
acute aortic
coarctation in conscious and anesthetized dogs. tion. Am J Physiol 1977; 232:F215-221
Am J Physiol. 44(Heart Circ Physiol 13):1983;H614-H621 12. Hall JE, Guyton AC, Jackson TE, Coleman TG, Lohmeir
4. l3ailie MD, Donoso BS, Gonzalez NC. Role of the renin- TE, Trippodo NC. Control of glomerular filtration rate by
angiotensin system in hypertension after coarctation of the renin-angiotensin system. Am J Physiol. 1977;233:F366-
aorta. J Lab Clin Med. 1984;104:553-562 F372
5. Bagby SP, Fuchs EF. Chronic MK421 fails to modify evo- 13. Williams GH. Converting-enzyme inhibitors in the treat-
lution of hypertension in neonatally coarcted pups. Hyper- ment of hypertension. N EngI J Med. 1988;319:1517-1525
ten.sion. 1989;13:91-101 14. Steinman TI, Silva P. Acute renal failure, skin rash, and
6. Caste A, Conti VR, Talabi A, Brouhard BH. Effective use eosinophilia associated with Captopril therapy. Am J Med.
of Captopril in postoperative paradoxical hypertension of 1983;75:154-156

When CHV became unresponsive to primary tumor


Primary Central Hyperventila-
management with radiation therapy and adminis-
tion in a Child With a Brainstem tration of dexamethasone, oral morphine was ad-
Glioma: ManagementWith Con- ministered
nate. Although
in an attempt to decrease
some decrease
his respiratory
in respiratory rate
tinuous Intravenous Fentanyl was noted, the effect was brief (30 to 60 minutes)
and excessive sedation with an inability to handle
oral secretions necessitated discontinuing its use.
Alveolar ventilation and respiratory rate are neg- CHV eventually was controlled with the narcotic
ulated by central respiratory centers in the pons agent, fentanyl, which was administered as a con-
and medulla, which are influenced by both neural tinuous infusion. We are unaware of previous re-
and humonab input. Aberrations in control mecha- ports concerning the use of fentanyb to control
nisms can bead to apnea, hypoventilation, or hyper- CHV.
ventilation. Although hyperventilation usually oc-
curs as a compensatory mechanism for metabolic CASE REPORT
derangements, primary central hyperventilation
An 11-year-old boy had a 3-week history of progressive
(CHV) has been reported with brainstem gliomas,
tachypnea, ataxia, and diplopia. Initial examination re-
central nervous system bymphoma, supratentonial
vealed a respiratory rate of 72 breaths per minute with a
lesions, and head trauma.13
primary respiratory alkabosis. Magnetic resonance imag-
We present an 11-year-old boy with a brainstem ing of the brain revealed a diffuse and symmetric pontine
glioma whose initial symptoms included CHV. mass with evidence of extension into the superior me-
dulla, consistent with a brainstem (pontine) glioma. Dex-
amethasone therapy was started and the patient was
referred to St. Jude Children’s Research Hospital where
he was treated with hyperfractionated radiation therapy.
Received for publication Jan 4, 1991; accepted Feb 20, 1991.
This therapy initially controlled the CHV and his respi-
Reprint requests to (J.D.T.) Division of Pediatric Anesthesiol-
ogy/Critical Care Medicine, St. Jude Children’s Research Hos- ratory rate ranged from 28 to 40 breaths per minute.
However, toward the end of the 6-week course of radia-
pital, :3:32 N. Lauderdale, Memphis, TN 38101.
PEDIATRICS (ISSN 0031 4005). Copyright © 1991 by the tion therapy, his respiratory rate began to increase and
American Academy of Pediatrics. was unresponsive to an increase in his dexamethasone

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818 PEDIATRICS Vol. 88 No. 4 October 1991
Captopril-Induced Reversible Acute Renal Failure in an Infant With Coarctation of
the Aorta
ELLEN G. WOOD, TIMOTHY E. BUNCHMAN and ROBERT E. LYNCH
Pediatrics 1991;88;816

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Captopril-Induced Reversible Acute Renal Failure in an Infant With Coarctation of
the Aorta
ELLEN G. WOOD, TIMOTHY E. BUNCHMAN and ROBERT E. LYNCH
Pediatrics 1991;88;816

The online version of this article, along with updated information and services, is located on
the World Wide Web at:
http://pediatrics.aappublications.org/content/88/4/816

Pediatrics is the official journal of the American Academy of Pediatrics. A monthly publication, it has
been published continuously since 1948. Pediatrics is owned, published, and trademarked by the
American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois, 60007.
Copyright © 1991 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 1073-0397.

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