Treatment of Congenital Telangiectatic Vascular Malformations With the Pulsed-Dye Laser (585 nm)

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Administration of ipecac has been observed to

pro-duce potentially fatal cardiac myopathy as well as

skeletal myopathy and gastrointestinal symptoms

both in adults71 and children.2”7’1216 In older

chil-dren, ipecac toxicity can occur with therapeutic

ad-ministration after toxic ingestions7 or in abuse by

bulimic or suicidal patients.6’17 In younger children,

surreptitious administration by caregivers has been

described as an additional source of noncardiac

mor-bidity #{149}2,4,1216 To our knowledge, ipecac-related

car-diac disease from MSBP has been reported only

twice. Day et al5 described a 4-year-old patient with

gastrointestinal and progressive cardiac symptoms

who died after chronic maternal ipecac

admin-istration. An echocardiogram revealed dilation of all

four chambers, tricuspid and mitral insufficiency,

and decreased left ventricular contractility, but no

quantitative measures were provided. Sutphen and

Saulsbury4 described a 16-month-old patient with

vomiting, diarrhea, muscle weakness, and

arrhyth-mia who had probably received ipecac repeatedly

from his mother. His echocardiogram was normal.

The exact mechanism of ipecac cardiotoxicity

re-mains unclear,18 and the significance of its effects on

the heart has been the subject of debate.19 However,

the association of unexplained cardiomyopathy and

gastrointestinal symptoms mandates a high level of

suspicion by the clinician. In patients with a

long-standing history of unexplained vomiting,

examina-tion of body fluids for constituents of ipecac is

im-portant both for medical and legal purposes. Their

detection in body tissues and fluids, including blood,

urine, gastric secretions, and vomitus, currently

re-quires advanced technologies.6

Syrup of ipecac is prepared from Cephaelis

acumi-nata and contains I .23 to I .57 mg of ether-soluble

ipecac alkaloids per milliliter, and 90% of the

alka-bids are emetine and cephaeline.1 Their

concentra-tions observed in reported cases are comparable with

the levels detected in our pafient.2.4SlZl3 Negative

examinations of the serum (as obtained twice by us)

associated with positive urine findings are not

sur-prising, since ipecac constituents accumulate in the

kidneys, facilitating their detection in the urine

weeks after administration and disappearance from

the bloodstream.5 Tests for emetine and cephaeline

are not included in routine hospital drug screens, and

detection therefore requires a specific request based

on a high index of suspicion.

We conclude that the diagnosis of ipecac toxicity

should be considered in patients with unexplained

vomiting and skeletal or cardiac myopathy. The

symptoms and echocardiographic abnormalities are

reversible after discontinuation of the drug. Future

efforts should focus on increasing the rapid

avail-ability of sensitive detection assays for ipecac



We thank Lynn Waldrop and Sheri Fisher for their excellent technical assistance.




Dept of Pediatrics

*Divisiofl of Pediatric Gastroenterology :I:Division of Pediatric Cardiology

University of South Alabama College of Medicine

Mobile, AL


1. Do Smet PAGM, Vulto AG. Drugs used in non-orthodox medicine. In:

Dukes MNG, ed. Side Effects ofDrugs Annual ii. New York, NY: Elsevier Science Publishers; 1987:422-424

2. Johnson JE, Carpenter BLM, Benton J, Cross R, Eaton LA Jr, Rhoads JM.

Hemorrhagic colitis and pseudomelanosis coli in ipecac ingestion by

proxy. I Pediatr Gastroenterol Nutr. 1991;12:501-506

3. Rosen CL, FrostJDJr, Bricker T, TarriowJD, Gillette PC, Dunlavy S. Two

siblings with recurrent cardiorespiratory arrest: Munchausen syndrome by proxy or child abuse? Pediatrics. 1983;71:715-720

4. Sutphen JL, Saulshury Fl’. Intentional ipecac poisoning: Munchausen syndrome by proxy. Pediatrics. 1988;82:453-456

5.Day L, Kelly C, Reed G, Andersen JM, Keljo JM. Fatal cardiomyopathy:

suspected child abuse by chronic ipecac administration. Vet Hum Toxicol. 1989;31 :255-257

6. Lachman MF, Romeo R, McComb RB. Emetine identified in urine by HPLC, with fluorescence and ultraviolet/diode array detection, in a patient with cardiomyopathy. Cli,: Chem. 1989;35:499-502

7. Manno BR, Manno JE. Toxicology of ipecac: a review. Cliii Toxicol.


8. Adler AG, Walinsky P. KraII RA, Cho SY. Death resulting from ipecac

syrup poisoning. JAMA. 1980;243:1927-1928

9. Palmer EP, Guay AT. Reversible myopathy secondary to abuse of ipecac

in patients with major eating disorders. N EngI IMed.


10. Mateer JE, Farrell BJ, Chou SSM, Gutman L. Reversible ipecac myopa-thy. Arch Neurol. 1985;42:188-190

11. Kuntzer 1, Bogousslavsky J, Deruaz JP, Janzer R, Regli F. Reversible emetine-induced myopathy with ECG abnormalities: a toxic myopathy.


Neurol. 1989;236:246-248

12. Colletti RB, Wasserman RC. Recurrent infantile vomiting due to inten-tional ipecac poisoning. I Pediatr Gastroenterol Nutr. 1989;8:394-396

13. Santangelo WC, Richey JE, Rivera L, Fordtran JS. Surreptitious ipecac administration simulating intestinal pseudo-obstruction. Aiiii liitcri: Med. 1989;110:1031-1032

14. Feldman KW, Christopher DM, Opheim KB. Munchausen syndrome! bulimia by proxy: ipecac as a toxin in child abuse. Child Abuse Negl.

1989;1 3:257-261

15. McClung HJ. Murray R, Braden NJ, Fyda J, Myers RP, Gutches L.

Intentional ipecac poisoning in children. AJDC. 1988;142:637-639

16. Berkner I’, Kastner 1, Skolnick L. Chronic ipecac poisoning in infancy: a case report. Pediatrics. 1988;82:384-385

17. Ente G, Penzer PH. New abuse of ipecac. Pediatrics. 1986;77:134-135 18. GeIb BD. Metabolic heart disease. Emetine and ipecac. In: Garson A Jr.

Bncker J’, McNamara DG, eds. The Science and Practice of Pediatric cardiology. Philadelphia, PA: Lea &Febiger; 1990:1673

19. Isner JM. Effects of ipecac on the heart. N Eng! JMed. 1986;314:1253













The two most common vascular abnormalities of

childhood are port-wine stains and hemangiomas)

Port-wine stains are congenital capillary

malforma-tions, whereas hemangiomas are benign tumors of

Received for publication Jan 25, 1993; accepted Apr iS. 1993.

Reprint requests to (J.G.M.) Dept of Dermatology B-153, University of

CoIn-rado School of Medicine, 4200 E Ninth Ave. Denver, CO 80262.

PEDIATRICS (ISSN 0031 4005). Copyright © 1993 by the American

Acad-emy of Pediatrics.

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TABLE 1. Characteristics of Telangiectatic Vascular Malformations, Port-Wine Stains, and Telangiectatic Hemangiomas


Telangiectatic Vascular Malformation Port-Wine Stain Telangiectatic Hemangioma

Always present at birth Always present at birth May be present at birth

Grows proportionately with child Grows proportionately with child Grows faster than child

Discrete telangiectasias present No apparent telangiectasias Telangiectasia clinically apparent

Capillary malformation Capillary malformation Tumor of endothelial cells

TABLE 2. Lesion and Treatment Data

Patient Location Size of Lesion


Age at First

Treatment (mo)

No. of


I Larm 34 8 3

2 3

L thigh R forehead

10.5 18

0.5 0.5

2 4

4 Lhand 92 7 3

5 6

Rthigh Larm

18 10





vascular endothelium.2 The natural history of each of

these lesions is distinct. Port-wine stains begin as

discrete pink/red macules and grow proportionately

with the child. As they mature they darken, and

vas-cular ectasia and blebbing, as well as soft tissue and

Fig 1. A: Left hand of a 7-month-old white female (patient 4) prior to laser treatment. B: Same hand 4 months later, after three laser treatments.

bony overgrowth of the affected area, can develop.

Hemangiomas undergo a very predictable natural

history, progressing through a rapid growth phase

out of proportion to the child’s growth, followed by

a regressive phase and eventual involution in 90% of

cases. A vascular malformation which at birth can

easily be confused with either port-wine stains or

hemangiomas is the telangiectatic vascular

malfor-mation. This type of congenital vascular

malforma-tion, like port-wine stains, is a capillary

malforma-lion and it is identified by the presence of clinically

distinct telangiectasias within the lesion. The

telan-giectasia may be either diffuse or relatively

conflu-ent. When this type of lesion presents as diffuse

tel-angiectasia, it is most often mistaken for the

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Patients were between the ages of 2 weeks and 9 months of age at the time of initial treatment. None of the patients had a coexisting port-wine stain.

All patients were treated with a pulsed (450 microseconds) dye laser (585 nm) (Candela SPTL-1, Candela Corp. Wayland, MA). The entire lesion was treated at each session.

All treatments were performed with a laser energy of 6.0 to 6.5 J/cm.2 Patients were treated every 4 to 12 weeks. No anesthesia was used. Posttreatment care consisted of the frequent application of bacitracin ointment. None of the patients received any previous or concomitant treatment.


In all patients, the lesions totally cleared with two

to four treatments (Table 2, Figs I and2). The patients

with the more confluent lesions required four

treat-ments to clear, whereas the patients with the less

confluent lesions required only two or three

treat-ments. Residual hypopigmentation was noted in

pa-tients with lesions that contained more concentrated

telangiectasias (Fig 2, B), but these lesions were on a

hypopigmented background prior to therapy and the

resulting hypopigmentation may not be related to

the laser treatment of the malformation. Skin texture

remained normal and no infections occurred.

Pa-tients have been followed for 8 to 27 months without

any signs of recurrence.


Fig 2. A: Right thigh of a 9-month-old white female (patient 5) prior to laser treatment. B: Same thigh 9 months later, after four laser treatments.

telangiectatic presentation of a hemangioma. When

the telangiectasias are more concentrated the lesions

appear more like port-wine stains. It is important to

differentiate this type of lesion from port-wine stains

and hemangiomas, not only for discussion of the

natural history of the lesions, but also because of the

excellent response of these lesions to the pulsed-dye

laser (585 nm) (Table 1). These lesions will not

spon-taneously regress, will not fade, and will grow

com-mensurately with the child. If a telangiectatic lesion

has been present since birth and has not changed

over the first 2 months of life, it is likely to be a

vascular malformation and not a hemangioma.

The pulsed-dye laser (585 nm) was designed using

the principle of selective photothermolysis as an

im-proved treatment for port-wine stains.3 This laser is

safe and effective in the treatment of port-wine stains

and other congenital and acquired vascular

malfor-mations and tumors consisting of capillary-sized

blood vessels. The major drawback in the

treat-ment of port-wine stains using this laser is the

re-peated number of treatments required for clearing.7

We report on the treatment of six children with

con-genital telangiectatic vascular malformations distinct

from port-wine stains.


Six infants with congenital telangiectatic vascular malforma-tions were treated at the Birthmark Treatment Center at the Uni-versity of Colorado School of Medicine, Denver. The location and size of the lesions and the results are summarized in Table 2.

It is very important to differentiate congenital

tel-angiectatic vascular malformations from

hemangio-mas and port-wine stains. This can be difficult if the

patient is seen shortly after birth. Congenital

telan-giectatic vascular malformations are true capillary

vascular malformations which have distinct

telangi-ectasias within them and grow proportionately with

the child and do not undergo a rapid growth phase

as do hemangiomas. If the lesions have not changed

by 2 months of age, they can be assumed to be

vas-cular malformations.

All of our patients responded to the pulsed (450

microseconds) dye laser (585 nm) therapy with

nearly complete clearing in two to four treatments.

The number of treatments required to clear the

le-sions was related to the amount of telangiectasia

pre-sent. Port-wine stains require fewer treatments to

reach 50% clearing when treatment is begun before 6

months of age than they do when treatment is started

at a later age,8 but complete clearing in less than four

treatments is unlikely regardless of the age at the

beginning of treatments.4’9 In contrast, the more

rapid clearing of the telangiectatic vascular

malfor-mations is likely to be due to the fact that there are

fewer total vessels present in the telangiectatic

mal-formation than in a true port-wine stain, thus

allow-ing for a greater percentage of the vessels to be

de-stroyed with a given treatment.

The recognition of telangiectatic vascular

malfor-mations as a separate and distinct entity from

port-wine stains and hemangiomas will allow for

im-proved counseling for families with children who

have this type of vascular malformation.



Dept of Dermatology

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University of Colorado School of Medicine Denver


1. Jacobs AH, Walton RG. The incidence of hirthrnarks in the neonate.

Pediatrics. I 976;58:21 8-222

2. Mulliken JB. Classification of vascular hirthmarks. In: Mulliken JB,

Young AE, eds. Vaccilar !lirth,narkc: th’pii,ii’iotiio iid Malformations.

Philadelphia, PA: WB Saunders; 1988

3. Anderson RR, Parrish JA. Selective photothermolvsis: precise microsur-gery by selective absorption of pulsed radiation. Science. 1983;220:524-527

4. Tan OT, Sherwood K, Gilchrest BA. Treatment of children with

port-wine stains using the flashlamp-pulsed tunable dye laser. N Engl IMed. 1 989;320:41 6-421

5. Garden JG, Bakus AD, Faller AS. Treatment of cutaneous hemangiomas

by the flashlamp-pumped pulsed dye laser: prospective analysis. I

Pc-diatr. 1992;120:555-560

6. Geronemus RG. Treatment of spider telangiectasia in children using the

Ilashlamp-pumped pulsed dye laser. Pediatr Derinatol. 1991;8:61-63

7. Morelli JG, Weston WL. Pulsed dye laser treatment of port-wine stains in children. In: A4anac’enu’nt it,,! Trt’atnu’nt of Be,ii’n Cutaiu’ous Vascular IA’SUfllS. Malvern, PA: Lee & Fehiger; 1992:100-106

8. Ashinoff R, Geronemus RG. Flashlamp-pumped pulsed dye laser for

portwine stains in infancy: earlier versus later treatment. I Am Acad Pi’rn,atol. 199124:467-472

9. Reycs BA, Geronemus RG. Treatment of port-wine stains during

child-hood with the flashlamp-pumped pulsed dye laser. IAm Acad Der,natol. 1990;23:1142-1I48








a Premature









ABBREVIATIONS. PPHN, persistent pulmonary hypertension of the newborn; PVR, pulmonary vascular resistance; HMD, hyaline membrane disease; RDS, respiratory distress syndrome; NO, nitric oxide; ECMO, extracorporeal membrane oxygenation; HFOV, high-frequency oscillatory ventilation; GBS, group B

Streptococ-cus; Fio,, fraction of inspired oxygen.

Persistent pulmonary hypertension of the

new-born (PPHN) is a clinical syndrome, characterized by

sustained elevation of pulmonary vascular resistance

(PVR) with right-to-left shunting across the ductus

arteriosus and/or foramen ovale, causing severe

hy-poxemia.1’2 Although generally associated with

dis-eases of term or near-term newborns, including

group B streptococcal sepsis,3’4 PPHN has been

de-scribed in preterm neonates as well.59 Recent

echo-cardiographic studies have demonstrated increased

PVR in preterm neonates with hyaline membrane

disease (HMD), which correlated with disease

sever-ity and mortality.911 Severe HMD was associated

with lower aortopulmonary pressure gradients and

left pulmonary artery blood flow velocities during

the first 72 hours after suggesting that high

Received for publication Feb 26, 1993; accepted Apr 5. 1993.

Reprint requests to (S.H.A.) Pulmonary Medicine, 0-395, The Children’s

Hospital. 1056 E Nineteenth Aye, Denver, CO 80218-1088.

PEDIATRICS (ISSN 0031 4005). Copyright © 1993 by the American Acad-emy of Pediatrics.

PVR contributes to the mortality of respiratory

dis-tress of premature neonates. These findings refute

the belief that the developing lung circulation is

in-capable of significant vasoconstriction.11 Case reports

of improved oxygenation with tolazoline in selected

cases of HMD further support a role for pulmonary

vasospasm in the pathophysiolog’ of severe

respira-tory distress syndrome (RDS).12’1 However, therapy

with tolazoline or other pharmacologic vasodilators

is often limited by lack of responsiveness, inability to

sustain vasodilation, or harmful side effects,14 and

vasodilator treatment for preterm infants with PPHN

has not been extensively studied.

Nitric oxide (NO) or an NO-containing product

has been identified as an endogenous

endothelium-derived relaxing factor which contributes to the

regu-lation of vascular tone in many circulations,

includ-ing the perinatal lung.14’15 Since NO is a gas,

inhalational NO therapy has been studied for its

p0-tential efficacy in causing potent and selective

pul-monary vasodilation in experimental and clinical

settings.16-21 Roberts et al17 and others2#{176} have

dem-onstrated that inhaled NO causes marked

improve-ment in oxygenation in term newborns with severe

PPHN who met criteria for extracorporeal membrane

oxygenation (ECMO) therapy. Early findings in a

small number of patients suggest that continuous,

low-dose NO therapy for PPHN may hasten

recov-ery without the need for ECMO.2#{176} Premature

new-borns with severe respiratory failure and pulmonary

hypertension were not included in these initial

stud-ies. In these patients, ECMO is not an option because

of their small size and risks associated with systemic


Therefore, we report the clinical course of a

pre-term neonate with severe respiratory distress and

group B streptococcal sepsis, who was treated with

inhaled NO because of critical hypoxemia and

marked pulmonary hypertension, which was

refrac-tory to conventional and high-frequency oscillatory

ventilation (HFOV), high inspired oxygen

concentra-tions, and cardiotonic support. We found that

in-haled NO improved oxygenation, lowered PVR, and

allowed for ventilation at lower mean airway

pres-sure. This response suggests the potential efficacy of

inhalational NO therapy for severe PPHN and

marked hypoxemia in the preterm infant and

dem-onstrates that the immature pulmonary circulation is

responsive to exogenous NO.


An 1180-g female neonate was born at 28 weeks’ gestation to a white, 35-year-old woman (gravida 1,para 1), whose course was complicated by premature labor, requiring hospital admission 2 weeks prior to delivery for terbutaline therapy, monitoring, and bed rest. Despite these interventions, labor progressed. She was treated with erythromycin because of a positive cervical culture for group B Streptococcus (CBS), as well as steroids prior to deliv-ery. After vaginal delivery, the neonate had no spontaneous res-pirations and low heart rate. Apgar scores were 1 at 1 minute and 6 at 5 minutes. Resuscitation included chest compressions with hag-and-mask ventilation. Endotracheal intubation at 2 minutes improved the neonate’s color and heart rate. Physical examination revealed heart rate of 190 beats per minute, systolic blood pressure of 20 mm Hg, diffuse edema, poor perfusion, and cyanosis. Oxy-gen saturation by pulse oximeter was 50T while the neonate was receiving manual bag-and-mask ventilation with 100% oxygen.

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Laser (585 nm)

Treatment of Congenital Telangiectatic Vascular Malformations With the Pulsed-Dye


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Treatment of Congenital Telangiectatic Vascular Malformations With the Pulsed-Dye

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