EXPERIENCE AND REASON 1163
ISRAEL ALFONSO, MD
Department of Neurology Miami Children’s Hospital
Department of Neurology
University of Miami
OSCAR PAPAZIAN, MD
JEAN AICARDI, MD
Department of Neurology Miami Children’s Hospital
HOWARD E. JEFFRIES.
Tulane University
New Orleans, LA
REFERENCES
1.Daoust-Roy J, Seshia 55. Benign neonatal sleep myoclonus. A
differen-tial diagnosis of neonatal seizures. Am IDis Child. 1992;146:1236-1241 2. Coulter DL, Allen RJ. Benign neonatal sieep myoclonus. Arch Neurol.
198239:191-192
3. Blennow G. Benign infantile nocturnal myocbonus. Acta Paediatr Scand.
1984;74:505-507
4. Dooley JM. Myocbonus in children. Arch Neurol. 1984;41:138
5. Tardieu M, Khoury W, Navelet Y, Questiaux E, Landrieu P. Un
syn-drome spectaculaire et benin de “convulsions neonatales” les
myocbo-mes du sommeil profond. Arch Fr Pediatr. 1986;43:259-260
6. Resnick TJ, Moshe SL, Perotta L, Chambers HJ. Benign neonatal sieep myoclonus. Relationship to sleep states. Arch Neurol. 1986;43:266-268 7. Tsur M, Amit R. Benign neonatal sleep myocbonus. Harefuah. 1988;1 15:
179-180
8. Reggin JD, Johnson MI. Exacerbation of benign neonatal sleep
myoclo-nus by benzodiazepines. Ann Neurol. 1989;26:455
9. RichelmeC, Delpont E, Deswarte M, Dolisi C, Mariani R. Apropos d’un cas de myocbonies du sommeil profond du nouveau-ne. Pediatrie. 1990;
45:191-192
10. Quesada RR. Myoclonias del sueno del recien nacido. Neuroeje. 1991;2: 38-43
,I. Di Capua M, Fusco L, Ricci 5, Vigevano F. Benign neonatal sleep myoclonus: clinical features and video-polygraphic recordings. Mm’ Disord. 19938:191-194
12. Smith U, Thomas NH. Benign neonatal sleep myocbonus. AJDC. 1993; 147:817
13. O’Brien MJ, Lems YL, Prechtl HFR. Transient flattening in the EEG of
newborns: abenign variation. Electroencephalogr Clin Neurophysol. 1987;
67:16-26
14. Parker S. Zuckerman B, Bauchner H, Frank D, Vinci R, Cabral H.
Jitteriness in full term neonates; prevalence and correlates. Pediatrics.
199085:17-26
15. Vivegano F, Di Capua M, Barnardina BD. Startle disease: an avoidable
cause of sudden infant death. Lancet. 1989;1:216
16. Mizrahi EM. Diagnosis and treatment of neonatal seizures. mt Pediatr.
1089;4:180-187
17. Lane JC, Tennison MB, Lawless ST. Greenwood RS, Zaritsky AL Clin-ical and laboratory observation. Movement disorder after withdrawal of
fentanyl infusion. IPediatr. 1991;119:649-651
18. Scher MS. Pathologic myocbonus of the newborn: electrographic and
clinical correlations. Pediatr Neurol. 1985;1:324-328
19. Nolte R. Neonatal sleep myocbonus followed by myoclonic astatic epilepsy: a case report Epilepsia. 198%30:844-850
20. Volpe JJ. Neonatal seizures. In: Volpe JJ, ed. Neurology of the Newborn.
Philadelphia: WB Saunders Co; 1995:172-207
The
Progression
of Human
Papillomavirus
Lesions
in
Sexual
Assault
Victims
Human papifiomavirus (HPV) infections are seen
in up to 15% of adolescents who present to a
gyne-cology clinic.’ Anogemtal HPV develops in some
adolescents as a result of sexual assault. Sexual
as-sault protocols address detection and follow-up for chiamydia, gonorrhea, syphilis, human immunode-ficiency virus (HIV) and hepatitis,2’3 but follow-up
for detection of HPV lesions is not formally
ad-dressed. Early detection of HPV lesions is important for treatment and long-term management, because subtypes 6, 10, 11, 16, 18, 31, 33, and 35 have been associated with cervical cancer.4 Although 6 and II
are the most common subtypes found in
condylo-mata acuminata, types 1, 2, 10, 16, and 18 are also found in anogenital lesions.5 In one stud? HPV
cer-vical disease was found in 70% of patients with
vulvar condylornas.
Anogenital HPV has variable clinical appearances. Lesions may be flesh colored or purple,7 pink, or gray.’ Morphology may be papular,7 exophytic,7
flu-iform, or flat.’ Genital lesions tend to begin within the posterior fourchette and labia, later progressing to other genital sites.7 It is thought that HPV infects those areas traumatized by sexual activity or assault.8The incubation period for HPV is from I to 20
months,9 with an average of 2 to 3 months.’#{176}The use of a colposcope in the detection of early lesions of
anogenital HPV has been described.” Treatment of
anogenital HPV may vary with the extent of disease; smaller condylornas are amenable to topical treat-ments, whereas larger lesions may require laser or surgical treatment. Detection of HPV in earlier stages of development may spare patients from more inva-sive and painful methods of treatment.
We present the cases of two adolescents with ano-genital warts detected by colposcopy 12 and 34 days after sexual assault. Implications for clinical treat-ment and follow-up are discussed.
METhODS
Serial photographs with the Leisegang (Leisegang Medical Inc,
Boca Raton, FL) photocolposcope (magnification, x 15) were taken of two adolescents presenting for sexual assault examinations. Suspicious lesions were followed for up to 73 days after the assaults.
Case 1
RESULTS
This 15-year-old girl initially presented to the sex-ual abuse clinic 12 days after a sexual assault. She described digital-vaginal and vaginal-penile
penetra-tion by a gang member. She denied any sexual
ac-tivity before the assault. On initial examination, a cleft was noted at the 5 o’clock position, and friability was seen in the posterior vestibule. A 2-mm white bump resembling a half-moon was seen in the lateral vestibule at the 3 o’clock position (Fig IA). On mi-croscopic examination of vaginal secretions, 15 to 20 white blood cells per high-power field were noted. Vaginal and anal cultures for chiamydia and gonor-rhea were negative. Cultures for rapid plasma
rea-gin, HIV, and 3-human chorionic gonadotropin were
Received for publication Oct 24, 1994; accepted Dec 27, 1994.
Reprint requests to (ND-K.) University of Texas Health Science Center at San Antonio, Department of Pediatrics, Division of General Pediatrics, 7703
Floyd Curl Dr, San Antonio, TX 78284-7808.
PEDIATRICS (ISSN 0031 4005). Copyright t1 1995 by the American
Acad-emy of Pediatrics.
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Fig 2. Patient 2. A, 1 day after sexual assault. Submucosal
hem-orrhages are seen at the 7 and 12 o’clock positions. B, 34 days after
sexual assault. The hymen is reflected medially to reveal
condy-lomatous growths in the left lateral vestibule. C, 45 days after sexual assault. D, 73 days after sexual assault.
1164 EXPERIENCE AND REASON
Fig 1. Patient 1. A, 12 days after sexual
assault. B, 45 days after sexual assault.
C, 73 days after sexual assault.
negative. Patient I was treated for bacterial vaginosis
with metronidazole (Flagyl, C. D. Searle and Co.
Chicago, IL).
The patient was next seen 45 days after the assault. The lesion at the 3 o’clock position had enlarged (Fig
IB) and remained white-gray in color. When exam-med 73 days after the assault, the lesion at the 3 o’clock position was more prominent, and an addi-tional suspicious lesion was seen at the 6 o’clock position (Fig 1C). A 20% solution of podophyllum resin was applied to these areas, and the patient was referred to a gynecologist for a pap smear and fol-low-up. One month later, the result of the pap smear
was normal, and no condylomatous lesions were
seen.
Case 2
Patient 2 was a 16-year-old girl who initially pre-sented 36 hours after a sexual assault. She reported vaginal-penile, penile-oral, and penile-anal penetra-tion by at least two gang members. During the initial
visit, her recall of events was somewhat impaired by
alcohol intoxication and marijuana use. She reported sexual activity with at least six partners during the preceding 2 years but stated that her last consensual sexual contact was 8 months before the assault. On initial examination, there was diffuse vulvar and vaginal swelling, and submucosal hemorrhages were seen at the 7 and 12 o’clock positions (Fig 2A). Sev-eral acute anal tears were noted.
Patient 2 returned for follow-up 34 days after the assault. The submucosal hemorrhages had resolved, and clusters of 2-mm papular vascular lesions were seen in the vestibule at the 3 o’clock position (Fig 2B). At 45 days after the assault these lesions had prolif-erated, and additional condylomas were seen at the 6 and 8 o’clock positions in the vestibule (Fig 2C). At this time patient 2 was referred to a gynecology clinic for treatment and follow-up. She was seen by gyne-cologists 50 and 59 days after the assault. They noted
an “endocervical polyp,” which was normal on
bi-opsy. Gynecologists found “no evidence of condy-loma” and treated her for Candida vaginitis. Patient 2 returned to the sexual abuse clinic 73 days after the assault. Several coalescing papular vascular lesions were noted at the 3, 6, and 8 o’clock positions in the vestibular walls (Fig 2D). Results of all other cultures and tests for chlamydia, gonorrhea, HIV, and rapid
plasma reagin were negative. Patient 2 was then
referred to another gynecologist for treatment. At-tempts to contact the patient 4 months later were
unsuccessful.
DISCUSSION
These two cases demonstrate several points of in-terest. First is the need for follow-up of adolescents involved in high-risk sexual assault or activity. The perpetrators in both of these cases were gang mem-bers. Perpetrators who are gang members or at Viet Nam:AAP Sponsored on September 1, 2020
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EXPERIENCE AND REASON 1165 ers or whose sexual activity is prolific are more likely
to be infected with sexually transmitted diseases. Follow-up of sexual assault victims for HPV lesions is not addressed in published guidelines.2” A pro-spective study would be helpful in determining the actual risk for HPV infections after sexual assault. We suggest that adolescents involved in high-risk sexual activity or assault be examined for HPV le-sions I to 2 months after such an incident occurs.
In this case series, very early anogenital lesions were detectable by colposcopy at 12 and 34 days after
exposure. Although patient 2 may have become
in-fected with HPV 8 months earlier during consensual sexual activity, it seems most likely that the lesions were a result of the more recent gang rape. Clinical detection of HPV lesions during the earlier phase of growth may eliminate the need for more invasive and painful treatment,5 including surgical removal. Further studies are needed to determine whether early detection and treatment lower the recurrence rate of HPV lesions.
The HPV lesions in these patients were variable in morphology. In patient 1, the lesions were
white-gray, raised, and flat; in patient 2, the lesions were vascular, flliform, and clustered. Initially, gynecolo-gists did not detect the lesions in patient 2. The variable clinical appearances of anogenital HPV may hinder detection for clinicians not familiar with these presentations. In addition, anogenital HPV at times may be confused with condylornata lata, molluscum contagiosum, and normal anatomic variants, includ-ing epithelial papillae and sebaceous glands. Tech-niques that enhance detection and differentiation of
HPV lesions include acetowhitening with 3% to 5%
acetic acid applied to the vulva and vagina and
bi-opsy. Alternate detection techniques include DNA
methods such as ViraType (Digene Diagnostics,
mc,
Silver Spring, MD) and polymerase chain reaction,
which could be used in cases of acute sexual assault
to detect minute amounts of HPV DNA. Follow-up
for clinical evidence of HPV disease would be
mdi-cated in those patients in whom HPV DNA is
de-tected.
The initial locations of the HPV lesions in these
patients were surprisingly similar, involving the
lat-eral vestibule at or near the 3, 6, and 9 o’clock
posi-tions. In both patients condylornata acuminata
ap-peared initially at the 3 o’clock then the 6 o’clock
position. It is also of interest that in patient 2, who
had significant anal injuries, anal HPV lesions did
not develop during the follow-up interval. It is
pos-sible that the infected assailant penetrated her vagina
and not the anus. Alternately, the pattern of HPV
distribution in these two patients may reflect those
areas most traumatized during the assault and most
favorable for HPV colonization. Further studies are
necessary to address these questions.
Treatment of condylomatous lesions depends on
location, extent of disease, and degree of potential
discomfort.5 Topical treatment with podophyllum
resin or trichloroacetic acid are the most frequent
therapeutic approaches.’2 Podophyllum resin is most
effective when applied to small, moist lesions5 such
as the condylomas in patient 1. An 85% solution of
trichioroacetic acid applied weekly is slightly less
successful than podophyllum resin.’3 Although
re-peated weekly applications of topical agents for up
to 3 weeks is indicated 70% to 80% of the time,’3
patient discomfort tends to be minimal. Cryotherapy
is considered more effective for skin and mucous
membrane lesions but is more painful. Other more
invasive treatment methods are indicated for more
extensive lesions and lesions that do not respond to
topical treatment. These methods include surgical
removal and carbon dioxide laser treatment;
disad-vantages include moderate discomfort and the use of
general anesthesia in some patients.
Immunother-apy, 5-fluorouracil, and interferon are more
contro-versial methods of treatment.
In summary, these case reports demonstrate early
HPV condylornatous lesions in two victims of sexual
assault. The condylornas were variable in
morphol-ogy but are located within the same areas of the
vestibule. When lesions are detected earlier, less
in-vasive and less painful methods of treatment may
prove effective. In at least one patient a one-time
application of podophyllum resin was successful in
short-term follow-up. We recommend close
surveil-lance and careful examinations for HPV lesions in
adolescents involved in high-risk sexual experiences.
NANCY D. KELLOGG, MD
JUAN M. PARRA, MD, MPH
Department of Pediatrics
Division of General Pediatrics
University of Texas Health Science Center at San Antonio
REFERENCES
1. Brown HP. Recognizing STD’s in adolescents. Contemp Pediatr. 1989;6:
17-36
2. Centers for Disease Control and Prevention. 1993 sexually transmitted diseases treatment guidelines. MMWR. 1993;42(RR-14):99-102
3. American Academy of Pediatrics Committee on Child Abuse and
Neglect. Guidelines for the evaluation of sexual abuse of children.
Pediatrics. 1991;87:254-260
4. Emans SJ, Goldstein DP, eds. Human papilbomavirus (HPV) and human
immunodeficiency virus (HIV). Pediatric and Adolescent Gynecology. 3rd
ed. Boston: Little, Brown and Co; 1990:385-410
5. Boyd AS. Condybomata acuminata in the pediatric population. Am IDis Child. 1990;144:817-824
6. Martinez J,Smith R, Farmer M, et al. High prevalence of genital tract papilbomavirus infection in female adolescents. Pediatrics. 1988;82:
604-608
7. Stewart D. Sexually transmitted diseases. In: Heger A, Emans SJ, eds.
Evaluation of the Sexually Abused Child. New York: Oxford University Press; 1992:145-169
8. Shah KV. Biology of human genital tract papillomaviruses. In: Holmes
KK et al, eds. Sexually Transmitted Diseases. 2nd ed. New York: McGraw-Hill Information Services Co; 1990:425-431
9. Noble RC. Condyloma acuminata. Sexually Transmitted Diseases. Guide to Diagnosis and Therapy. Garden City, NY: Medical Examination Publish-ing Co; 1982:80-87
10. Oriel P. Genital warts. Sex Transm Dis. 1981;8:326-329
11. McCann J.Use of the colposcope in childhood sexual abuse examina-tions. Peditr Clin North Am. 199037:863-880
12. Davis JA, Emans SJ. Human papillomavirus infection in the pediatric
and adolescent patient. I Pediatr. 1989;115:1-9
13. Moscicki B. HPV infections: an old S revisited. Contemp Pediatr.
1989;6:12-48
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1995;96;1163
Pediatrics
Nancy D. Kellogg and Juan M. Parra
The Progression of Human Papillomavirus Lesions in Sexual Assault Victims
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Nancy D. Kellogg and Juan M. Parra
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