Retained Spur Following a Rooster Attack

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106 PEDIATRICS Vol. 90 No. 1 July 1992

disorder, where cutaneous inflammation along

Blaschko’s lines is either present at birth, or develops

shortly thereafter, proceeding through an evolution

to verrucous, pigmented, and ultimately normal or

hypopigmented skin. The recurrence of vesicular

in-flammatory lesions after infancy has been observed,’6

and one of the authors has seen this in association

with acute childhood illnesses, suggesting that

acti-vation (or reactivation) of an abnormal clone of cells

may indeed occur in response to infection (Ilona

Frieden, MD, and Anne Lucky, MD. Unpublished

observation. January 1991).

Other possible precipitating factors for the

devel-opment of lichen striatus could include cutaneous

injury, or as yet unspecified circulating factors. Nutter

et al have described an unusual annular eruption at

the periphery of an old burn scar with clinical and

histologic features of lichen striatus, suggesting that

the eruption develops in a particularly predisposed

region of skin, a so-called “locus minoris

resisten-tiae.”8”7 The presence of an atopic family history in

our patients may also be relevant. Toda found that

85% of patients with lichen striatus had a positive

family history of atopic dermatitis, asthma, or allergic jfljfi5#{149}8 The simultaneous occurrence of lichen

stria-tus in siblings, reported herein, suggests either a

common environmental (or infectious) stimulus, a

genetic predisposition, or both.

JOHN T. KANEGAYE, MD’

ILONA J. FRIEDEN, MD’S

Departments of ‘Pediatrics and

Dermatology

University of California, San Francisco

REFERENCES

I

.

Schachner L, Ling NS. Press S. A statistical analysis of a pediatric dermatology clinic. Pediatr Dermatol. 1983;1:157-164

2. Reed RJ, Meek T, Ichinose H. Lichen striatus: a model for histologic spectrum of lichenoid reactions. I.Cutan Pathol. 1975;2:1-18

3. Charles CR, Johnson BL, Robinson TA. Lichen striatus: a clinical, histo-logic and electron microscopic study of an unusual case. I.Cutan Pathol.

1974;1 :265-274

4. Burton JL, Rook A, Wilkinson DS. Eczema, lichen simplex, erythroderma and prurigo. In: Rook A, Williamson DS, Ebling FJG, et al, eds. Textbook of Dermatology. 4th ed. Oxford, MA: Blackwell Scientific Publication; 1986:414-415

5. Crounse RG. Lichen striatus. In: Demis DJ, Dobson RL, McGuire J, eds.

Clinical Dermatology. Hagerstown, MD: Harper and Row, Publishers; 1976; 1: 1-11

6. Lever WF, Schaumburg-Lever G. Histopathology of the Skin. 7th ed. Philadelphia. PA: J. B. Lippincott Co; 1990:152-184

7. Ramsay DL, Hurley HJ. Papulosquamous eruptions and exfoliative der-matitis. In: Moschella SL, Hurley HJ, eds. Dermatology. 2nd ed. Phila-delphia, PA: W. B. Saunders; 1985:499-556

8. Senear FE, Caro MR. Lichen striatus. Arch Dermatol Syph. 1941;43: 116-133

9. Staricco RG. Lichen striatus. Arch Dermatol. 1959;79:311-324

10. Grosshans E, Maroy L. Blaschkite de l’adulte. Ann Dermatol Venereol.

1990;1 77:9-15

I I

.

Jackson R. The lines of Blaschko: a review and reconsideration. Br

Dermatol. 1976;95:349-359

12. MacDonald RH, Sims RT. Linear lesions. BrJ Dermatol. 1969;81:72-79 13. Happle R. The lines of Blaschko: a developmental pattern visualizing

functional x-chromosome mosaicism. Curr Prob Dermatol. 1987;17: 5-18

14. Happle R. Cutaneous manifestations of lethal genes. Human Genet. 1986;

72:280

15. Happle R. Lethal genes surviving by mosaicism: a possible explanation for sporadic birth defects involving the skin. /Am Acad Dermatol. 1987;

I 6:899-906

16. Barnes CM. Incontinentia pigmenti. Report of a case with persistent activity into adult life. Cutis. 1978;22:621-624

17. Nutter AF, Champion RH. Lichen striatus occurring as an annular eruption: an acquired “locus minoris resistentiae.’ Br I Dermatol. 1979; 101:351-352

18. Toda K, Okamoto H, Horio T. Lichen striatus. mtIDermatol. 1986;25: 584-585

Retained

Spur

Following

a

Rooster

Attack

In many rural areas, families raise poultry as a

source of income and food. Chickens are often kept

close to living quarters. Children, especially those

who are young and unaware of the territorial

behav-ior displayed by roosters, are especially vulnerable to

attacks. Although such injuries are common, most do

not require medical attention. However, serious

claw-and peck-induced injuries to the face and upper torso

may occur. Injuries caused by rooster attacks have

been reported rarely.’3 We recently have cared for a

child with extensive facial lacerations who developed

a polymicrobial, chronic wound infection. Evaluation

revealed a retained rooster spur, an unexpected and

previously unreported complication of such injuries.

The case is reported to alert physicians to the potential

for such injuries and to urge that they counsel parents

about prevention.

CASE REPORT

While visiting relatives in a rural area, a 5-year-old boy at play

provoked an attack by a neighbor’s rooster. The bird jumped and

grasped his head. He sustained bilateral deep temporal lacerations

caused by the claws. He visited a local emergency department

where the wounds were closed with sutures and a 7-day course of

cefadroxil was prescribed. In the next week, the right temporal

laceration healed promptly and completely. One month after the

attack, the left temporal wound became erythematous, indurated,

and tender. The wound was incised and drained, and an additional

1 0-day course of cefadroxil prescribed. However, wound drainage persisted, inflammation increased, and he was admitted to a local hospital. He had no fever or signs of systemic infection. A computed

tomographic scan of the head was interpreted as normal and a

ssmTc radionuclide bone scan showed minimally increased activity in the left temporal area. A second incision and drainage procedure was performed, and a sinus tract in the temporal area was explored

and excised. Following the operation, ceftriaxone was begun and

continued for 6 days. Vancomycin and rifampin were substituted

when wound cultures grew Staphylococcus epidermidis,

Lactobacil-lus, and Streptococcus viridans. Cultures for anaerobic bacteria and

for fungi were negative. The child developed daily fevers to 39.5#{176}C postoperatively, and wound drainage continued. After several days

of fever, the family returned home. The patient subsequently was

admitted to the James Whitcomb Riley Hospital for Children at

Indiana University Medical Center, now, 2 months after the rooster

attack. On admission, a retained foreign body was suspected. A

head computed tomographic scan, performed this time with

high-resolution bone windows (Fig 1), showed a radiodense area at the

center of a left temporal soft tissue mass. At operation, a rooster

Received for publication Jan 13, 1992; accepted Feb 12, 1992.

Reprint requests to (M.B.K.) Division of Infectious Diseases, Riley Hospital for Children, 702 Barnhill Drive, Rm 5847, Indianapolis, IN 46202-5225. PEDIATRICS (ISSN 0031 4005). Copyright © 1992 by the American Acad-emy of Pediatrics.

at Viet Nam:AAP Sponsored on September 1, 2020

www.aappublications.org/news

(2)

Spur

Claws

Fig 1. Computed tomographic image showing radiodense lesion Fig 2. Anatomic detail of a rooster claw. (Reprinted, with

permis-within a soft tissue mass in the left temporal region. sion, from reference 8).

EXPERIENCE AND REASON 107

spur was found embedded in the fascia of the temporalis muscle;

however, it had not penetrated the cranial periosteum. The spur

was removed, and the surrounding abscess was drained. Cultures

of the abscess fluid were negative for bacteria, fungi, and acid-fast

organisms. Antibiotics were discontinued, and the child was

dis-charged 2 days later. At follow-up, his wounds were healed

com-pletely.

DISCUSSION

Although a relatively common occurrence in rural

areas (G. Sorrells, MD, oral communication, August

1991) physician visits for treatment of bird attacks

are unusual, and published reports concerning

chicken attacks are rare.’3 Only one report

describ-ing this type of injury to a child in the US could be

found.’ In 1985, an 18-month-old girl, while at play,

provoked a rooster and was attacked. She sustained

10 claw wounds of the face which required suture

repair. The child received prophylactic intravenous

antibiotics for 2 days although culture results were

not reported. In the same report, a 3 ‘/2-month-old

boy sustained rooster beak and claw wounds of the

head with three nonpenetrating skull fractures. A

wound culture grew only normal skin flora. He

re-ceived oral antibiotics for 7 days. Both children

re-covered without incident. Berkowitz et al2 described

a fatal outcome in a 1 6-month-old South African girl

who suffered a single peck wound on the left side of

her head. Four days after the attack, she developed

seizures and wound swelling. A computed

tomo-graphic scan of the head demonstrated a large left

temporal parietal brain abscess. Cultures of the

ab-scess fluid grew Streptococcus bovis, Clostridium ter-tium, and Aspergillus niger. The child died despite

operative drainage and antimicrobial therapy. Injuries

sustained during other types of bird attacks also have

been reported. Kuhl reviewed a series of 14 patients

with severe eye injuries reported in the European

literature from 1875 through 1970. All were

pene-trating ocular injuries some of which caused

perma-nent visual injuries and/or blindness. Long-legged

shore birds, such as storks and cranes, have been

reported to defend themselves against children by

pecking directly on the cornea.3 Several reports of

joggers attacked by European buzzards describe

in-juries which ranged from minimal abrasions to

lac-erations as long as 14 cm. An additional report

con-cerns joggers injured by blackbirds thought to be

defending their nests.47

The few published reports of rooster injuries do not

allow precise predictions of the microbial pathogens likely to infect such wounds. In the reports previously cited, cultures have grown a variety of aerobic,

an-aerobic, and fungal pathogens. Due to the expected

contamination of the beaks and claws of the roosters,

it can be presumed, that if infection does occur, it will

be polymicrobic, often including fecal flora. The

em-piric antibacterial treatment of infected wounds

should be guided by this assumption, and when

available, the findings of Gram-stained smears. Initial

empiric antibiotic selected should provide a broad

spectrum of antimicrobial activity. Treatment should

be modified when the results of cultures become

available. Prompt and adequate wound debridement,

especially if foreign bodies are present, is critical. If

local signs of inflammation and/or wound drainage

persist despite debridement and exploration, a foreign

body, such as a retained rooster spur or claw, should

be suspected. The anatomy of the foot of the domestic

fowl is shown in Fig 2.8 Each of the toes has a claw

which is strong and pointed. The tarsometatarsus of

young males, and sometimes of old hens, is a bonelike

pointed peg. The latter, directed caudomedially, forms

the basis of the spur. A strong horny sheath covers

the spur which is pointed and curved upward in old

birds. The spur generally is considered to be strong

and not subject to fracture. As occurred in the present

case, a routine head computed tomographic scan may fail to identify a small foreign body. In such circum-stances, a high resolution computed tomographic scan with bone windows may be helpful.

Except for individuals who come from rural areas,

few people recognize the risk of serious injury from

domesticated birds. Young children, especially infants

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108 PEDIATRICS Vol. 90 No. 1 July 1992

and toddlers, are completely unaware of such risks.

On the contrary, their perception of farm animals is

that of the gentle and lovable figures depicted in

books, stories, movies, and stuffed animals. Parents

of children in rural areas or those who plan to visit

farms should be aware that the territorial behavior of

many domestic animals, including roosters, may be a

risk to children. All children, especially infants and

toddlers, should be supervised by an adult who is

aware of such risks.

JOSEPH 0. COOLER, MD’

MARTIN B. KLEIMAN, MD’

KAREN WEST, MDt

JAY GROSFELD, MD

Division of Infectious Diseases, Department of Pediatrics’ Section of Pediatric Surgery, Department of Surgery Indiana University School of Medicine

The James Whitcomb Riley Hospital for Children Indianapolis, Indiana 46202

REFERENCES

1. Preiser G, Lavell TE. Rooster attacks on children. Pediatrics. 1987;79: 426-427

2. Berkowitz FE, Jacobs DWC. Fatal case of brain abscess caused by rooster pecking. Pediatr Infect Dis I.1987;6:941-942

3. Kuhl W. Augen verletzungen durch Vogel. Klin Monatsbol Augenheilkd.

1970;157:810-814

4. Itin P. Haenel A, Stadler H. From the heavens, revenge on joggers. N

EnglJMed. 1984;311:1703

5. Tanz RR. More on bird attacks. N EngI IMed. 1985;312:1066. Letter. 6. Green R, Hegenauer J, Toone B. More on bird attacks. N Engl IMed.

1985;312:1066-1067. Letter.

7. Phillips LH II. More on bird attacks. N EnglJMed. 1985;312:1067. Letter. 8. Nickel R, Schummer A, Seifeile E, Siller WG, Wight PAL. Anatomy of

Domestic Birds. New York: Springer-Verlag 1977:156-158

as having hypopituitarism after an extensive endocrinologic

eval-uation of delayed bone age and slow growth rate. This included

abnormal L-dopa stimulation and clonidine stimulation tests for

growth hormone. She had a history of mild allergic rhinitis but not

drug allergy. Immediately after a 2-mg intramuscular injection of

Humatrope, she developed hives at the injection site followed by

generalized pruritic urticaria which resolved in 1 hour after 25 mg

of oral diphenhydramine. She had no other systemic manifestations

of anaphylaxis. Thirty minutes before her next Humatrope injection

she was pretreated with 25 mg of diphenhydramine. Despite

pretreatment she developed generalized pruritic urticaria 30

mm-utes after the injection which lasted for 3 weeks despite antihista-mine treatment.

SKIN TEST RESULTS

Skin testing was performed with the usual

Huma-trope diluent, water with 0.3% m-cresol as a

preserv-ative and 1 .7% glycerin (Table 1). A full-strength

prick puncture skin test and an intradermal skin test

at 1 : 1 00 dilution were negative. Skin testing with

Humatrope was performed after reconstitution with

USP water and 0.9% benzyl alcohol to a final 1 mg/

mL concentration, which subsequently was diluted

1:1 with basic diluent (10 mL of USP water, 0.9%

benzyl alcohol, and 1 mL of the patient’s whole

blood). This diluent was suggested by Eli Lilly and

Company to prevent any binding of the recombinant

growth hormone to the glass vial. An epicutaneous

skin test (1:100 dilution) was negative. An intradermal

injection (1:10 000 dilution) showed a small flare

without a wheal. An intradermal injection (1:1000

dilution) resulted in a 5/20 mm (wheal/flare)

re-sponse. Skin test to the basic diluent alone was

neg-ative. An intradermal skin test with histamine

phos-phate (0.275 mg/mL) resulted in a 8/25 mm (wheal/

flare) skin response. Because the basic diluent

con-tamed the patient’s blood we were unable to safely

skin test normal controls.

Systemic

Reaction

to Human

Growth

Hormone

Treated

With

Acute

Desensitization

Recombinant DNA technology has led to increased

production and widespread use of recombinant

growth hormone. Systemic allergic reactions to

re-combinant growth hormone such as urticaria,

angioe-dema, or anaphylaxis have not been described in the

literature. We report a patient who developed

gener-alized urticaria from recombinant human growth

hor-mone (Humatrope, Eli Lilly and Company) in whom

we successfully desensitized to growth hormone

using a protocol modified from an insulin

desensiti-zation schedule.’

CASE REPORT

A 1 2-year-old girl with hypopituitarism and short stature had

been treated with 2 mg to 5 mg of Humatrope (depending on her

weight and responsiveness to treatment) intramuscularly 6 days a

week for 3 years without any problems. She had been diagnosed

Received for publication Sep 27, 1991; accepted Dec 12, 1992.

Reprint requests to (S.B.W.) 8301 161st Ave NE, Suite 208, Redmond, WA

98052.

DESENSITIZATION

Acute desensitization to Humatrope was performed

by doubling the concentration given subcutaneously

every 15 minutes starting with 0.1 mL of a 1:100 000

dilution to the final dose of 2 mg. The patient

toler-ated this procedure without any adverse reactions

(Table 2).

The day after desensitization, an intradermal skin

test to Humatrope (1:1000 dilution) was negative, and

a positive 7/30 mm (wheal/flare) response to a

his-tamine control was obtained. The patient

subse-quently has been maintained on daily intramuscular

injections of Humatrope (2 mg) without any adverse

reactions other than occasional flares at the injection

site.

DISCUSSION

Hypersensitivity has been reported to occur after

the administration of endogenous hormones such as

tniodothyronine, L-thyrOxine,2 and insulins including

human insulin.3 Although the immunologic

mecha-nism involved in these reactions is not always known,

it appears that many insulin reactions are

IgE-me-diated. This is true even for recombinant human

insulin where it is postulated that tertiary

conforma-tional structural differences between native insulin

and recombinant insulin may allow immunologic

(4)

1992;90;106

Pediatrics

JOSEPH O. COOLER, MARTIN B. KLEIMAN, KAREN WEST and JAY GROSFELD