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Amebic

Liver Abscess

in Children:

Clinical

and

Epidemiologic

Features

H. Robert Harrison, DPhil, MD, MPH,

C.

Peter Crowe, MD, and

Vincent A. Fulginiti, MD

From the Department of Pediatrics, Section of Infectious Diseases, University of Arizona, Arizona Health Sciences Center, Tucson

ABSTRACT. Amebiasis, that is, infection with Entameba

histolytica, continues to be endemic in the United States, with liver abscess occurring as an infrequent but constant complication. Seven cases are reported, with epidemio-logic investigation of two. Reliable findings in hepatic abscess include fever, abdominal pain, respiratory dis-tress, tender abdomen, and large, tender liver. Anemia, elevated white count with left shift, and the radiographic findings ofan elevated right hemidiaphragm are constant. Epidemiologically, amebiasis occurs in clusters in the United States with person-to-person transmission pre-dominant in spread. Infection is associated with poor sanitation and crowding. Investigation of the families of two patients documented 9/21 carriers and an additional 3/21 who were seropositive, as well as crowding and poor sanitation. In this country, treatment of a patient with amebic disease should include investigation of his home and family. Pediatrics 64:923-928, 1979; amebiasis, liver abscess, colitis, metronidazole.

It has been estimated that 3% to 7% of the

Un-traveled United States population harbors

Enta-meba histolytica,’3 with a higher figure (10%) for

the southern United States. Recent Center for

Dis-ease Control data4 suggest that far less than 3% of

specimens submitted to State Health Department

laboratories show E histolytica. However, this

fig-ure underestimates the prevalence of asymptomatic

carriers. Community5 and family6 foci of amebic

disease have been reported in the United States. In

these outbreaks person-to-person transmission,

rather than common source exposure, has been

Received for publication Aug 12, 1978; accepted March 5, 1979. Reprint requests to (H.R.H.) Department of Pediatrics, Section of Infectious Diseases, University of Arizona, Arizona Health Sciences Center, Tucson, AZ 85724.

PEDIATRICS (ISSN 0031 4005). Copyright © 1979 by the

American Academy of Pediatrics.

important, with infection rates correlating with

crowding, poor sanitation, and use of common toilet facilities.

Although amebic hepatic abscess is thought to be

less common in children than in adults, it is found

as a disease complication in all endemic areas.

McCarty et al,7 in a recent literature review, found that in children liver abscesses were most common in those under 3 years of age.

In southern Arizona a significant proportion of

the population travels to and from northern Mexico, a highly endemic amebiasis region. Our experience

with seven cases of hepatic abscess, four within the

last year, and our epidemiologic investigation of

two of these should alert US physicians, especially

in southern border areas, to the continuing presence of amebic liver disease and its symptoms, signs, and clinical variability. Furthermore, our experience

should serve to underscore the principle that

ame-biasis can occur in clusters in the United States and should help to identify the public health investiga-tion necessary after index case identification.

The two cases in which epidemiologic

investiga-tion was possible are detailed below, with the

re-maining five summarized in Table 2.

CASE REPORTS

Case I

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On admission he was afebrile, lethargic, and in respi-ratory distress. Auscultation of the chest was normal, but the child had a markedly distended, tympanitic abdomen without bowel sounds, an enlarged liver, and a possible right lower quadrant mass. The rectum was edematous and nodular, with an anterior mass narrowing the lumen and preventing passage of the examining finger beyond 4 cm. Chest roentgenograms showed right upper lobe ate-lectasis and an elevated right hemidiaphragm. Abdominal roentgenograms revealed dilated bowel and a possible right lower quadrant mass corresponding to the one

pal-pated on abdominal examination. The hematocrit was

23%; the white blood cell count was 14,000/cu mm with 33% neutrophils and 39% juvenile forms. The SGOT was 124 IU. Proctoscopy to 5 cm revealed edematous, friable mucosa with spontaneous bleeding and ulceration. A wet preparation from the border of an ulcer was negative for amebae on fresh examination by an experienced observer.

After multiple blood, urine, and stool specimens were obtained for bacterial culture, therapy with ampicilhin and gentamicin was started, and the infant’s fluid and electrolyte status stabilized over the rest of the first day. With a presumptive diagnosis of gangrenous, perforated appendix with abscess, ileus, and sepsis, he was operated upon approximately 24 hours after admission. A gangre-nous, nonperforated appendix and an area of necrotic

cecum were found; the appendix was removed and a

cecostomy tube was placed. On day 3 carbenicillin was substituted for ampicillin for confirmed Pseudomonas aeruginosa bacteremia. A chest roentgenogram after res-piratory deterioration showed an opaque right hemi-thorax; thoracentesis yielded 200 ml of very thick, brown-ish fluid. On day 4, histology of the appendix revealed numerous amebic trophozoites. Chest tube and cecos-tomy drainage at that time did not show organisms. On day 5 a nuclide scan ofthe liver depicted a large posterior-superior defect suggesting amebic abscess. Despite addi-tion of intravenous metronidazole on day 4 and continued vigorous supportive care the infant died on day 7. Amebic serology by immunodiffusion on day 6 was positive.

Postmortem examination revealed extensive colonic ulceration and necrosis, with perforations of the trans-verse colon and numerous trophozoites, even in the ser-osa. The liver contained one large abscess with perfora-tion through the diaphragm into the right thorax.

Case 2

C.C. (No. 1490-05-7), a 1-year-old Mexican-American

girl was admitted to AHSC with possible sepsis and

bloody diarrhea. Twelve days earlier, shortly after return-ing from Mexico, she developed fever and bloody stools, which continued through seven days of ampidillin ther-apy. A urinalysis five days before admission reportedly led to diagnosis of a urinary tract infection and addition of sulfisoxazole. Two days later trimethoprim-sulfame-thoxazole was substituted for both when the urine culture grew i04 Escherichia coli. She was admitted three days later with continued fever, pyuria, and diarrhea.

She was febrile (38), irritable, and tachypneic, with a distended tender abdomen and enlarged liver, and inter-mittent “rushes” of bowel sounds. The hematocrit was 27%. The white blood cell count was 20,200 cu mm with

49% neutrophils and 17% juvenile forms. The urinalysis was normal and the urine culture negative for bacteria.

The SGPT was 49 IU, the SGOT 94 IU, and the lactic

dehydrogenase 90 IU. Chest roentgenograms and intra-venous pyelogram were nondiagnostic. Ultrasonography on day 3 revealed a large cystic mass in the right lobe of the liver and subsequent amebic serology (immunodiffu-sion) was positive. Three stool samples were negative for trophozoites. She received five days of intravenous and 12 days of oral metronidazole and became afebrile on day 6 of therapy. On day 8, 200 ml of thick creamy fluid was drained from the abscess by percutaneous needle aspira-tion. Complete clinical resolution occurred, with subse-quent sonograms demonstrating healing of the abscess.

EPIDEMIOLOGIC INVESTIGATIONS

Case I

The patient is the fourth of four children of a

19-year-old unmarried Mexican-American woman

liv-ing in Pinal County, AZ, and a Mexican man living

in Mexico. The mother and four children inhabit a

three-room suite with inside bath in a motel court.

Samples of drinking water did not reveal evidence

of fecal contamination. Amebic serologies by

indi-rect hemagglutination were as follows: siblings M.R.

(3 years old) 1:512; J.R. (2#{189}years old) 1:1028; G.R.

(1’/2 years old) <1:64; mother S.R. 1:128. J.R. also

had amebae in stools, and he and his pregnant

mother, S.R., had visited Mexico with our patient. During our patient’s first 2 months oflife he had on

occasion shared the bottle used to feed J.R. The

father of the family could not be examined. The

mother and three siblings were all well and without

symptoms. Those with positive stool cultures and!

or serobogies were treated with metronidazole.

Case 2

This cluster consists of three related family units

(see Table 1) that inhabit three separate dwellings

on the same property. All three share a common

toilet located in one of the units. There is no sink or

handwashing facilities in proximity to the toilet,

and general sanitary conditions are poor. Many of

the family members of all three families visit

rela-tives in Mexico frequently. The last two members

of unit 2, and the last member of unit 3, while not

siblings, are close relatives living in the units.

Stool cultures and serologies are shown in Table

1. Our patient was a member of unit 1. All

culture-positive and seropositive individuals were

asymp-tomatic. Those with positive stool cultures and/or serologies were treated with metromdazole.

DISCUSSION

Although amebic liver abscess is an infrequent

(3)

TABLE 1. Serologic Data on Family Cluster of Case 2*

Family Age/Sex Stool Serology

1. C. family (proband’s family)

L.C. (mother) 24/F Pos Neg

D.C. (sibling) 2/F Pos Pos (ID) 1:4096(IHA)

2. H. family

C.H. (aunt) 34/F Pos Neg

G.H. (uncle) 36/M Neg Neg

G.H. 12/M Neg Neg

J.H. 11/M Neg Neg

E.H. 9/F Pos Neg

G.H. 7/M Neg Neg

M.J.M. 18/Ft Pos Neg

V.M. 9/12/F Neg Neg

3. C. family

J.C. (grandmother) 51/F Neg Neg

M.C. (grandfather) 46/M Pos Neg

L.D. 8/F Pos Neg

A.C. 3/M Neg 1:1024 (IHA)

M.C. 13/M Neg Neg

L.C. 10/F Neg Neg

M.L. 21/M Pos Neg

* Abbreviations used: Pos, positive; Neg, negative.

t

Pregnant.

important to recognize, since morbidity and

mor-tality are appreciable. Despite maximum therapeu-tic intervention, two infants (cases 1 and 3) died,

with shock and Pseudomonas sp sepsis as terminal

events. Three had prolonged, complicated courses

characterized by multiple courses of drugs and

sev-eral surgical procedures. Only two patients had

uncomplicated recoveries. Early recognition and

treatment can prevent enlargement and perforation of abscesses into the thorax (especially those in the right lobe), or into the pericardium (left lobe), an

especially severe complication. In addition, rapid

treatment of an associated active colitis (present in two of our children) is necessary to prevent necrosis of the bowel with perforation and secondary sepsis,

often with Pseudomonas sp. Fever is a hallmark of

liver abscess9 and is prominent in those pediatric patients reported.7”#{176}’5 Other prominent findings

include abdominal pain and distention, and an

en-larged, tender liver.7”3’6 There is usually anemia

and some degree of leukocytosis with a left

shift.7”#{176}17 Diagnostic clues on the chest radiograph include an elevated right or left hemidiaphragm, small pleural effusions, or right basilar pneumonitis or atelectasis.7’8”2’4 Our children certainly ifiustrate

these findings; their salient features are summarized

in Table 2. Six of seven children were febrile and

had distended abdomens. In six children abdomens

were tender and in all five in whom the liver could

be palpated, it was enlarged. In addition four of

seven had evidence of ileus and five were anemic.

Six of seven had elevation of the white blood cell

count, and all seven exhibited a left shift. In child

1, the hematocrit was probably falsely elevated due

to the presence of severe fluid deficit. On chest

roentgenogram the right hemidiaphragm was

ele-vated in five of seven patients, and the left leaf was

elevated in the one patient with a large abscess in

the left lobe. In addition child 1 had upper lobe

atelectasis, child 4 had a basilar opacification, and children 5 and 7 had pleural effusions. In support of

the observation of McCarty et al7 six of the seven

children were less than 3 years old.

Children 1 and 3 had evidence of active colitis,

and child 1 abdominal findings mimicking

perfo-rated appendiceal abscess and pathologic findings

of gangrenous appendix and cecum and numerous

areas of necrotic colon. In a series of seven children in Sri Lanka with severe colitis and perforation,’8

three were noted to have a gangrenous cecum, and two of these had gangrenous, perforated appendices

as well. This should indicate that, if colitis is

pres-ent, other localized intra-abdominal events beside

liver abscess may be occurring.

As ifiustrated by case 1, much of the morbidity

and mortality from amebic hepatic abscess in the

United States is probably due to our failure to

include this condition in our differential diagnosis.’9

In England and Wales, the diagnosis of amebiasis is

reportedly missed in 40% of patients with lethal

amebic infection.#{176} In only two of our seven cases was amebic disease suspected, even at

hospitaliza-tion. In case 3 amebae were seen in the stool, and

in case 1 in the appendix only; in none of the

remaining five were amebae seen either in stool or

abscess material. Sulfonamides, as administered to

child 2, are known to interfere with stool examina-tion.2’ According to Barrett-Conner,8 the stools

con-thin organisms in less than 50% of patients with

(4)

pre-TABLE 2. Clinical Features of Seven Cases with Liver Abscess

Patient Data 1 2 3 4 5 6 7

Age 3#{189}mo lyr 2yr 2#{189}yr 23/4yr 7yr 22mo

Sex Male Female Female Female Female Female Female

Race* M-A M-A Indian M-A M-A M M-A

History

Fever + + + + + + +

Colitis + + + - - - +

Respiratory distress + - - - - - +

Vomiting - - - + - - +

Physical Examination

Fever - + + + + + +

Respiratory distress + + + + + - +

Distended abdomen + + + + + - +

Tender + + + + + +

-Tender liver ? + ? + + ?

-Large liver ? + ? + + ? +

Ileus + - + + + -

-Chest film

Elevated diaphragm + + - + + + +

Pneumonia - . - - + - -

-Atelectasis + - - - - -

-Effusion - - - + - +

White blood count

Total 14,000 20,200 15,800 27,300 7800 20,600 22,200

Neutrophils (%) 33 49 2 53 17 50 77

Juveniles (%) 39 17 67t 38t 48 21 0

Hematocrit (%) 23 27 41 26 28 37 29

* M-A, Mexican-American; M, Mexican.

t

Includes juveniles plus all more immature forms.

vious reports.7”#{176}’4 When the stool is examined for

amebae, procedures that optimize detection should

be used. Supravital stains such as methylene blue

may be used to show nuclear detail and thus distin-guish amebae from fecal leukocytes. The definitive

examination of the stool is performed on slides of

fresh stool fixed in polyvinyl alcohol and suitably

stained.2’ The use of an experienced laboratory is

mandatory. Recent epidemiologic investigations22

have indicated that a number of laboratories have

overdiagnosed amebiasis by confusing fecal

leuko-cytes with organisms.

Serologic testing for suspected amebic abscess is

quite useful. Both indirect hemagglutination (IHA)

and immunodiffusion (ID) are 95% to 100% positive

in patients with liver abscess and 85% positive in

diagnosing dysentery.23’24 Moreover, the

combina-tion of IHA and serum immunoelectrophoresis can

be used to differentiate between active disease and

persistent antibody after cure.25 In this country, a

positive IHA is not common in the general

popula-tion.26 In our series, serologies were positive in all

six children in which they were performed. In the

seventh child amebae were seen in the stool.

Al-though uncommon, patients such as child 5

(posi-tive IHA, negative ID) do occur: in a study of 65

selected patients with amebic liver abscess,

Mad-dison and others27 found one negative by both tests

and one negative by ID and positive by IHA.

Demonstration of abscess cavities may be

accom-pushed by radioisotope liver scanning or

ultraso-nography.2’ Although a single abscess is the most

common finding, the presence of multiple cavities

does not exclude the diagnosis of amebic abscess.

Two of our patients (Nos. 3 and 5) had multiple

scattered abscesses. In addition, in a recent review

from Malaysia,’6 62 of 167 patients with amebic

liver abscess had more than one cavity present.

Epidemiologically, major common source

out-breaks of amebiasis have occurred as a result of

water supply contamination. However, it is

impor-tant to note that, at this time in the United States,

amebic infection in the community tends to cluster

in household foci with person-to-person

transmis-sion playing the major role in endemic disease. In

a community study in Arkansas,5 Spencer and

oth-ers showed infection to be endemic, with

signifi-cantly higher rates of stool and seropositivity seen

in households with crowding and poor sanitation.

No evidence for transmission by food or water was

found. In a further exploration which is of special relevance to our findings, Spencer and colleagues6 extensively investigated the family of two

(5)

town who were found to have amebic liver

ab-scesses. The survey of 183 extended family members

by Spencer et al revealed that 45.7% of 162 were

IHA positive and that 12.6% of 111 had positive

stools on a single examination. Five family members

had amebic liver abscesses. Only 0.3% of a random

sample of the community had a positive serology.

Homes of this family were significantly more

crowded, with fewer indoor toilets. Indeed, cluster-ing of seropositivity occurred in homes without that

facility. Water supplies were not contaminated, and

person-to-person transmission was implicated.

In the family cluster of child 1, three of four

members had serologic evidence of infection and at

least one was actively infected. In the cluster of

child 2, investigation of 17 family members detected

eight asymptomatic carriers and one additional

in-dividual with a positive serology. Person-to-person

transmission seems implicated in the families of

both cases and crowding in the cluster surrounding child 2. It is clear from the literature and our own data that, once an index patient is identified, family investigation is a very high-yield public health pro-cedure for case finding. Since asymptomatic carriers are infectious, this is a relatively cheap and effective public health measure.

Treatment of patients and positive contacts is

not completely settled. In our situation, all contacts with positive stools or serologies were treated with

metronidazole for ten days because adequate

fol-low-up could not be assured. Krogstad et al2’ have

recently reviewed amebiasis and its treatment, as

has the Medical Letter on Drugs and

Therapeu-tics.28 Metronidazole is currently the drug of choice

for treatment of symptomatic intestinal disease and

hepatic abscess. Child 5 exhibited a slow or incom-plete response to metronidazole resulting in the use

of chloroquin and dehydroemetine, and child 7 was

refractory to both chloroquin and metronidazole

and required surgical procedures. These children

support case reports already extant of liver

ab-scesses unresponsive to metronidazole but

respon-sive to other types of drug therapy. Intravenous

metronidazole may replace other drugs in patients

unable to take oral medication, but this drug is

investigational. For the asymptomatic carrier,

di-loxanide furoate, a nonadsorbable intestinal

ame-bicide, is the drug of choice. It is available, however,

only through the Center for Disease Control,

Par-asitic Disease Section, Atlanta.

Uncomplicated deep liver abscesses may, for the

most part, be managed conservatively, that is, with

oral metronidazole and observation. The patient’s

clinical condition can be used as a guide to the

effectiveness of therapy, and isotope scanning or

ultrasound used to follow abscess size. For the

re-fractory patient, a different drug regimen and/or

percutaneous aspiration or open drainage may be

necessary. For active subcapsular subphrenic

ab-scesses, percutaneous decompression should be

per-formed early since rupture into the pleural cavity

or pericardium is to be avoided.

Associated active colitis should be treated

vigor-ously with metronidazole and superimposed

bacte-rial sepsis with appropriate antimicrobial agents. For the refractory patient, surgery with creation of

an ileostomy and sigmoid mucus fistula may

im-prove survival.29 Patients with colon perforation

should undergo resection coupled with the above.

In summary, amebiasis still exists in endemic foci

in the United States, with person-to-person

trans-mission the predominant mode of spread. These

foci may be more numerous in southern border

areas in contact with heavily endemic regions. If a

substantial portion of the population is infected,

even low-incidence complications such as liver

ab-scess will occur with some frequency. In other

North American areas with lower endemicity,

ame-biasis and liver abscess should be suspected, espe-cially if travel to an endemic area has occurred prior to a clinically suspicious illness. E histolytica must

therefore be sought for in applicable patients with

colitis or signs of liver abscess. In addition, it must

be stressed that, once a case of amebic disease has

been diagnosed, investigation of the child’s family

or close contacts may be as important a duty as

care of the child himself.

ACKNOWLEDGMENTS

We wish to thank Bruce Porter, MPA, of the Pima

County Health Department and Virginia Barber, RN, of the Pinal County Health Department for their coopera-tion in the investigation of cases 1 and 2, and Kai Haber, MD, Picker Scholar, James Picker Foundation, of the Department Radiology for his help with ultrasonographic examinations.

REFERENCES

1. Brooke MM: Epidemiology of amebiasis in the United States. JAMA 188:519, 1964

2. Doxiadis T: Amebiasis: A nontropical disease. Med Times

97:86, 1969

3. Burrows RB: Prevalence of amebiasis in the United States and Canada. Am J Trop Med Hyg 10:172, 1961

4. CDC Intestinal Parasite Surveillance Annual Summary for

1977, Atlanta, Center for Disease Control, September 1978

5. Spencer HC, Hermos JA, Healy GR: Endemic amebiasis in an Arkansas community. Am J Epidemiol 104:93, 1976 6. Spencer HC, Muchnick C, Sexton DJ: Endemic amebiasis in

an extended family. Am J Trop Med Hyg 26:628, 1977

7. McCarty E, Pathmanand C, Sunakorn D: Amebic liver ab-scess in childhood. Am J Dis Child 126:67, 1973

8. Barrett-Conner E: Amebiasis, today, in the United States.

CalifMed J 114:1, 1971

9. Debakey MD, Ochsner A: Hepatic amebiasis: A 20 year experience and analysis of 236 cases. Surg Gynecol Obstet

(6)

10. Burnside WW, Cummins SD: Amebic abscess of the liver in a six-month old infant. J Pediatr 55:516, 1959

11. Walt F: Amebic liver abscess in infancy. Afr Child Health 1:

77, 1959

12. Jessee WF, Ryan JM, Fitzgerald JR, et al: Amebic liver abscess in childhood. Cliii Pediatr 14:134, 1975

13. Wadlington WB, Faber R, O’Neill JA: Recent experience wit hepatic amebiasis. Clin Pediatr 14:163, 1975

14. Das BM, Mitra SK, Walla BNS: Amoebic liver abscess in

children: A report of five cases. Indian Pediatr 13:113, 1976

15. Ramachandran S: Hepatic amoebiasis. Ceylon Med J 20:69,

1975

16. Chellappa M, Rengabashyan N: Amoebic liver abscess: A

review and study in 167 cases. Med JMalaysia 21:192, 1977

17. Ibarra-Perez C, Selman-Lama N: Diagnosis and treatment of amebic abscess of the liver with thoracic complications.

Am J Surg 134:283, 1977

18. Wijesundera C deS, DeSilva CC: Amebic perforation of the intestine in children. Pediatrics 30:937, 1962

19. Dorrough RL: Amebic liver abscess. South Med J 60:305, 1967

20. Stamm WP: Amoebiasis: A neglected diagnosis. J Clin Pa-thol 29:83, 1976

21. Krogstad DJ, Spencer HC, Healy GR: Current concepts in

parasitology, amebiasis. N EngI J Med 298:262, 1978 22. Krogstad DJ, Spencer HC, Healy GR: Amebiasis:

Epidemi-ologic studies in the United States 1971-1974. Ann Intern

Med 88:89, 1978

23. Krupp IM, Powell SJ: Antibody response to invasive ame-biasis in Durban, South Africa. Am J Trop Med Hyg 20:414, 1971

24. Kotcher E, Miranda M, Garcia de Salgado V: Correlation of clinical, parasitological, and serological data of individuals infected with Entamoeba histolytica. Gastroenterology 58: 388, 1970

25. Krupp IM, Powell SJ: Comparative study in the antibody response in amoebiasis. Am J Trop Med Hyg 20:421, 1971 26. Milgram EA, Healy GR, Kagan IG: Studies on the use of the

indirect hemagglutination test in the diagnosis of amebiasis.

Gastroenterology 50:645, 1966

27. Maddison SE, Powell SJ, Elsdon-Dew R: Comparison of hemagglutinins and precipitins in amebiasis. Am J Trop Med Hyg 14:551, 1965

28. Abramowicz M (ed): Drugs for parasitic infections. Med Lett

20:17, 1978

29. Vargas M, Pena A: Toxic amebic colitis and amoebic colon perforation: Improved prognosis. J Pediatr Surg 11:223, 1976

GROWTH OF THE CHILD

Observations of working- and middle-class American families consistently

reveal that lower-middle-class Caucasian mothers talk less to their infants, are

less likely to encourage cognitive development, especially of language, and are

more intrusive and autocratic in their discipline. This is not a recent trend.

Thirty years ago, Alfred Baldwin and colleagues observed working- and

middle-class Caucasian mothers and their young children in rural Ohio and reported

that working-class mothers were more autocratic and restrictive in their

prac-tices with their children. They intruded more often into the activities of the

child and were less disposed to explain punishments or give reasons for their

prohibitions. Several years ago, we observed 90 firstborn Caucasian children at

home over a five- to six-hour-period on several occasions and qualified the

encounters that involved maternal commands, prohibitions, and children’s

re-quests. There was an inverse relation between the number of prohibitions she

issued, a rate of one every five minutes for lower-middle-class parents versus

one every ten minutes for middle-class parents, a finding in complete accord

with Baldwin’s data gathered 30 years earlier.

From Kagan J: The Growth ofthe Child. New York, WW Norton & Co, 1978.

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1979;64;923

Pediatrics

H. Robert Harrison, C. Peter Crowe and Vincent A. Fulginiti

Amebic Liver Abscess in Children: Clinical and Epidemiologic Features

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1979;64;923

Pediatrics

H. Robert Harrison, C. Peter Crowe and Vincent A. Fulginiti

Amebic Liver Abscess in Children: Clinical and Epidemiologic Features

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