Vol.

35(3) September, 2011

ISSN 0304 4904

PAKISTAN
PAEDIATRIC
JOURNAL

A JOURNAL OF PAKISTAN PAEDIATRIC ASSOCIATION

Indexed in EMBASE/Excerpta Medica & Index medicus WHO IMEMR
pakpaedjournal@gmail.com

www.ppa.org.pk

http://www.pakmedinet.com/PPJ

ISSN 0304-4904

Founder
Prof. SMK Wasti (Late)

PAKISTAN PAEDIATRIC
JOURNAL

Patron
Prof. SM Haneef

Chief Editor
Prof. Said ul Haque

Managing Editor

-------------------------------------------------------Pak Paed J 2011, 35(3)

Prof. M Ashraf Sultan

CONTENTS

Editors
Prof. AG Nagi
Prof. A Hameed
Prof. Akmal Laeeq
Prof. Ayesha Arif
Prof. DS Akram
Prof. Humyaun Iqbal Khan
Prof. Iqbal Memon
Prof. Shakila Zaman
Prof. Tahir Msood
Prof. Nadeem Khawar
Prof. ZA Bhutta
Dr. Abdul Rehman

Article

Editorial
Review article

Apnea of Prematurity: Brief Review of

Pathogenesis and Pragmatic Guidelines for Its
Management in Resource Limited Countries

Editorial Board

KHALID N. HAQUE, AHMED QUDDUSI

1.

2.

3.

International
David Southall (UK)
Mobeen Rathore (USA)
Prof. Peter Raine (UK)
Prof. Charlotte M Wright (UK)

Statistical Adviser
Prof. Amanullah

Oral Hygiene and Dietary Habits among Primary

School Children, in Urban Karachi

128-34

MARIUM IQBAL, IBRAHIM SHAKOOR,

MOHSINA NOOR IBRAHIM, Laeeq-uz Zaman

Biochemical Types of Dehydration and Risk

Factors for Sodium Imbalance in Children with
Acute Watery Diarrhea

BUSHRA
FATIMA,
MUHAMMAD
FAHEEM
MUHAMMAD ASHRAF SULTAN, Asif Hanif

Developmental Assessment
Intervention
in
Children
Developmental Delay

135-38

AFZAL,

and Effect of
with
Global

139-44

SHAZIA MAQBOOL, EHSAN ULLAH, TAYYABA KHAWAR BUTT,

4.

National
Prof. Afroz Ramzan
Prof. A H Haquani
Prof. Asma Fouzia Qureshi
Prof. Atta Ullah Mazhar
Prof. Ayesha Mehnaz
Prof. Pervaz Akbar
Prof. Qamar ud din Nizami
Prof. Salman Ali (Brig)
Prof. Tariq Bhutta
Dr. Asad Hafeez
Dr. Liaquat Ali
Dr. Tayyaba Khawar Butt

118-27

Original article

Editorial Executive
Committee
Prof. Agha Shabbir Ali
Prof. Abdul Waheed
Prof. Javaria Mannan
Prof. Muhammad Ali Khan
Prof. Sajid Maqbool

Page
115-17

5.

Wajeeha Zahra, Mian M Shariff

Is Lumbar Puncture Necessary among Children

with First Febrile Seizure?

MUHAMMAD SAEED, TAHIR NADEEM, SAMIR M. AL-NUFIEE

Pattern of Neonatal Diseases in Special Care

Baby Unit (SCBU) Khyber Teaching Hospital,
Peshawar.

145-48

149-54

QAMAR ALI KHAN, HAMID IQBAL, HABIB UR REHMAN

Pakistan Paediatric Forum

1.
2.

Dengue Fever Guidelines: Its Controversies

ABDUL REHMAN, HUMAYUN IQBAL KHAN

Pakistan Cardiac Society Guidelines for

Prevention of Rheumatic Fever and Rheumatic
Heart Disease

155-61
162-68

NAVEED AKHTAR, MASOOD SADIQ, FAIZ UL HASSAN RIZVI,

Haseena Chagani, Asad Hafeez, Adnan Gul,

Madeeha Hina

Case report
1.
2.
3.

Nephrogenic Diabetes Insipidus

SHAAFIA FATIMA, HAFSA MUHAMMAD, AYESHA ARIF

Histiocytosis Syndromes of Childhood

JOVARIA MANNAN, MUHAMMAD NAVEED, ATTIA KALIM

Pseudohypoaldosteronism, Hypothyroidism and

Hypoparathyroidism in a Two-Year-Old Boy

ABDULMONEIM AL-AGHA

Abstract service
News and views

169-70
171-74
175-77

178-79
180-81

II

PAEDIATRICIANS AND MEDICAL PRACTITIONERS

All paediatricians can become member of
Pakistan Paediatric Association. And, also, all
those who take care of children in their practice
may become associate member of the Pakistan
Paediatric Association.
Please enroll as a Member of the Pakistan
Paediatric Association by contacting any one of
the followings in your region.
1. Prof. Amir M K Jogezi, President Centre,
C-31, GOR Colony, Air Port Road, Quetta.
E-mail: amir_jogezai@hotmail.com
2. Dr. Zareen Fasih, General Secretary Centre,
114, 33rd Street, Off. Khayabane-e-Mohafiz,
Phase 6, DHA, Karachi 75600.
E-mail: z_fasih56@yahoo.com
3. Dr. Imtiaz Ali Khan, President Sindh Branch,
No. 48, Talha Mansion, Ground Floor Flat
No. 1, Block # 3, Karachi Memon Cooperative
Housing Society, Karachi 74800.
E-mail: driakhan12@yahoo.com
4. Dr. Hasina S Chagani, Secretary Sindh Branch,
A-428, Block-C, North Nazimabad, Karachi-33.
E-mail: hasina_chagani@hotmail.com

8. Prof. Amin Jan Gandapur, Secretary Khyber

Pakhtoon Khwah House No. 15, Street No. 3,
K-1, Phase III Hayatabad Peshawar.
E-mail:
9. Prof. Mahmood Jamal, President Federal
Branch, H. # 66, St. 16, F-11/2, Islamabad
E-mail: mahmoodjamal@hotmail.com
10. Dr. Shehzad Munir, Secretary Federal Branch,
H. # -E, St. # 20, Sector G-7/2, Islamabad.
E-mail: smunir9933@hotmail.com
11. Prof. Waqar Hussain, President Punjab Branch,
122-A, PSCIR Colony, Phase 1, West Canal
Bank, Lahore.
E-mail: gwar@lhr.paknet.com.pk
12. Dr. Muhammad Nasir Rana, Secretary Punjab
Branch, E-22 New Super Town Opp: Toheed
Mosque, Lahore cantt.
E-mail: dr_nasirrana@yahoo.com
13. Prof. Saidul Haque Chaudhry, Chief Editor,
Pakistan Paediatric Journal (PPJ), 180-H Block,
Phase-II, Johar Town, Lahore.
E-mail: drsaidulhaque@gmail.com

5. Prof.
Bashir
Ahmed
Kakar,
President
Balochistan Branch, House # 10, 9/450-A Opp.
GOR Colony, Main Shahboo Road, Quetta
E-mail: nil

14. Prof. Muhammad Ashraf Sultan, Managing

Editor, Pakistan Paediatric Journal (PPJ),
124-SD House, Askari Housing Complex,
Walton, Gulberg-III, Lahore.
E-mail: drmas@brain.net.pk

6. Dr. Lotf Ali, Secretary Balochistan Branch,

H # 2, Aziz Marri Colony of Mir Mitha Khan
Street, Brewary Road, Quetta.
E-mail: lotfoof@yahoo.com

Please inform the editorial office about

your membership so that your name is placed on
mailing list of the Pakistan Paediatric Journal.

7. Prof. Asmat Ara Khattak, President Khyber

Pakhtoon Khwah Branch, 33 Shami Road, St.
EDITOR
No. 3, Behind Bilal Masjid, Peshawar Cant.
E-mail:
------------------------------------------------------------------------------------------------------------------------------------------------------Pakistan Paediatric Journal is published quarterly in March, June, September and
December. Inland annual subscription for 2011 is Rs.600. The price of single copy is Rs.150.
Special rates are applicable for postgraduates and for subscribers from Mid Eastern,
SAARC and developing countries. Separate rates for institutions in Pakistan and abroad.
Annual subscription for United Kingdom: 40, USA, rest of the world and for those having
sub-office in Pakistan US $ 50.
Pakistan Paediatric Journal: No part of this journal may be reproduced in any form or by
any means mechanical or electronic including information storage and retrieval system
without the written permission of the publisher.
Recognized by PM&DC, Indexed in index Medicus WHO IMEMR & EMBASE/Excerpta
Medica & Global Health/CAB Abstracts.
Declaration No.PC.PB/25573/17951 dated 07-09-1977

www.ppa.org.pk

III

PAKISTAN PAEDIATRIC JOURNAL

INSTRUCTIONS FOR AUTHORS
INFORMATION FOR CONTRIBUTORS

EDITORIAL AND PEER REVIEW PROCESS

Pakistan Paediatric Journal is the official

publication
of
The
Pakistan
Paediatric
Association. The first issue was published in 1977
as Pakistan Paediatric Journal, ISSN No.0304-4904.
Since then, the journal has been published without
interruption
and
has
contributed
tremendously to several advances in paediatrics
in Pakistan. Our journal covers clinical and
research works on all aspects of the healthcare
of children. The journal aims to contribute to cure
of the paediatric diseases and improvement of
the health of children. The manuscripts are
categorized as review articles, original articles
and case reports. The journal is published
quarterly and official language of Pakistan
Paediatric Journal is English. The journal is
distributed to all members of The Pakistan
Paediatric Association, medical colleges, libraries
and related institutes. The journal is also
expedited to libraries of several major universities
in the world.

Editorial and Review Board of Pakistan Paediatric

Journal reviews all the received materials. The
manuscripts are sent to three most relevant
investigators for review of the contents including
statistical analysis. The editor selects peer referees
from the specialist database owned by the
Editorial and Review Board. For review, names
and their affiliations of the authors are blinded.

Manuscripts for publication are accepted from

authors both within the country and abroad.
These should be prepared in accordance with
the fifth edition of Uniform Requirements for
Manuscripts Submitted to Biomedical Journals
established by Vancouver group (International
Committee of Medical Journal Editors, ICMJE)
originally published in New England Journal of
Medicine 1997; 336:309-15. The complete
document, updated December, 2010, appears
at http:/www.icmje.org/index.html and should
not have been offered for publication elsewhere
or published previously. If so permission for republication must be enclosed from the
editors/copy holders. Authors should disclose at
the time of submission, information on financial
conflicts of interest that may influence the
manuscript.
Manuscript should be submitted by the
corresponding authors, who should indicate the
address, phone number, fax number, and e-mail
address for correspondence in the title page of
manuscript.

Acceptance of the manuscript is decided, based

on the critiques and recommended decision of
the referees. A referees decision is made as
acceptance without revision, acceptance
after revisions, review again after revisions,
rejection and additional review by outside
reviewers. If there is marked discrepancy in the
decisions between the three referees or in
opinions between the author and referees(s), the
Editor may send the manuscript to another
referee
for
additional
comments
and
recommended decision. Names and decisions of
the referees are masked. A final decision on
acceptance or rejection for publication is
forwarded to the corresponding author from the
Editorial Office.
The usual reasons of rejection are insufficient
originality, serious scientific flaws, poor quality of
illustrations. Rarity itself of a disease condition is
not an acceptable condition of case reports. The
peer review process takes usually six weeks after
the manuscript submission. Revisions are usually
requested to take account of criticism and
comments made by referees. Three copies of
revised manuscript should be submitted,
including one set of original illustration. Failure to
resubmit the revised manuscript within two
months is regarded as a withdrawal. The
corresponding author must indicate clearly what
alterations have been made in response to the
referees comments point by point. Acceptable
reasons should be given for noncompliance with
any recommendation of the referees. Once
accepted, original articles will be published within
three months.

www.ppa.org.pk

IV
General
Two complete copies of the manuscript should
be sent to the Editors, Pakistan Paediatric Journal.
101, H-Block, Gulberg-III/GPO Box:308, Lahore,
Pakistan. These will not be returned unless
requested at the time of submission. Authors
should keep one set of the entire manuscript with
them.
Manuscripts and references should be typed in
double line spacing with a 4 cm margin on the
left side. Pages must be numbered and each
page carries a running title. Submission of articles
online would be preferred. If this facility is not
available to the author then he/she may send
article on re-writeable CD.
Articles are submitted for peer review and the
editors may make such alterations as considered
necessary. The views expressed are those of the
authors and may not reflect the policies of the
Journal or the Association. Concise Oxford English
dictionary is used as a reference for spellings and
hyphenation.
All measurements must be in SI units except blood
pressure (mm Hg) and drugs (metric units).
Generic names of drugs must be used.
In statistical analysis of data, 95% confidence
intervals must be employed.
Use terms from the medical subject headings
(MeSH). Uncommon abbreviations should be
avoided and should be preceded by the full
word before their next appearance in the text.
Abbreviations for some of the commoner units
are Gram (gm); Kilogram (kg); Milligram (mg);
Microgram (ug); Nanogram (ng); Picogram (pg);
Hour (hr); Second (sec); Cubic Millimeter (mm3);
Millimeter (mm); Centimeter (cm); Milliliter (ml);
Pound (lb); Milliequivalent (mEq); Micron (u);
Percent (%). Plural words have the same
abbreviation.
Tables should be typed in double line spacing
without ruled lines and should include essential
data. Avoid crowding. Main heading should be
in capital letter. Below this a caption in small
letters must be included.
Illustrations and figures should preferably be
professionally drawn. These should be given
capital letters and numbers eg Figure-2 and

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table-4. Tables and figures must bear a number

corresponding to a similar number in the text.
Except for especially complicated drawings,
which show large amounts of data, all figures are
published at one single page width, the smallest
parts of the figure must be legible.
All the legends for figures should be typewritten in
double space. Do not use a separate sheet for
each legend. Figure legend should describe
briefly the data shown, explain any abbreviations
or reference point in the photographs, and
identify all units, mathematical expressions
abscissas, ordinates and symbols.
Photographs should be uncounted, black & white
on glossy paper, and submitted in a separate
envelope backed by a stiff card board. The
name of author, title of paper and top or bottom
must be marked on the back of illustrations and
photographs. Pictures, scans etc should be
arrowed ( ) an overlay to show specific areas or
attach explanatory drawings, sketches etc.
Color photographs will be published if the Editor
decide them absolute necessary. The entire
expense of reproducing colour photographs will
be charged to the author. The author is
responsible for submitting prints that are of
sufficient
quality
to
permit
accurate
reproduction, and of approving the final colour
galley proof. All photographs should be correctly
exposed, sharply focused, and submitted on
glossy white paper
Pakistan
Paediatric
Journal
assumes
no
responsibility for the quality of the photography
as they appear in the Journal. Current estimates
for color reproduction can be obtained from the
Editors Office.
A legend for each light microscopic photograph
should include name of stain and magnification.
Electron microscopic photographs should have
an internal scale marker. All kinds of figures may
be reduced enlarged or trimmed for publication
by the Editor.

GENERAL CATEGORIES
Include invited review articles, Original
articles, Short reports, Annotations/Editorials,

V
Letters to the editors, Book reviews and Notes and
Notices.
1. Invited review articles describe concise
review on important subjects of paediatrics.
The review articles are accepted after
editorial evaluation.
2. Original Articles: should normally include a
title, Abstract, Introduction, Materials &
Methods, Results, Discussion and Conclusions,
Acknowledgements, References.
Title: use a separate page. Give the title of
the article, names(s) and academic degrees
of author(s) place(s) where the work was
done, address for correspondence and a
running title (that is carried on subsequent
pages). Title should have not more than 10
words.
Abstract: (separate page) should comprise of
not more than 150 words and should include
what was done, the main findings and their
implications. Details should be avoided.
Introduction: should briefly state the purpose
of study, pertinent but not extensive review of
the subject with 5-6 references.
Materials and Methods: should describe the
criteria for selection of material and identify
clearly the methods, materials and apparatus
used. Avoid using names of patients or other
clues that can lead to disclosure of their
identity.
We endorse the principles embodies in the
Declaration of Helsinki and expect that all
investigations involving human materials have
been performed in accordance with these
principles. For animal experiment, the
Guiding Principles in the Care and Use of
Animals approved by the American
Physiological Society have to be observed.
Method of statistical analyses and criteria of
significance level should be described. In
case reports, case history or case description
replace the Materials and Methods section as
well as Results section.
Results: should be presented systematically

Preferably in one format only i.e. script, tables

or figures without repetition as far as possible.
Discussion and Conclusions: comment on the
observations, conclusions drawn, implications
of the study, its limitations and how the study
compares with other similar or relevant
studies. Recommendations for further study
may be recorded when indicated.
Acknowledgements: should be recorded on
a separate paper.
References: These must be numbered in the
order according to which they appear in the
text and should include all information
(Vancouver style). Abstracts and personal
communications may be cited in text but
should not be included in the references.
Authors are responsible for the accuracy of all
references. These cannot be checked by the
editors.

3. Short Reports
These must not exceed 1000 words, including
an abstract of no more than 50 words, 1 or 2
tables or illustrations and 5-6 references. The
table title should be less than 8 words.
4. Annotation/Editorial
Suggestions for topics and for authors are
welcome. Usually these are written by the
editors.
5. Letter to Editor
Should contain not more than 300 words with
few references and should be signed by all
the authors. Readers are invited to freely
contribute to this column as regard their
experience,
importance
of
paediatric
research.
6. Book reviews
Are welcome from readers.
7. Notes & Notices
Association
news,
forthcoming
events,
conferences and other academic and
literary pursuits etc are included.

www.ppa.org.pk

VI

LETTER OF UNDERTAKING
This is to confirm that the manuscript entitled ---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------submitted for publication in Quarterly Pakistan Paediatric Journal has not been offered for
publication to, or published in, any other journal and if accepted for publication it will not
be published in any other medical periodical in Pakistan or overseas.
Name of the authors*

Signature

1. ------------------------------------------

------------------------------------------------

2. ------------------------------------------

------------------------------------------------

3. ------------------------------------------

------------------------------------------------

* Please mention role of co-authors.

(This letter must be signed by all the authors)

ELECTRONIC SUBMISSION OF ARTICLES

PAKISTAN PAEDIATRIC JOURNAL now accepts electronic submission of articles via email, attachment in MS Word format at following address

pakpaedjournal@gmail.com
Note: The figures should be sent in the format of JPEG or GIF to
ensure good quality images

Electronic submission saves time, postage costs and allows the

manuscript to be handled in electronic form throughout the publication process.

www.ppa.org.pk

VII

THE FINAL CHECKLIST

The authors must ensure that before submitting the manuscript for publication, they have taken
care of the following:-

Double spaced typing in A4 size white paper with 12-point font

Sequence of title page, abstract and keywords, introduction, materials and methods,
results, discussion, acknowledgments, reference, tables and figure legends. All pages
should be numbered consecutively starting from the title page

Title page with article title, authors full name(s) and affiliation, address for
correspondence (including telephone, fax number and e-mail address), running title
(less than 10 words) and footnotes if any.

Check the total/percentage in the table carefully

Abstract in structured format for original article and in unstructured format for case
report within 250 words, and key words as in MeSH.

Two copies and one original text, tables and figures.

All take and figure numbers found in the text.

Reference listed in proper format. Check that all references listed in the references
section and cited in the text and vice versa.

A covering letter

An undertaking signed by all the authors stating the material is not published
previously, and will not be submitted for publication elsewhere, and stating conflicts of
interest of all listed authors, if any.

CD disk with manuscript in Microsoft Word format

www.ppa.org.pk

EDITORIAL

Pakistan Paediatric Journal

-----------------------------------------------------------------Pak Paed J 2011;35(3): 115-17

Dengue Epidemic 2011

With the onset of monsoon in Lahore cases of
dengue infection started appearing this year. This
was followed by a full-fledged dengue epidemic,
probably the worst recorded in history. Though
the official figures of confirmed dengue
infection were 15,235 up to 9th October 2011 and
dengue related deaths during this period were
195, the actual number of people suffering from
this infection is much more. This is because of
gross under-reporting (large number of cases go
to private medical facilities rather than public
sector hospitals and are not reported), and the
criteria for labeling is not appropriate. The
diagnosis of dengue in an epidemic situation is
usually made clinically and serological and
virological confirmation is not possible neither
practical in vast majority of the patients. The
government figures include only those patients in
which secological tests were done and ware
positive. Now when floods are wreaking havoc in
a large part of the country dengue epidemic
can easily spread to these areas as well.
Dengue is Aedesborne disease caused by
dengue viruses that belong to genus Flavivirus.
There are four serotypes: DEN1, DEN2, DEN3 and
DEN4. The long-term immunity is serotype specific.
More than 90% of the patients are asymptomatic.
Half of the symptomatic patients have
undifferentiated fever. Remaining patients of
dengue infection have classical dengue fever
that is non-fatal. However the disease is very
disabling, the suffering quite intense, and the
period of recuperation may be long. Dengue
hemorrhagic fever is a separate disease and may
be deadly. Classical Dengue fever primarily
occurs in non-immune adults and children of all
ages. However when the disease becomes
endemic outbreaks are more commonly seen in
children and incidence of dengue hemorrhagic
fever rises.

Epidemics of Dengue are often very explosive

with an attack rate of 50-80%. When such
epidemics occur whole communities are seriously
affected. This infection is primarily tropical, Its
principal vector is Aedes egypti and accessory
vectors include Aedes albopicus. Aedes is
exceedingly domestic, and has a very short flight
range. Multiple household cases are therefore
common. Transmission of disease occurs from
viremic to healthy individual through the above
mentioned mosquito vectors. Transmission may
also occur by mechanical means. Mosquito while
feeding on a viremic patient when interrupted
bites another susceptible person immediately
infecting the later as well. Non-Aedes mosquito
may also contribute to spread of the disease in
this fashion. With effective vector control Aedes
can be eradicated. Since all these vectors are
day time biter, avoidance of bite through
individual protective methods is also helpful. In
addition cases of the disease must be screened
from mosquitoes for example by using nets and
viremic individuals should not be allowed to
move around to prevent viral transmission.
The treatment of dengue fever and dengue
hemorrhagic fever is supportive. Paracetamol is
given for fever in addition to measures like
sponging. For the management of dengue
hemorrhagic fever identification of critical phase
of the disease is imperative. During this phase
calculated amount of fluids are administered
with strict monitoring of the patient. This requires
hospital administration in high dependency area.
Platelet transfusions are given only in selected
patients who have severe thrombocytopenia.
There is no role of prophylactic platelet
transfusion. Similarly the management of dengue
shock is also a medical emergency that requires
meticulous fluid administration. Sometimes colloid
solution like Dextran 40 may be required
especially for the treatment of dengue shock
syndrome. Dextran is however not a magic drug
that would cure dengue. This is given in bolus

www.ppa.org.pk

Editorial

116
form if crystalloids do not improve the
hemodynamic status. It should however be kept
in mind that most of the patients of dengue
infection have dengue fever. They neither require
hospitalization nor intensive monitoring.
The governments all-out efforts this year were on
improvement of treating facilities for dengue
patients. All teaching hospitals of the province
were converted into dengue hospitals. Though
this approach may have saved many lives but
cannot be recommended as on ongoing policy
keeping in view the misery of a huge number of
non-dengue patients who did not receive
appropriate and on time management. In
addition fumigation drive to exterminate adult
mosquito is not very helpful. Poor hygienic
conditions that lead to stagnant water provide
excellent breathing sits for Aedes. To avoid a
dengue-related catastrophe in coming years not
only government but organizations like Pakistan
Paediatric Association must launch a well
designed and motivated campaign to increase
public awareness about the hazards of poor
hygiene and how people can contribute in
improving these conditions. Surroundings must be
kept lean, water drained from empty cans, trapholes, tires, etc, and potted plants must also be
well drained. Health managers should also keep
an eye on emergence of other arboviral diseases
like chikungunya and yellow fever. Larvacidal
drugs should also be sprayed at appropriate
time. Remedial and preventive measures are the
key to control the menace of these infections.

Prof. Humayun Iqbal Khan,

Professor of Pediatrics,
Postgraduate Medical Institute/
Lahore General Hospital,
Lahore.

PAEDIATRIC DENTISTRY
Paediatric Dentistry is a sub-specialty of Dental
Surgery, also called oral medicine. The Paediatric
Dentistry has got further sub-specialties. There are
many oral diseases, which may which include
genetic and developmental, acquired and may
effect not only the health of a child but also
leads to speech, esthetic and psychological

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defects thus the child and the adolescence

needs special attention and may some time
have to include other experts in the team for
management. Due to modern life style, child has
to experience dental caries and periodontal
diseases and adults are also suffering.
The tooth decay is a common problem of
children of today due to modern food and
change of life style. Researchers have now
discovered and studied the glucansherose
enzyme that is responsible for dental or bacterial
plaque sticking to teeth. This has been obtained
or isolated from lactic acid bacterium
lactobacillus.
This
bacteria
uses
the
glucansnerose enzyme to convert sugar into long
sticky sugar chains. They use this glue to attach
themselves to tooth enamel. The main cause of
tooth decay in addition to this bacterium is
streptococcus mutans of mouth that also use this
enzyme. Thus, these bacteria ferment sugar
releasing acids that dissolve calcium in teeth.
One of the commoner sequels of cause is dental
abusers with or without systemic effects. There are
other factors which govern the childs subcreepily to carries, which may include genetic
and developmental factors. This is a new dental
problem developing in children.
The preventive measure against dental caries
include decreasing frequent sugar ingestion, use
of plastic dental sealants on the pit and fissure of
molars, improving oral hygiene by daily burshing
especially with fluoridated toothpaste, and use of
oral fluoride. Water fluoridation is the most cost
effective, most convenient, and most reliable
method of providing optimal fluoride because it
does not depend on individual compliance.
Numerous studies have shown decay rates to be
reduced by between 25 and 65% depending on
the population group.
There is need for awareness of mothers and
children. They should avoid eating sticky sugar
containing food or fast food. Many children visit
the Hospitals or dentist for pain in milk teeth due
to unhealthy eating habits. The child stops eating
food and develop low resistance in body.
Sometime symptoms are sudden pain, swelling
due to infected teeth. The child feel difficulty in
eating.
To prevent the dental caries, the
pregnant mothers diet is important. During 42
weeks of embryonic life, the fetus needs proper
balanced food. There is need to eat healthy diet

117

Editorial

and to avoid drinking alcohol during pregnancy.

This is way of preventing dental carries. There is
need to improve maternal health so that a
healthy child is born with full resistance.
Paediatric dentistry should achieve the goals of
education of doctors, dental surgeons, public
and child in order to reduce tooth loss due to
dental caries in early age.
The periodontal disease is another problem. This is
due to neglect of parents and children.
According to our own survey, more than 75% of
children have got either dental caries or
periodontal disease. Pericronitis may also be seen
in addition to gum soreness in early and late
childhood. Modern diet and lack of breast
feeding also creates dental diseases in children.
Most mothers put the child on bottle feeding.
Such childrens masticating muscles cannot
develop properly and dental arches are not
formed. There is need of education to parents
and teachers. Irregular teeth and arches destroy
esthetics of face and such children need
orthodontic treatment, in this way tooth
movement is carried out.
An insidious threat to health, periodontal disease
has been associated with an increase in systemic
diseases. Toxic products generated by bacteria
trigger an inflammatory response from host tissue,
which can lead to progressive periodontal
disease. Pathogens, bacteroides, such as P.
gingvalis are most commonly associated with
localized active periodontal disease. While C.
rectus, P. micros, F. nucleatum, B. forsenthesis and
A.
actinomycetemcomitans
fusiformis
are
implicated in both localized and generalized
disease. The bleeding from gums or bad smell
from mouth should be properly checked by a
qualified periodontal surgeon. If periodontal
pockets remain for some time, they will effect the
general health badly.
Oral hygiene is important for general health, and
it can be controlled by observing prevention and
proper hygiene and healthy eating habits and
optimum use of flouride in drinking water. The
bad oral health creates pockets in the gums

micro organism from pocket get into blood

stream and causes cardiac, joint problems and
redness of eyes. The maintenance of oral
hygiene should be given urgent attention by the
teaches, parents, doctors so that oral health
should be improved by such preventive measures
to save the general health, mothers can play
role in this regard. The medical well-being of the
individual of the society is very much needed. In
this regard intention should be paid to the
importance of public health education be made
vigorously to keep the children away from
diseases. Prevention is better than cure.
Researcher have now shown that oral health is
related to systemic diseases, thus need attention
by all those who are related to health of the
patient. There is no dental health plan for
manpower. According to W.H.O present dental
manpower to population ratio is very much low.
Even school health service does not exist in
Pakistan, thus child population is the most sufferer
due to lack of planning as compared to other
countries. All our institutions lack in human
resources, teachers and para dental workers to
meet the requirement of the population in
Pakistan. There is need for attracting Pakistani
scholars serving abroad to come to Pakistan for
the welfare of the people of Pakistan.
However, there is need to get proper check up
and if required, treatment should be done by the
qualified persons. A dental care programme from
neonate to adolescent be prepared and
implemented by the health caring authorities, till
such time we may follow the recommendation of
the American Academy of Paediatrics, American
Society of dentistry for children, British Paediatrics
Association. Society and the pediatricians may
supervise in the best interest of the notion A
healthy nation.
Prof. M. A. Soofi
48-Lawrance Road,
Lahore.

www.ppa.org.pk

REVIEW ARTICLE

Apnea of Prematurity: Brief Review of Pathogenesis and

Pragmatic Guidelines for Its Management in Resource
Limited Countries
KHALID N. HAQUE, AHMED QUDDUSI

-----------------------------------------------------------------ABSTRACT
Authors affiliations
-----------------------------------------Correspondence to:Khalid N. Haque*
276, Club Drive, San Carlos,
California 94070, USA
E-mail:
Khalidnh99@yahoo.com

Pak Paed J 2011; 35(3): 118-27

Apnea of prematurity (AOP) is diagnosed in more than 50% of premature

infants and is inversely related to gestational age at birth. Nearly all
infants born at < 29 weeks or weighing < 1000 Grams at birth are
affected, 54% born at 30-31 weeks, 15% born at 32-33 weeks and 7% born
at 34-35 weeks.
Though it is a common problem there is lack of consensus amongst
caregivers on the criteria used to diagnose AOP, and to its management
and long-term significance.
This review present the current thinking about the etiology, diagnosis and
management of AOP and suggests an evidence based management
guideline suitable for resource limited countries.
Key words: Apnea of Prematurity. Management Guidelines

INTRODUCTION:
Apnea of prematurity (AOP) is diagnosed in more
than 50% of premature infants and in nearly all
the infants who weigh less than1000 g at birth1.
Whilst literature clearly defines clinically significant
apnea in infants as pauses in breathing that last
for >20 seconds or for >10 seconds if associated
with bradycardia or oxygen desaturation (SpO2 <
80% for > 4 seconds and heart rate < 2/3rd of base
line for > 4 seconds)2. There is no consensus about
the frequency or duration of apnea required to
diagnose AOP. Nor is there consensus on the
degree of change in oxygen saturation, or
severity of bradycardia required to diagnose
significant apnea that requires therapy to be
initiated. Bradycardia is reported to occur in 10%
of infants when apnea lasts between 10 and 14
seconds, around 34% with apnea lasting 15 to 20
seconds and in 75% of infants who have apnea
lasting for more than 20 seconds1.
Whilst it would be logical to assume that apnea

www.ppa.org.pk

associated
with
either
bradycardia
or
desaturation may affect neurodevelopmental
outcome due to disturbance in cerebral blood
flow. No direct link has been demonstrated
between
AOP
and
neurodevelopmental
outcome. This may be due to various
confounding comorbidities that influence the
neurodevelopmental outcome of premature
infants. Thus, it is also not clear whether AOP has
clinically important long-term effects. Never-theless when faced with a premature infant with
AOP there is an immediate and irresistible urge
amongst clinicians to respond to apnea.
Clinicians are able to respond successfully to
apnea events with drugs or physical and or
mechanical interventions, but it remains
unproven which of these interventions are
beneficial and/or have any long-term effects.
This review will therefore discuss the pathogenesis,
diagnosis, causes and risk factors, associated
conditions, management modalities, prognosis
and conclude by suggesting a pragmatic

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Apnea of Prematurity, Management Guidelines

diagnostic and management guideline for use in

resource limited countries.
Pathogenesis: AOP affects mainly preterm infants
due to immaturity of their respiratory control
centers in the brainstem, medulla oblongata,
central and peripheral chemoreceptors in the
brain, aortic arch, and carotid arteries.
Immaturity of the mechanical stretch receptors in
lungs is also involved. Whilst the pathogenesis
remains unclear, current thinking is that AOP may
be related to one or more of the following
factors; 1) up-regulation of inhibitory neurotransmitters, 2) impaired central chemo-sensitivity,
3) hypoxic ventilator depression and or 4)
impaired astrocyte development.

The fetus transits from an oxygen-poor

environment, with PaO2 of 2327 mmHg, to an
oxygen-rich environment soon after birth leading
to a fourfold increase in PaO23. This postnatal rise
in PaO2 significantly dampens the peripheral
chemoreceptors, resulting in delayed onset of
spontaneous breathing, especially when the
baby is exposed to 100% oxygen during postnatal
resuscitation4.
It is also thought that enhanced sensitivity to
inhibitory neurotransmitters, such as gammaamino-butyric acid (GABA), adenosine, serotonin,

and prostaglandin, a feature of the premature

infants respiratory control system plays a role in
the pathogenesis of AOP5.
Exaggerated activation of the laryngeal mucosa
(a chemo-reflex mediated through the superior
laryngeal afferent nerve) in premature infants is
another factor that may lead to AOP6.
Diagnosis: AOP is inversely related to gestational

age at birth with nearly all infants born at < 29

weeks of gestation being affected, 54% born at
30-31 weeks, 15% born at 32-33 weeks and 7%
born at 34-35 weeks3. The diagnosis of AOP is
made after excluding; 1) central apnea (10%-25%
of cases) defined as total cessation of inspiration
without evidence of obstruction, 2) obstructive
apnea (10%-25% of cases) defined as attempted
inspiration with upper airway obstruction resulting
in chest wall motion without airflowand 3) mixed
apnea (50%-75% of cases) defined as obstructed
respiratory efforts usually following central
causes7Table 1. It is equally important for
clinicians to differentiate AOP from periodic
breathing (though uncommon in preterm infants)
where there the infant breaths for 10-15 seconds
then has apnea for 5-10 seconds with no change
in heart rate or colour.

TABLE 1:- Comparison of different types of Apnea and Periodic Breathing

Criteria
Duration of cessation of
breathing
Respiratory Effort
Movement of Air
Bradycardia/Desaturations

Central Apnea
At least 20
seconds
Absent
Absent
May Occur

Obstructive Apnea
At least 20 seconds

Mixed-Type Apnea
At least 20 seconds

Periodic Breathing
5 10 seconds

Present
Reduced/Absent
May Occur

Absent/Present
Reduced/Absent
May Occur

Absent
Reduced/Absent
No

AOP usually presents after the 2nd day and within

the first 10days of life. Presence of apnea may be
obscured if the baby requires ventilator support
or is having seizures. Spell of apnea is often
preceded by gross body movements suggestive
of arousal (such as squirming, crying, eye
opening)
bradycardia
and/or
oxygen
desaturation. This is because apneic spells usually
occur during either active rapid eye movement
or transitional stage sleep and are uncommon
during quite sleep. Episodes of AOP may be
accentuated or precipitated by medications
such as narcotics, prostaglandins or magnesium
sulphate8.
Clinicians diagnose AOP when there is no other

cause for apnea (diagnosis of exclusion) such as

sepsis, pneumonia, asphyxia, seizures, and intracranial haemorrhage, anemia or temperature
instability. It is important to also rule out metabolic
disturbances like hypoglycemia, hypocalcaemia,
hyponatremia and conditions like gastrooesophegeal reflux that may precipitate or coexits with AOP.
Risk Factors: The likely risk factors that are well

known to be associated with apnea (not

necessarily AOP) include hypoxic-ischemic
encephalopathy, seizures, intra-cranial bleeding,
infection/sepsis,
glucose
and
electrolyte
disorders, fluctuating environmental temperature,
and airway obstruction due to any cause.

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120

Haque KN, Quddusi A

Recently two important risk factors associated

with increased risk of AOP have been identified.

There is thus NO evidence that GER is either

temporally or causally related to AOP12.

a)

Investigations: All babies, born at or less than 35

b)

Based on a retrospective cohort study of

317 premature twin pairs the heritability of
AOP in the same gender twins was found to
be 87% (CI 49-97), and genetic factors were
associated with 99% variance in male twins
(CI 89-100) and 78% in female twins (CI 49
94%)9. These workers also identified other risk
factors i.e. low gestational age (p <0.991),
cesarean delivery (p=0.017) and IVF
conception
(p=0.008).
Thus,
genetic
predisposition and gender are significant
factors associated with AOP.
A trial of 103 preterm infants weighing
between 500 and 1300 Grams who were
allocated either a liberal blood transfusion
policy (transfusion if hematocrit (Hct) < 46%
in mechanically ventilated infants or Hct<
38% for infants receiving continuous positive
airway pressure (CPAP) or supplemental
oxygen and Hct< 30% for not requiring
respiratory therapy) or a restrictive blood
transfusion policy (transfusion for Hct< 34% in
mechanically ventilated infants, Hct < 28%
for infants on CPAP or supplemental oxygen
and Hct < 22% for infants not requiring
respiratory therapy. Infants in the restrictive
group had more frequent episodes of
apnea (median 0.84 vs. 0.43 episodes/day,
p = 0.004) and more grade 4 intraventricular
hemorrhage or periventricular leukomalacia (12% vs. 0%, p=0.012, Number to Harm
{NNH} 8)10. Making anaemia a significant
causative factor for AOP.

A condition that is also common in very preterm

infants; gastro-oesophgeal reflux (GER) is
frequently thought to be either the cause or is
associated with AOP. However, an observational
study of 119 preterm infants monitored for 12
hours
using
respiratory
inductance
plethysmography, heart rate, oxygen saturation
and esophageal pH studies failed to show any
causal relationship between GER and AOP11. In
another study 19 preterm infants were monitored
for apnea and GER for 26 hour sessions during
2,039 episodes of apnea. Frequency of apnea
occurring within 20 seconds of GER was not
significantly different from apnea occurring
without GER12.

www.ppa.org.pk

weeks of gestation should be monitored for

apneic spells. As the diagnosis of AOP is a
diagnosis of exclusion clinicians often resort to
perform investigations to rule out associated
causes of apnea alluded to earlier by estimating
blood gases, urea and electrolytes, sugar,
calcium, hematocrit and often perform a sepsis
screen. Whilst these tests appear to be necessary,
their yield in AOP is poor.
Clinicians also perform a number of tests that are
specifically designed to diagnose GER e.g.
transthoracic impedance pneumography, nasal
thermistor, ultrasound whilst baby is being fed
etc. All these tests have significant drawbacks as
their sensitivity and specificity is poor.

Gastric and esophegial pH studies are

considered to be the gold standard for the
diagnosis of GER. Since infants receive frequent
milk-based feedings, which continually buffer
stomach acid, measured pH may be neutral or
even alkaline in some cases. Therefore,
esophageal pH may significantly underestimate
episodes of reflux in premature infants and not
identify AOP events resulting from nonacid reflux.
Multichannel intraluminal impedance technology
has been used toprovide a more comprehensive
measure of reflux. In conjunction with pH
measurement,
multichannel
intraluminal
impedance can increase the sensitivity of reflux
detection and the identification of both acid and
nonacid reflux13. But despite improved detection
no association has been found between gastrooesophageal reflux and AOP. As a result, there is
no scientific evidence to support the use of antireflux medications for thetreatment of AOP13.
Treatment: Whilst it is not clear if AOP causes a

clinically important effect on outcome or in itself

is harmful, providing no treatment when an infant
stops breathing is not an option. The immediate
and irresistible urge to respond to apnea is based
partly on the uncertainty about exactly what
causes the apneic episode and whether AOP
may harm the brain or other organs/systems or
produce a long-term effect on neurodevelopment14.
Although caregivers are able to respond
successfully to apnea events with either drugs or

121

Apnea of Prematurity, Management Guidelines

physical and mechanical interventions, it remains

un-proven, which of the interventions offer most
benefits.
Management strategies for AOP are based on
any or combination of the following;
a)
b)
c)
d)
e)
f)

Emergency Treatment
Positioning
Physical or Kinesthetic stimulation
Respiratory support
Medication
Carnatine supplementation

Emergency Treatment

1.

3.
4.
5.
6.

Position the neck in slightly extended

position.
2. Suck the oropharynx gently if required
(avoid vigorous suctioning).
Tactile stimulation for 1-2 seconds.
Oxygen by funnel, nasal cannula to
maintain oxygen saturations between 87
and 93%, or till the baby starts to breath.
If the infant remains apneic start bag and
mask ventilation.
If bag and mask fail then consider
ventilation.

Prone positioning can improve

thoraco-abdominal synchrony and stabilize the
chest wall without affecting breathing pattern or
SpO215. Several studies have demonstrated that
prone position reduces AOP16.
Positioning:

Though extension of the neck 15 from the prone

position (referred to as the head elevated tilt
position), had been found to decrease episodes
of oxygen desaturation by 48.5% and a more
comfortable three-stair-position (that maintains
the head and abdomen in a horizontal position
had
reported
improvement
in
apnea,
bradycardia, and desaturation17. However,
recent cross over trial using these positions was
unable to show any significant difference in
combined event rate of bradycardia or oxygen
desaturations18. Equally, head elevated tilt
position or the three-stair-position with concurrent
aminophylline therapy also did not show any
reduction
in
rates
of
bradycardia
or
desaturations.
However, we think that the head elevated tilt
position and three-stair-position are easy to
provide and may be helpful without any side
effects, they should be considered as a first-line

intervention in infants with AOP particularly in

resource limited situations.
and or Kinesthetic stimulation: Simple
interventions like physical or olfactory stimulation,
oscillating water or air mattresses are often used
and they most likely work by generating
excitatory, nonspecific neuronal activity in the
brainstem center to stimulate respiratory
activity19. However, Cochrane systematic review
has suggested that there is insufficient evidence
to recommend kinesthetic stimulation to reduce
episodes of clinical apnea20.
Physical

Kangaroo care: Though recommended by some21

kangaroo care for treatment of AOP still requires

further study.
Other measures
CO2 Inhalation: Recently, a randomized controlled

trial22 of theophylline versus CO2 inhalation for

treating AOP suggested that inhalation of a low
CO2 concentration (0.8%) in premature infants
was as effective as theophylline therapy in
decreasing apnea. Long-term effects of exposure
to CO2 are not known and its use should be
considered experimental at this stage.
Feeding tube placement: Upper airway resistance
plays asignificant role in causation of AOP.
Nasogastric tubes have been documented to
increase nasal airway resistance by 50%.
Therefore, oro-gastric
feeding tubes are
sometimes preferred in premature infants with
apneic events. However, a recent randomized
controlled trial showed that the placement of
nasal feeding tube had no significant effect on
AOP23.
Temperature control: In a recent study,less apnea
was found at an incubator temperature of 30.4C
than at 32.5C 24. However, no specific
environmental temperature to reduce the
incidence or severity of AOP is known. More
research is required.
Red Cell Transfusion: As eluded to earlier, a
randomized trial10 comparing a liberal versus
restrictive transfusion policies in premature infants
found that infants had more frequent apnea in
the restrictive transfusion group. However, a
retrospective study on the risks and benefits of
transfusions in extremely low birth weight preterm
infants found that frequent red blood cell
transfusions was associated with increased risk of

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122
bronchopulmonarydysplasia
and necrotizing
enterocolitis25,26. Based on these data, there is
insufficient evidence to recommend routine red
cell transfusion to treat AOP.
Respiratory Support: Respiratory support to reduced
work of breathing is thought to be beneficial in
the management of AOP. This can be achieved
by providing oxygen and distending pressure via
either synchronized NIPPV or variable flow nasal
continuous positive airways pressure (nCPAP)
devices. In an earlier publication we have shown
how to make and deliver bubble nCPAP cheaply
using
commonly
available
equipment27.
Cochrane systematic review of randomized or
quasi-randomized
trials
comparing
nasal
intermittent positive pressure ventilation (NIPPV)
vs. nCPAP for apnea showed that NIPPV may
reduce apnea frequency more than nCPAP but
that there was insufficient evidence to
recommend NIPPV as standard therapy for
AOP28. There was some suggestion that NIPPV or
nCPAP using variable flow ventilator was more
effective than conventional ventilator, but a
recent study29 found no significant difference in
event rate between the NIPPV/conventional
ventilator and bubble nCPAP. Therefore if
required bubble nCPAP should be the preferred
respiratory support. However, if ventilation is
required it should be as gentle as possible e.g.
peak pressures of 10-12 cm of water, end
expiratory pressure of 3-5 cm of water with a rate
of 20-25/minute with an inspiratory time of 0.350.40 seconds and inspired oxygen between 30 to
50%.

Methylxanthines such as caffeine,

theophylline, and aminophylline have been used
to treat or prevent AOP30. Whilst methylxanthines
are powerful central nervous system stimulants
they are likely to reduce apnea by multiple
physiological and pharmacological mechanisms.
They are non-selective antagonists of adenosine
receptors
that
improve
diaphragmatic
contraction and respiratory muscle function,
increase minute ventilation, CO2 sensitivity, and
respiratory drivewhile decreasing the hypoxic
depression of breathing31.
Medicines:

Systematic reviews of methylxanthine therapy in

AOP clearly demonstrate that both caffeine and
theophylline are equally effective inreducing
apnea. Caffeine however is safer and has a
wider therapeutic range and longer half-life (100

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Haque KN, Quddusi A

hours vs. 30 hours) thantheophylline32. Studies on

long-term safety and efficacy ofmethylxanthine
therapy for the treatment for AOP have shown
that
caffeine
reduced
the
rate
of
bronchopulmonary
dysplasia
and
neurodevelopmental disabilities33.
Caffeine: Caffeine the drug of choice is
commercially available in most western countries
as caffeine citrate. In the largest randomized
clinical trial34 to date involving 2,006 infants from
five countries who were less than 10 days old and
weighed between 500 and 1,250 Grams
compared caffeine vs. normal saline. This
randomized clinical trial (RCT) was an intention to
prevent or treat apnea or facilitate extubation
trial. Caffeine citrate was given as 20 mg/kg
intravenously as a loading dose followed 5
mg/kg/day intravenously or orally. The dose of
caffeine was increased up to 10 mg/kg/day if
apnea persisted. The dose of caffeine was
adjusted weekly according to weight of the
infant. Caffeine was discontinued either at the
discretion of the treating clinician or after five
consecutive days without use of positive airway
pressure or there were signs/symptoms of
caffeine toxicity (seen in 2.3%). Caffeine reduced
rates of broncopulmonary dysplasia (6.3% vs.
46.9%, p <0.001, number to treat {NNT} 10) bot not
mortality. Caffeine therapies also seem to reduce
the need to treat patent ductus arteriosus (29.6%
vs. 38.2%, p=<0.001, NNT 12) and there was no
significant difference in the incidence of
necrotizing enterocolitis.

Number of studies have reported beneficial

results using varying dosage regimens (loading
from 10 to 40 mg/kg and maintenance from 2.5
mg/kg/day to 5 mg/kg/day)35, 36.The high-dose
groups in all the studies showed significant
reductions in AOP, extubation failure and apnea
after extubation. Thus, it would seem that a
higher dose of caffeine appears to be more
effective in preventing AOP. However, Hoecker
et al37 found that loading doses of 25 mg/kg or
more of caffeine citrate reduced blood flow
velocity in cerebral arteries of premature infants
by about 20%, whereasa loading dose of 10
mg/kg of caffeine also resulted in reduction of
cerebral blood flow velocity but it recovered
within four hours38. Thus, caffeine at a loading
dose of 10 - 20 mgkgfollowed by 5 - 8 mgkgday
maintenance may be adequate and only if AOP

Apnea of Prematurity, Management Guidelines

persists a higher dose should be considered.

There is evidence that caffeine used in these
doses reduces the incidence of incidence of
neurodevelopmental disability (p = 0.008, NNT 17)
and cerebral palsy 4.4% vs. 7.3% (p = 0.009, NNT
35)3. Based on observational studies it appears
that monitoring of therapeutic levels may not be
necessary39, making caffeine therapy highly cost
effective40.
Thus it behooves neonatologists practicing in
resource-limited countries to seek availability of
caffeine citrate for use in AOP.
Methylxanthines: Aminophylline and Theophylline

are readily available and isused. Recommended

loading dose is 56 mg/kg, followedby
maintenance doses of 26 mg/kg/day divided
into two or three daily doses. Aminophylline differs
from theophylline only by the addition of
ethylenediamine to its structure and may differ in
amount of molecules of water of hydration
according to individual manufacturer. 100 mg of
aminophylline (hydrous) contains approximately
79 mg of theophylline (anhydrous) and 100 mg of
aminophylline
(anhydrous)
contains
approximately 86 mg theophylline (anhydrous).
Conversely, 100 mg of theophylline (anhydrous) is
equivalent to 116 mg of aminophylline
(anhydrous) and 127 mg aminophylline (hydrous).
Methylxanthines do not appear to be less
efficacious in treating AOP than caffeine citrate
but caffeine has a much better safety profile41.
Toxic levels of methylxanthines may produce
tachycardia, cardiac dysrhythmias,and feeding
intolerance or, at high doses, may precipitate
seizures thus they frequently require serum levels
to be estimated. Mild diuresis and delayed
gastricemptying has also been observed.
Methylxanthines
also
increase
energy
expenditure, possibly leading to reduced growth
rates in premature infants, suggesting extra
caloric requirement may be necessary in
infantstreated with theophylline42, 43.

Cochrane systematic review suggests that there

is limited evidence of theophylline being more
effective than nCPAP or kinesthetic stimulation in
treating AOP20, 44.
There is no consensus on how long either caffeine
or methylxanthine therapy should be continued.
As long-term therapy with either of the two drugs
is associated with poor growth, therapy should be

123

given for shortest possible period. Personal

practice has been to stop the therapy after 10 to
12 full apnea free days or when the corrected
gestation reaches 34 weeks.
Doxapram: Doxapram is a potent respiratory
stimulant used for management of apnea45. It
may have similar efficacy to methylxanthines in
the short term but46 its use is controversial due to
its reported adverse effects i.e. increase in
cerebral oxygen consumption and decrease in
oxygen delivery secondary to decreased
cerebral blood flow47. Therefore, doxapram is not
routinely recommended for AOP. However, a
study has suggested that addition of Doxapram
in low dose to methylxanthines may reduce
mortality and frequency of AOP48 but this needs
to be studied further.
Other Drugs: Clinicians often use off-label drugs
that have been approved for gastro-esophageal
reflux disease (a common condition in premature
infants) with the belief that such treatments may
also have an impact on AOP, although this link
has never been demonstrated. A number of
studies using cisapride, rinatidine, domperidone
or metoclopramide have all shown thattheir use
individually or in combination does not affect
either the frequency or severity of AOP49, 50.

Carnitine51 or oral cretinesupplementation52 have

been tried in small-randomized trial but neither
has been found to be beneficial in AOP.
Prevention: Prophylactic use of either caffeine or
methylxanthies or carnitine does not reduce the
risk
of
AOP
but
prophylactic
use
of
caffeine/methylxanthine reduces the duration of
ventilation in very low birth weight babies53
hence current evidence does support their use
for preterm infants who are ventilated and at risk
of apnea.
Prognosis: The long-term consequences of AOP

are difficult to determine due to co-morbidities in

the preterm infants. A number of studies have
found that a higher frequency and severity of
AOP is associated with a higher incidence of
neurodevelopmental
impairment
such
as
cerebral palsy and blindness at 3 years of age54, 55
but this aspect of AOP remains controversial.
As a whole, the lower the gestational age, the
more likely is AOP and it may last for a longer
period. In most infants AOP disappears by 36 to

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124

Haque KN, Quddusi A

40 weeks post-conceptional age. However,

infants born between 24 28 gestational weeks

may continue to have AOP beyond 38 to40

weeks post-conceptional age56.

Recommended Guidelines for Management of AOP in Resource Limited Situations

Neonate with Apnea
Emergency Treatment (Airway, Breathing, Circulation)
Maintain Temperature

Investigations: Blood Sugar, Ca,

Urea, Electrolytes, CBC
Others if required

Evaluate to exclude other causes of Apnea:

Seizures, Hypoxemia,
Sepsis, Anemia, GER, Other

Diagnosis: AOP
Position: Head elevated tilt position and three-stair-position

ApneaResponds

No Response
Start Theophylline/Aminophylline:
Loading dose 5 -6 mg/kg
Maintenance: 2 4 mg/kg/day in 2 or 3
divided doses

No Response

Start nCPAP/NIPPV 4-6 cm of water.

Apnea Responds:
Stop medication after 10-12 days of continuous
apnea free period or at corrected gestational
age of 35 weeks.

No response:

Initiate mechanical ventilation

1.
2.

Some clinicians give prophylactic Caffeine or Methyxanthine to babies born at or before 29 weeks of
gestation (level of evidence is poor).
24 hours prior to extubation from a ventilator caffeine or methylxanthine should be started to prevent postventilation spells of apnea (level of evidence is good)

Follow-up: Home monitoring is often used where

services are well developed and financed. In

resource limited countries this facility is usually not
available but will be briefly discussed for

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completion of a review of the subject. Where

resources are limited, parents should be
educated about signs and symptoms of apnea,
given instructions on resuscitation, preferably in

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Apnea of Prematurity, Management Guidelines

the form of well illustrated document.

Home monitoring may be required for infants at
high risk of recurrent apnea, bradycardia and
hypoxemia after hospital discharge. It should be
discontinued in any case by 43 weeks of postconceptional age unless the infant is dependent
on respiratory support. Home monitoring should
not be prescribed to prevent sudden infant
death syndrome.If home monitoring is provided
the monitor should be equipped with an event
recorder and parents or caregivers should be
trained in its use and cardio-pulmonary
resuscitation.

7.

St-Hilaire M, Samson N, Duvareille C, et al.

Laryngeal stimulation by an acid solution in
the pre-term lamb. Adv Exp Med Biol 2008;
605:15458.

8.

Abu-Shaweesh JM, Martin RJ. Neonatal

Apnea: Whats new. Pediatr Pulmonol. 2008;
43(10): 937-44.

9.

Bloch-Salisbury E, Hall MH, Sharma P, et al.

Heritability of apnea of prematurity: a
retrospective twin study. Pediatrics 2010;
126(4): 779-87.

10.

Bell EF, Strauss RG, Widness JA et al.

Randomized trial of liberal versus restrictive
guidelines for red blood cell transfusion in
preterm infants. Pediatrics 2005; 115(6):
1685-91.

11.

Di Fiore JM, Arko M, Whitehouse M, et al.

Apnea is not prolonged by acid
gastroesophageal reflux in preterm infants.
Pediatrics 2005; 116(5):1059-63.

12.

Peter CS, Sprodowski N, Bohnhorst B, et al.

Gastroesophageal reflux and apnea of
prematurity: no temporal relationship.
Pediatrics 2002; 109(1): 8-11.

13.

Corvaglia L, Mariani E, Aceti A et al.

Combined oesophageal impedance-pH
monitoring in preterm newborn: comparison
of two options for layout analysis.
Neurogastroenterol Motil 2009; 21(10): 1027
81.

--------------------------------------------------------------Authors affiliations
Prof. Khalid N. Haque
Department of Neonatal Medicine, 276, Club Drive,
San Carlos, California 94070, USA
Ahmed Quddusi
Department of Neonatology, Childrens Hospital &
Institute of Child Health, Abdali Road, Multan, Pakistan

REFERENCES
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the appearance of apnea of prematurity.
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Stokowski LA. A Primer on Apnea of

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Haque KN, Quddusi A

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intermittent positive pressure ventilation
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3): 2023.

22.

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Mueni E, Opiyo N, English M. Caffeine for

the management of apnea in preterm
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M. Oral versus nasal route for placing
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Caffeine for Apnea of Prematurity Trial
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35.

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dose caffeine citrate for extubation of
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trial. Arch Dis Child Fetal Neonatal Ed 2004;
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transfusion in anemic infants with apnea of
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Apnea of Prematurity, Management Guidelines

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Tracy MB, Klimek J, Hinder M et al. Does

caffeine impair cerebral oxygenation and
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neonates:
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Yamazaki T, Kajiwara M, Itahashi K, et al.

Low-dose doxapram therapy for idiopathic
apnea of prematurity. Pediatr Int 2001;
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Kimball AL, Carlton DP. Gastroesophageal

reflux medications in the treatment of
apnea in premature infants. J Pediatr 2001;
138(3): 355-60.

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Wheatley E, Kennedy KA. Cross-Over Trial of

Treatment for Bradycardia Attributed to
Gastroesophageal Reflux in Preterm Infants.
J Pediatr 2009; 155(4): 516-21.

51.

Kumar M, Kabra NS, Paes B. Carnitine

supplementation for preterm infants with
recurrent apnoea. Cochrane Database Syst
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52.

Bohnhorst B, Geuting T, Peter CS, et al.

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supplementation (not effective) for apnea
of prematurity. Pediatrics 2004; 113(4): 30307.

53.

Henderson-Smart DJ, De Paoli AG.

Prophylactic methylxanthine for prevention
of apnoea in preterm infants. Cochrane
Database Syst Rev 2010; (12): CD000432.

54.

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is associated with neurodevelopmental
impairment in very low birth weight infants. J
Perinatol 2004; 24(12): 76368.

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Pillekamp F, Hermann C, Keller T et al.

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of
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91(3): 15561.

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Ducrocq S, Biran-Mucignat V, Boelle PY. et

al (2006) Apnea of prematurity: risk factors
and ambulatory treatment with caffeine
citrate. Arch Pediatr; 13(10): 12991304.

Dukhovny D, Lorch SA, Schmidt B, et al.

Caffeine for Apnea of Prematurity Trial
GroupPediatrics. Economic evaluation of
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Pediatrics 2010; 127(1): 146-55.

41.

Henderson-Smart DJ, Steer PA. Caffeine

versus theophylline for apnea in preterm
infants. Cochrane Database Syst Rev2010;
20 (1): 2010: CD000273.

42.

Adn U. Methylxanthines during pregnancy

and early postnatal life. Handb Exp
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methylxanthines on periodic respiration and
acid gastroesophageal reflux in newborn
infants. Monatsschr Kinderheilkd 1990;
138(3): 12327.

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PG. Continuous positive airway pressure
versus theophylline for apnea in preterm
infants. Cochrane Database Syst Rev 2001;
(4): CD001072.

45.

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treatment for apnea in preterm infants.
Cochrane Database Syst Rev 2004; 18(4):
CD000074.

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versus methylxanthine for apnea in preterm
infants. Cochrane Database Syst Rev 2000;
(2): CD000074.

47.

Yost CS. A new look at the respiratory

stimulant doxapram. CNS Drug Rev 2006;

12(34): 23649.

www.ppa.org.pk

ORIGINAL ARTICLE

Oral Hygiene and Dietary Habits among Primary School

Children, in Urban Karachi
MARIUM IQBAL, IBRAHIM SHAKOOR, MOHSINA NOOR IBRAHIM, Laeeq-uz Zaman

---------------------------------------------------------------Pak Paed J 2011;35(3): 128-34

ABSTRACT

Objective: To measure the occurrence of oral hygiene habits and

dietary practices in 6 - 12 years old children, to set a bench mark for
later studies on similar groups.
Authors affiliations

Study Type: Cross sectional study.

-------------------------------------------

Subjects, Materials and Methods: The data was collected through self
responding questionnaires sent to the parents of primary school
children from urban Karachi. We received 610 appropriately filled
forms. Inclusion criteria were student age and parental consent to
provide information. There were no exclusion criteria, except to
exclude grossly incomplete forms.

Correspondence to:Marium Iqbal,

Operative Dentistry, Jinnah
Medical and Dental College
# 22, 23, Shaheed-e-Millat
Road, Karachi, Pakistan.
E-mail:
mariumdeens@hotmail.com

Results: We observed a comparable mix of practice patterns as we

match up the results with similar national and international studies.
There were no discrete extremes of prevalence, either of poor or of
good habits and/or practices.
Conclusion: We concluded that in such a diversity of practices,
particularly at a crucial stage of life (being transition to permanent
dentition and habit formation), school children could substantially
benefit from interventions like prevention programs.
Key Words: Oral hygiene habits, dietary practices, primary school, risk
factors, children, Karachi, Pakistan.
Future opportunities: We look forward to researchers using this data to
put up more detailed studies to explore the impact of interventions
directed at preventive programs.

INTRODUCTION
The role of poor dietary, hygienic, and social
habits is known and established for their
individual and cumulative effects on caries
predisposition and etiology1. Based on this
ground, we set out to learn the prevalence of
these habits in primary school children.
There is ample of research evidence that favors
the correlation between the triad of chronic
dental problems (like caries), oral hygiene
habits and dietary practices2. They have also
favored mass awareness through health
services professionals3.

www.ppa.org.pk

Unfortunately, it is often observed that the

prevalence of caries has not declined enough
in the less developed parts of the world as
much as it has in the developed world. This has
economic, social, and overall health status
explanations at its back, but more sadly, it also
has health status, social and economic
implications, explaining the vicious circle4.
It can therefore be concluded that the
measurement and change of childs health
and nutrition habits and practices, can directly
contribute to impact analysis of such
interventions as prevention programs, as well as
help strategize these programs.

Oral Hygiene and Dietary Habits among Primary School Children, in Urban Karachi

Literature search showed a dearth of research

evidence
on
prevalence
of
the
aforementioned practices at national or local
level5-6. We therefore designed this survey, to be
conducted in various primary schools in
Karachi.

SUBJECTS AND METHODS

This is a cross sectional study, where data was
collected
through
self
responding
questionnaires given out to the parents of the
study subjects - primary school children,
operationally sent and collected by the school
administration of the selected private schools
from urban Karachi. Letters of invitation were
sent to various schools of the city and four
schools were randomly selected from those
who agreed to participate. More than 700
questionnaires were sent out (in excess of the
required number) Out of the received forms,
610 were found up to the standards for data
entry and analysis. Student inclusion criteria
were student age and parental consent to
provide information. There were no discrete
exclusion criteria, however grossly incomplete
forms were excluded from data entry and
subsequent exercise. In more than 30 questions
we
collected
demographic
data
and
information on 11 practices and habits.
The practices questions were identified by
reviewing the pertinent literature and in
consideration of the authors experience,
contributed mostly by the first author. The
selection of included questions was also in
consideration of our local social and cultural
context.

RESULTS
The study was conducted in Karachi, the
economic hub of the country, and it is therefore
not representative of the complete national
status (rural and urban). We believe however,
that it may well represent the larger cities of
Pakistan. This may also represent a tilt towards
the higher socio-economic stratum of the
society.
Demographic Profile
Age: The mean age of our studied group was
6.79 years, with a SD of 1.61 years (n=596; 14
missing)

129

Distribution: Total 610: Males 51.5%

(n=314); females 47.2% (n=288); missing 1.3%
(n=08).

Gender

Mothers domestic status: Total 610: Working

mothers 8.4% (n=51); House wives 91.1% (n=556);
missing 0.5% (n=03)

Practices and habits

Tooth Brushing: We found that 51.0% (n=311) of
the studied children brushed their teeth once or
less daily; 46.7% (n=285) brushed twice or more
daily; while the missing (or un-comprehendible)
answers were 2.3% (n=14). The data also
showed details of brushing patterns as shown in
Table 01. In the sequence of frequency, the
largest number 45.2% (n=276) brushed before
breakfast only; and 33.8% (n=206) brushed
before breakfast and before bed. The other
patterns, some very interesting, are detailed in
the table. Overall, brushing was supervised in
58.0% (n=354), and unsupervised in 38.5%
(n=235); while no answer was given by 3.4%
(n=21).
Dentifrice Use: Toothpastes were used by 98.9%
(n=603), and not used by 0.5% (n=03), while
0.7% (n=04) did not answer.
Dental flossing: Most of the respondents were not
flossing their teeth 73.8% (n=450); those flossing
were 13.8% (n=84); and 12.5% (n=76) did not
answer. When asked for how often do they
floss, the answers were: With every tooth
brushing 4.4% (n=27); most of the times 5.4%
(n=33); sometimes or almost never 29.7%
(n=181); and 60.5% (n=369) did not answer.
Milk consumption: 86.9% (n=530) consumed milk,
while 12.1% (n=74) did not consume milk; and
1% (n=06) did not answer. Milk was consumed in
one go by 67.0% (n=409); distributed over a day
by 21.1% (n=129); while no answer was given by
11.1% (n=68). Also 34.6% (n=211) consumed
unsweetened milk; 59.5% (n=363) sweetened;
and No answer was given by 5.9% (n=36).
Feeder bottle use: We found that amongst these

primary school children a mug or cup was used

by 93.9% (n=573); bottle or feeder by 03.8%
(n=23); Sippy cup or trainer mug by 00.8%
(n=05); and no answer was given by 01.5%
(n=09). When asked for use of feeder while
sleeping, they replied with no 93.4% (n=570); yes
2.5% (n=15); or did not answer 4.1% (n=25).

Sweets and candies: When asked about the use

of chocolates / sticky candies / toffees, etc.
22.5% (n=137) marked for once or more almost

www.ppa.org.pk

130
everyday; 71.6% (n=437) marked for sometimes
or rarely; and 5.9% (n=36) did not answer. 56.4%
(n=344) of our studied children eating
chocolates and sweets after meals; 29% (n=181)
during or ahead of meals; and 10.7% (n=65) did
not answer.
Sticky foods: When inquired, the response
towards their consumption was: once or less
than once a day 80.7% (n=492); twice or more
daily 17.9% (n=109); and no answers by 1.5%
(n=09).
Cheese: We found that cheese consumption

was positive in 21.1% (n=129); negative in 75.1%

(n=458); and the question was not answered by
3.8% (n=23).
Salads / fresh fruits / fresh vegetables: We were

exploring the use of salads / fresh fruits / and

fresh vegetables for their favorable mechanical
cleansing effects and also for their nutritional
value of minerals and various vitamins. We
learned that 69.3% (n=423) consumed salad or
fresh vegetables; 27.4% (n=167) did not
consume them; and 3.3% (n=20) did not
answer. When asked specifically whether the
child regularly consumes apple (defined as an
apple every one or two days), the responses
were positive for 60.7% (n=370); negative for
37.0% (n=226); and no answer was given by
2.3% (n=14).
Drinks: We asked for three types of drinks these
children would most usually consume: Soft
(aerated) drinks; packed (not necessarily fruit)
juices; and fresh fruit juices. We found that
regular consumption was highest for packed
juices 13.9% (n=85) and lowest for soft drinks
6.1% (n=37), while only 2.8% (n=17) or less did
not answer these questions. Further details are
in Table 02.
Dental Visits: When inquired about the frequency

of dental visits, 10.2% (n=62) visited the dentist

once or twice a year; 85.1% (n=519) visited per
need; and 4.8% (n=29) did not answer.
Consumption of beetle leaves / beetle nut: We

found that 90.3% (n=551) did not consume

them; 5.6% (n=34) consumed them; and 4.1%
(n=25) did not answer. We also found that
family members (parents, grand parents, aunts
or uncles) were also consuming the same in
36.9% (n=225); 58.2% (n=355) were not
consuming; and 4.9% (n=30) did not answer.

www.ppa.org.pk

Iqbal M, Shakoor I, Ibrahim MN, Zaman LU

TABLE 1: Tooth brushing patterns in the studies

children
Brushing time
Before breakfast
After breakfast
Before bed at night
After every meal
Before breakfast and after
breakfast
Before breakfast and
before bed
After breakfast and
before bed
Before bed and after
every meal
Before breakfast, before
bed and after every meal
Total
No Answer
Total

Percentage

Number

45.2
03.1
09.3
02.6
00.3

276
19
57
16
2

33.8

206

03.0

18

00.7

00.3

98.4
01.6

600
10

100.0

610

TABLE 2: Frequency and use of various drinks by the

children
Frequency

Soft
Drinks
6.1%
(n=37)

Packed
Juice
13.9%
(n=85)

Fresh
Juice
11.5%
(n=70)

Less than once

a day

91.1%
(n=556)

84.6%
(n=516)

86.2%
(n=526)

No Answer

2.8%
(n=17)

1.5%
(n=09)

2.3%
(n=14)

Almost
once
everyday
or
more

DISCUSSION
Prof. WD Millers published scientific work in 1891
provided scientific grounds to the theories of
Milles proposed in 1881, which state the role of
acids in decaying and thereby weakening the
protective structure of the teeth. The more
contemporary versions of these theories is
based not only on the diet, the tooth
susceptibility, and time, but also upon
frequency and duration of exposure to
cariogenic nutrients, the individual immunity,
and the use of fluorides. Factors like socioeconomic stratum of the individual, the level of
education and lifestyle behaviors are also
indicted1,2. However, it can perhaps be argued
equally strongly that most of them are
eventually secondary contributors to the
original sinners, the sugar and the microbes.

Oral Hygiene and Dietary Habits among Primary School Children, in Urban Karachi

A study conducted in Pakistan Institute of

Medical Sciences (PIMS), Pakistan, on children
between 6 and 9 years of age, showed similar
findings5. Another study conducted as a nation
wide survey of children aged 12, made
comparative assessments with a similar survey
conducted earlier. The findings of this survey
showed an overall improvement but a mean
(Decayed, Missing, Filled Teeth (DMFT) of 0.9.
While the rate of caries decreased substantially,
there rate of untreated caries remained at an
alarming 90%6. Apart from these two studies, we
could not find much research evidence to
document dental caries factors in the primary
school children in Pakistan.
Demographic Parameters
Mothers domestic status: We could not find this
parameter in the studies we reviewed. This
could be a likely contributor to supervision of
favorable practices and forbidding the bad
practices. We assume that all the non-working
mothers are available at home to the children
after school. It must however not be interpreted
in social isolation, since families with the working
mothers may still have childrens attendants or
other family arrangements (as is not uncommon
in this part of the world). Also, non working
mothers should not be confused with uneducated mothers, for an educated mother
may choose to be non-working. We found that
8.4% of our studied mothers were working (part
time or full time), and 91.1% were house wives.
Only 03 questionnaires were received with no
answer to the question.

Oral hygiene practices

Tooth brushing and Flossing: The habit of tooth

brushing is acquired in early childhood,

preferably the toddler stage. However, to try
establishing it in early school years is better than
giving up on it. The role of tooth brushing
against the commonest caries is unquestionably
established. Outcomes of a study conducted
by Gibson and Williams on pre-school children
aged 1.5 to 4.5 years are very interesting,
establishing an apparently greater role of tooth
brushing than dietary restrictions7. Although
these were the pre-primary school children, it
gives a reason to think the same for mixed
dentition stage. We found that 51.0% (n=311) of
our studies children brushed their teeth once or
less daily; and 46.7% (n=285) brushed their teeth
twice or more daily. A Scottish interventional
study on young children at the early stage of
permanent dentition eruption showed that

131

twice daily brushing controlled caries in first

permanent molars better than did once daily
brushing. More importantly however, this study
related the significance of outcomes to
parents beliefs8. If the parents are also
sympathetically (not compulsively) involved in
supervising their childrens tooth brushing, the
outcomes are essentially known to yield better
outcomes. Another study on Scottish children
(who have the highest prevalence of caries
throughout Europe) endorsed the positive role
of supervised brushing with fluoridated
toothpaste9. In our observations, brushing was
supervised in 58.0% (n=354), and unsupervised
in 38.5% (n=235) children. An intervention study
conducted in London over school going
children in various ages showed lesser caries
incidence in children submitted to teachersupervised tooth brushing with 1450 ppm
fluoride toothpaste. When compared to the
controls, the difference in the results was
statistically significant and in favor of the
intervention group10. This is unlike our schools
setting which has virtually no school health
program.
Scientific literature published as recently as 2003
in a Swedish study, established statistical
grounds for at least three findings: Firstly, the
role of fluoridated toothpastes (compared with
placebo) in young permanent dentition;
secondly the quantity of fluoride being 1500
ppm to be superior to (the more usual) 1000
ppm available in the toothpastes when used for
young permanent dentition; and thirdly the
positive role of supervised brushing as
compared to unsupervised. These establish a
prominent role of high fluoride toothpastes and
regular-supervised tooth brushing in children at
the time of early permanent dentition11.
Researchers have stated that children who
brush their teeth independently [unsupervised]
experienced more caries as compared to those
who were supervised by their mothers12-13.
Waerhaug in his study showed the positive role
of flossing by way of physically removing the
inter-proximal plaque from between the teeth
and therefore a reduced risk of inter-proximal
caries14.
A systemic review of six studies, with a total
subject population of 808 patients, and age
range from 4 to 13 years, showed that even
amongst the children with low fluoride
exposures, a regular professional flossing (on
school days) for 1.7 years, reduced the risk of
dental caries by 40%, unlike two other studies

www.ppa.org.pk

132
with three monthly professional flossing for 3
years, and self performed flossing for two years,
did not reduce the risk of caries. However, the
former study was conducted on primary
dentition, while the latter were conducted on
teeth of young adolescents15. Most of our
respondents were not flossing 73.8% (n=450);
leaving only those flossing 13.8% (n=84); and
12.5% (n=76) not answering. This underscores
the need for education in dental practices.
Use of Tooth paste: Researchers have found a

significant role of daily use of fluoride

toothpaste for caries prevention in children,
when compared with placebo controls.
Supervised
brushing,
particularly
when
conducted twice daily and complemented
with 1500 ppm fluoride, accentuated the
caries prevention effects. These finding are
broadly congruent to the earlier stated Swedish
study which showed similar results. This study did
not recommend the age of practice
commencement. However, an interesting
observation was that the use of high
concentration fluoride (adult toothpaste)
induced a higher risk of fluorosis in low-caries
prevalence communities, but not in socially
deprived, high-caries communities11. The use of
adult dentifrices (with higher fluoride content,
compared to pediatric dentifrices) may
therefore be arguable in socially disprivileged
communities. Another review conducted in
Manchester, found similar evidence for higher
fluoride concentrations, particularly above 1000
ppm16. We found that 98.9% (n=603) children
used toothpastes and 0.5% (n=03) did not. The
high rate of toothpaste use may be attributable
to toothpaste advertisements on television and
billboard media. A study over practice patterns
of Board-Certified Pediatric Dentists, in USA,
provided evidence on the positive contribution
of fluoridated toothpastes, flossing, and proper
brushing7.
Dietary Habits
Sweets, sticky sugars and snacks: Diets low in

sugars (and fermentable carbohydrates), but

high in calcium may be more favorable to the
re-mineralization / demineralization balance.
The over all incidence of caries is a sum total of
chemo-parasitic insults and protective factors1718. Apart from individual predisposition, the
determinants of caries susceptibility are factors
like quantity, frequency, oral retention, nutrient
composition, salivary stimulation, and the foods
combination19-20. Chocolates, sticky candies

www.ppa.org.pk

Iqbal M, Shakoor I, Ibrahim MN, Zaman LU

and toffees, all have a high retention time on

the tooth surface. 22.5% (n=137) of our studies
children used them once or more often, every
day; 71.6% (n=437) consumed them sometimes
or rarely; and 5.9% (n=36) did not answer.
A comparable study conducted in Maglore,
Bharat, on 5-13 years old children, provided
evidence to the correlation between sugar
intake and caries21.
Evidence suggests that a daily dietary extrinsic
sugar intake per person exceeding 30 gram for
pre-school and early childhood years and 60
grams for teenagers and adults, is directly
related with increased risk of dental caries22.
Other than pure sweets, sticky foods like chips,
biscuits and other packed snacks could also
prove to be deleterious. 80.7% (n=492) of our
studied children consumed them once or less
often each day and 17.9% (n=109), twice or
more daily.
A study by Mustahsen-ur-Rehman and
colleagues on 11-14 years-olds in Sharjah
showed that the prevalence of caries was
higher, 79.01%, in those who consumed sugary
snacks between meals, compared to its
presence, 59.3%, in those who had sugary
snacks during [as part of the] meals23. We found
our studied children eating chocolates and
sweets more often after meals 56.4% (n=344),
than during or before meals 29% (n=181).
Researchers
have
proposed,
even
demonstrated through physical evidence, how
food treatment causes changes in stickiness to
the tooth enamel20. As a result variously
processed foods have various stickiness and
thereby caries predisposition.
Drinks (other than milk): Studies have reported

changing patterns in liquid consumption

amongst children24-25. This pattern is now
common among the dwellers of large
metropolitans around the world. We found that
our studied children, apart from drinking water,
most frequently consumed packed juices
13.9% (n=85), fresh juices 11.5% (N=70), and soft
drinks 6.1% (n=37). Most frequently was
defined as once or more often, daily
consumption. Sohn, Burt and Sowers have also
implied that a higher use of aerated drink has
direct etiologic contribution to caries, as well as,
a supposed association with similar binge
diets26.
Milk: Milk has physical and chemical properties

like

saliva27

and

bovine

milk

is

non-

Oral Hygiene and Dietary Habits among Primary School Children, in Urban Karachi

cariogenic28-29. Another study shows that routine

milk consumption is protective to primary
dentition30. Our study showed that 86.9%
(n=530) of our studies children consumed milk,
while 12.1% (n=74) did not. Milk was consumed
as single intake by 67.0% (n=409) and
distributed over a day by 21.1% (n=129). The
protective role of milk is limited only when
consumed without added sugar. Unfortunately,
in our study, 34.6% (n=211) consumed
unsweetened milk and 59.5% (n=363) took it
sweetened. A high consumption of soft drinks,
absolute or relative to milk or pure fruit juices,
exposes the child to higher risk of caries31.
Cheese: The role of cheese through its dietary
role of calcium post-absorption, as well as
direct availability of calcium and casein, and
by stimulating saliva, has been proposed as
anti-carious by Papas and colleagues32. Within
our studied group, 21.1% (n=129) consumed
cheese; 75.1% (n=458) did not consume it.
Frequency of dental visits: It is a common
observation that dental visits are usually not
given enough importance. It could be a lower
personal priority or the fact that dental
problems often take years before becoming
evident. Irrespective of the cause, researchers
in a study in southern China on 12 year old
children found that within the urban subjects,
about 50% of them attended a dentist in the
last year, while 13% never visited a dental
surgeon. Within their rural subjects however,
about 13% visited the dental surgeon in the last
year and 51% never visited a dental surgeon33.
In our studies children, 10.2% (n=62) visited the
dentist once or twice a year; and 85.1% (n=519)
visited per need.

CONCLUSION
Measurement and healthy change in childs
practices can contribute to limit the
occurrence of caries, particularly at this crucial
stage of life when habits are being formed and
ingrained.

Jinnah Medical and Dental College (year 2010),

who helped collect the data.
----------------------------------------------------------------------Authors affiliations
Marium Iqbal,
Operative Dentistry, Jinnah Medical and Dental
College # 22-23, Shaheed-e-Millat Road, Karachi,
Pakistan.
Ibrahim Shakoor,
Department of Paediatrics, Karachi Medical and
Dental College, Abbasi Shaheed Hospital, Karachi.
Mohsina Noor Ibrahim,
National Institute of Child Health, Rafiquee Shaheed
Road, Karachi, Pakistan.
Laeeq-uz Zaman
ProtoMed, Karachi, Pakistan.

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Gibson S, Williams S. Dental caries in preschool children: associations with social

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Pine, C, McGoldrick P, Burnside G, Curnow

M, et al. An intervention programme to
establish
regular
toothbrushing:
understanding
parents'
beliefs
and

Efforts should be directed at planning

preventive school and community based
programs that are school based and
community based, that could help encourage
favorable habits and practices.

ACKNOWLEDGEMENT:
The researchers gratefully acknowledge the
efforts of the final year student volunteers of

133

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motivating children. Int Dent J 2000; 50

(S6-Part1): 312-23.

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Mobley C, Dodds MW. Diet and dental

health. Top Nutr 1998; 7: 118.

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Curnow MM, Pine CM, Burnside G, et al. A

randomised controlled trial of the efficacy
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Sudha P, Bhasin S, Anegundi RT.

Prevalence of dental caries among 5-13year-old children of Mangalore city. J
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Jackson RJ, Newman HN, Smart GJ, et al.

The effects of a supervised toothbrushing
programme on the caries increment of
primary school children, initially aged 5-6
years. Caries Res 2005; 39(2): 108-15.

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Sheiham A. Dietary effects on dental

diseases. Public Health Nutr 2001; 4(2B):
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Rehman MM, Mahmood N, Rehman B.
The relationship of caries with oral hygiene
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Twetman S, Axelsson S, Dahlgren H, et al.

Caries-preventive
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of
fluoride
toothpaste: a systematic review. Acta
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Kuriakose S, Joseph E. Caries prevalence
and its relation to socio-economic status
and oral hygiene practices in 600 preschool children of Kerala-India. J Indian
Soc Pedod Prev Dent 1999; 17(3): 97-100.
Sarnat H, Kagan A, Raviv A. The relation
between mother's attitude towards
dentistry and oral health status of their
children. J Pediatric Dent 1984; 6(3): 12831.

14.

Waerhaug J. Healing of the dentoepithelial junction following the use of

dental floss. J Clin Periodontol 1981; 8(2):
144-50.

15.

Hujoel PP, Cunha-Cruz J, Banting DW, et

al. Dental flossing and interproximal caries:
a systematic review. J Dent Res 2006;
85(4): 298-305.

16.

Walsh T, Worthington HV, Glenny AM, et

al. Fluoride toothpastes of different
concentrations for preventing dental
caries in children and adolescents.
Cochrane Database Syst Rev 2010; (1):
CD007868.

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Sohn W, Burt BA, Sowers MR. Carbonated

soft drinks and dental caries in the primary
dentition. J Dent Res 2006; 85(3): 262-66.

27.

Samarawickrama DY. Saliva substitutes:

how effective and safe are they? Oral Dis
2002; 8(4): 17779.

28.

Bowen WH, Lawrence RA. Comparison of

the cariogenicity of cola, honey, cow
milk, human milk, and sucrose. Pediatrics
2005; 116(4): 92126.

29.

Peres RC, Coppi LC, Franco EM, et al.

Cariogenicity of different types of milk: an
experimental study using animal model.
Braz Dent J 2002; 13(1): 2732.
Levy SM, Warren JJ, Broffitt B, et al.
Fluoride, beverages and dental caries in
the primary dentition. Caries Res 2003;
37(3): 15765.
Lim S, Sohn W, Burt BA, et al. Cariogenicity
of soft drinks, milk and fruit juice in lowincome african-american children: a
longitudinal study. J Am Dent Assoc 2008;
139(7): 959-67.
Papas AS, Joshi A, Palmer CA, et al.
Relationship of diet to root caries. Am J
Clin Nutr 1995; 61(2): 423-29.
Wong MC, Lo EC, Schwarz E, et al. Oral
health status and oral health behaviors in
Chinese Children. J Dent Res 2001; 80(5):
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of caries prevention. J Am Dent Assoc
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Van Houte J, Upeslacis VN, Jordan HV, et

al. Role of sucrose in colonization of
Streptococcus mutans in conventional
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Woodward M, Walker ARP. Sugar

consumption and dental caries: evidence
from 90 countries. Br Dent J 1994; 176(8):
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Harnack L, Stang J, Story M. Soft drink

consumption among US children and
adolescents: nutritional consequences. J
Am Diet Assoc 1999; 99(4): 436-41.
Heller KE, Sohn W, Burt BA, et al. Water
consumption in the United States in 199496 and implications for water fluoridation
policy. J Public Health Dent 1999; 59(1): 311.

33.

ORIGINAL ARTICLE

Biochemical Types of Dehydration and Risk Factors for

Sodium Imbalance in Children with Acute Watery
Diarrhea
BUSHRA FATIMA, MUHAMMAD FAHEEM AFZAL, MUHAMMAD ASHRAF SULTAN, Asif Hanif

-----------------------------------------------------------------Pak Paed J 2011;35(3): 135-38

ABSTRACT
Background: Acute watery diarrhea (AWD) is defined as passage of 3 or
more loose stools/day or more frequent for the individual with duration of
less than 14 days. Dehydration is biochemically categorized according
to serum sodium concentration as isonatremic (135-145mEq/L),
hyponatremic(<135mEq/L) and hypernatremic dehydration(>145mEq/L).
Objective: To determine the biochemical types of dehydration and
determine the risk factors for sodium imbalance in children with AWD.
Authors affiliations

Study design: Cross sectional study.

---------------------------------------------

Setting: Department of Paediatrics Unit-I, King Edward Medical University/

Mayo Hospital, Lahore.

Correspondence to:

Duration: March to August 2010.

Bushra Fatima,
Department of Paediatrics
Unit-I, King Edward Medical
University/ Mayo Hospital,
Lahore.

Subjects and Methods: A total of 500 children of age 1month-12 years

with AWD were included in the study by non probability purposive
sampling. After consent, demographica data was recorded. Each child
was examined for degree of dehydration, and was investigated for
serum sodium level. ANOVA was applied to find out the association of
age and Chi square was applied to find out association of sex, feeding
pattern, nutritional status, degrees of dehydration with type of
dehydration. Each child was treated according to WHO plan of
treatment for some or severe dehydration.

E-mail:
fatimaalvi2000@yahoo.com

Results: Mean age was 2.53 years. Clinically severe dehydration was
found in most children (51%). Highest and lowest serum sodium level was
166 and 117 mEq/L respectively with mean of 1346 mEq/L. Isonatremic
dehydration was found in 51% children followed by hyponatremic
dehydration (46%). There was positive association of nutritional status and
degree of dehydration. (p value 0.05 each) More malnourished and
more severely dehydrated the child was more was the chance of having
sodium imbalance.
Conclusion: Isonatremic dehydration is most common type of
dehydration. Malnutrition and clinically severe dehydration are
significantly associated with biochemical type of dehydration.
Key words: isonatremic, hyponatremic, hypernatremic dehydration,
acute watery diarrhea.

www.ppa.org.pk

Fatima B, Afzal MF, Sultan MA, Hanif A

136
INTRODUCTION
Acute watery diarrhea (AWD) is defined as
passage of 3 or more loose stools/day or more
frequent for the individual with duration of less
than 14 days. Diarrheal disease is the second
leading cause of death in children under five
years of age. Globally, it is causes about two
billion cases and 1.5 million deaths every year1.
Dehydration is a state of negative fluid balance
that leads to depletion of extracellular fluid and
electrolytes resulting in reduction of plasma
volume
with
consequent
disturbance of
physiologic functions2. Serum sodium is the
dominant
cation
and
determinant
of
extracellular osmolality. Dehydration can also be
categorized according to serum sodium
concentration as isonatremic (serum sodium level
135-145
mEq/L),
hyponatremic
(serum
sodium<135
mEq/L),
or
hypernatremic
dehydration
(serum
sodium>145
mEq/L).
Isonatremic dehydration is the most common (7080%) type of dehydration. Hypernatremic and
hyponatremic types of dehydration each
comprise 10-15% of cases. Both types can lead to
neurological symptoms3.
Based on this review, this study was conducted to
help determine the biochemical types of
dehydration and the risk factors for sodium
imbalance in children with AWD, so that patients
at risk can be identified earlier and special
treatment strategies can be instituted regarding
rehydration of these patients so that mortality
associated with this preventable disease may be
reduced.

MATERIAL AND METHODS

This cross sectional study was conducted from
March to August 2010 in the Department of
Paediatrics
Unit-I,
King
Edward
Medical
University/Mayo Hospital, Lahore. Sample was
collected by non probability purposive sampling.
A total of 500 children of age 1months-12 years of

AWD were included in the study. Consent was

taken from parents/guardian. All parents of the
children, who were approached, consented for
the study. Each child was examined for degree of
dehydration (sunken eyes, skin pinch, conscious
level, thirst), and nutritional status according to
modified Indian Gomez classification. (>80%
classified as No Malnutrition, 70-80% as Grade I
Malnutrition, 60-69% as Grade II Malnutrition,
50-59% as Grade III Malnutrition and <50% as
Grade IV Malnutrition). Each child was
investigated for serum sodium level. Other
electrolytes as serum bicarbonate level, serum
creatinine, blood urea were performed as per
individual case, but since it was beyond scope of
the objective of the study, these electrolytes
were included in data analysis. Data was entered
in SPSS 17. ANOVA was applied to find out the
association of age with type of dehydration. Chi
square was applied to find out the association of
sex, feeding pattern, nutritional status, degree of
dehydration with type of dehydration. p value of
0.05 was considered to be statistically
significant. Each child was treated according to
the individual merit.
RESULTS
Mean age was 2.53 years. Most common age
group was infancy (53%).(Fig 1) There was over all
male preponderance. In children less than 2
years of age, majority was top fed (51%).
Clinically severe dehydration was found in most
children (51%). Highest and lowest serum sodium
levels were 166 and 117 mEq/L respectively with
mean of 1346 mEq/L. Isonatremic dehydration
was found in 51% children followed by
hyponatremic dehydration (46%). There was
positive association of nutritional status and
degree of dehydration (p value 0.05). More
malnourished and more severely dehydrated the
child was, more was the chance of sodium
imbalance. (Table I & 2) However, there was no
significant association of age, sex, and feeding
pattern with type of dehydration (p value 0.914,
0.836 and 0.546 respectively).

TABLE 1: Comparison of type of dehydration with Nutritional Status (n=500)

Type of
Dehydration

No Malnutrition
n (%)

Grade I
n (%)

Grade II
n (%)

Grade III
n (%)

Grade IV
n (%)

Total

Isonatremic
46 (9.2)
49 (9.8)
51 (10.2)
67 (13.4)
43 (8.6)
256
Hyponatremic
51 (10.2)
63 (12.6)
55 (11)
35 (7)
25 (5)
229
Hypernatremic
02 (0.4)
03 (0.6)
05 (1)
04 (0.8)
01 (0.2)
15
Total
99 (19.8)
115 (23)
111(22.2)
106(21.2)
69(13.8)
500
(Association of nutritional status with biochemical type of dehydration was statistically significant; p value was 0.05
by Chi square)

www.ppa.org.pk

137

Issonatremic, hy
yponatremic,, hypernatrem
mic dehydratio
on, acute watery diarrhea

T
TABLE
2: Deg
gree of dehyd
dration (n=500)
A
Age
Issonatremic
H
Hyponatremic
c
H
Hypernatremic
c
T
Total

Some
n (%)
142 (28.4)
96 (19.2)
6 (1.2)
244 (48.8)

Severre
n (%
%)
114 (22.8)
133 (26.6)
9 (1.8)
256 (51.2)

Total
256
229
15
500

cal dehyd
dration with
(Association of clinic
b
biochemical
l type of dehydration was
w statistically
s
significant;
p value was 0.05
0
by Chi square)
s

16%

32%
%

15%
16%

21%

1<6months

6<12m
months

2<5years

512ye
ears

12
2<24months

F 1: Age disstribution (n=

Fig
=500)
M
MeanS
D 2.53
3 years

D
DISCUSSION
N
Diarrhea is most
D
m
common in childrren especially
t
those
betwe
een 6monthss to 2 years of
o age. Major
c
complication
ns of diarrhea include dehydration,
abnormalitties and malnutrition.
e
electrolyte
P
Present
study
y had age range 1 mo
onth up to 12
1
y
years
with a mean ag
ge of 2.53
3 years. Mo
ost
c
common
ag
ge group was
w
infancy
y [268 (53%
%)]
T
These
results are co
onsistent with a stud
dy
c
conducted
on children
n with diarrrhea in 200
05
m
mentioning
that most of
o the child
dren sufferin
ng
from AWD were
w
betwee
en 6 months up to 4 yea
ars
o age4. The prevalence of diarrhea is also high in
of
c
children
be
elow 5 years in western world
d5.
A
Although
A
AWD
is not sex speciific howeve
er,
p
present
stud
dy showed preponderan
p
nce of male
es
(57%). This coincides witth a local sttudy6 showin
ng
6
60%
male ca
ases in AWD
D. This may be
b due to th
he
fact that ma
ales with severe infectio
ons are more
frequently brought
b
to the hospita
al than the
eir
female coun
nter parts in our
o culture.
Present stud
P
dy had pre
edominance
e of clinica
ally
s
severe
dehydration (52%
%), while 51%
% children ha
ad

ydration. Wa
athen7 repo
orted 96%
isonattremic dehy
childrren of AWD
D with isona
atremic deh
hydration.
Local study co
onducted in Lahore reported
ydration as 81%8. This difference
d
isonattremic dehy
may be
b due to th
he fact that we
w included
d children
with clinically
c
som
me and sev
vere dehydration. In
this studied population, 3% children had
d
hyperrnatremic dehydration
. These results are
comp
patible with other
o
studiess7,8 in which 3.3% and
7% patients
p
had hypernatremic deh
hydration.
Present study had
d 46% hypon
natremic deh
hydration
which
h is compa
atible with internationa
al report
(56%)9. However, it was 12% in a local sttudy from
s
had statistically
s
significant
Lahorre.8 Present study
assoc
ciation of biochemica
al dehydrattion with
nutritional status which is comparable with
w
study
by Caksen
C
et al10. Prese
ent study had no
statisttically signific
cant associa
ation of bioc
chemical
dehyd
dration with
h type of feeding. However,
H
hyperrnatremic dehydration
d
is reported
d to be
more commonly
y associate
ed with hy
ypertonic
ng preparatiions11.
feedin
Present study ha
as certain limitations. This was
ed out from March to August
A
(peak season
carrie
of AW
WD) which did not in
nclude all the four
seaso
ons. If the study
s
had included
i
th
he whole
calen
ndar year, the result might hav
ve been
differe
ent. Factors contributing
g to all three
e types of
dehyd
dration were
e not studied and we could
c
not
get in
nformation on
o consump
ption of OR
RS before
presenting to ho
ospital. Elec
ctrolytes oth
her than
sodium
m were not included in data.
d

CONCLUSION
We co
onclude from
m present sttudy that isonatremic
dehyd
dration is mo
ost common
n type of deh
hydration
follow
wed by hyp
ponatremic and hypernatremic
dehyd
dration wh
hose timely
y identification is
necesssary for furrther manag
gement. Ma
alnutrition
and
clinically
severe
dehydration
n
were
al type of
significantly associated with biochemica
dehyd
dration.
--------------------------------------------------------------------------------Authorrs affiliations
a Fatima, Muhammad
M
Faheem Affzal, Prof.
Bushra
Muham
mmad Ashraff Sultan
Deparrtment of Pae
ediatrics Unit-I, King Edward
d Medical
Univerrsity/ Mayo Ho
ospital, Lahore
e.
anif
Asif Ha
Biostattistician, Annals
Univerrsity, Lahore.

of

Kin
ng

Edward

Medical

www.p
ppa.org.pk

Fatima B, Afzal MF, Sultan MA, Hanif A

138
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Hafeez A, Tariq P, Ali S, Kundi ZU, Khan A,

Hassan M. The efficacy of Saccharomyces

www.ppa.org.pk

7.

boulardi in the treatment of AWD on

children:
A
multicentre
randomized
controlled trial. J Coll Physicians Surg Pak
2002; 12: 432-34.
Wathen J E, Mackenzie T, Bothner J P.
Usefulness of the serum electrolyte panel in the
management of pediatrics dehydration
treated with intravenously administered fluids.
Pediatrics 2004; 114: 1227-34.

8.

Sarfraz M, Iqbal SMJ, Azhar IA. Incidence and

outcome of various types of dehydration
(biochemical) in children with acute diarrhea.
Pak Paed J 2002; 26: 191-94.

9.

Shah GS, Das BK, Kumar S, Singh Mk, Bhandari

GP. Electrolyte disturbances in diarrhea.
Pediatric On call [serial online] 2006 [cited 2008
November
1].
Available
from:
http://www.pediatriconcall.com/fordoctor/Me
dical_original_articles/electrolyte_disturbances
_diarrhea.asp.

10.

Caksen H, Odabas D, Sar S, Celebi V,

Arsalan S, Kuru M et al. Hyponatremic
dehydration: an analysis of 78 cases. Int Urol
Nephrol 2001; 33: 445-48.

11.

Hussain S, Hassan S. Management of

hypernatremic dehydration and its outcome in
children. Pak Paed J 2003; 27: 121-26.

Developmental Assessment and Effect of Intervention in Children with Global Developmental Delay

139

ORIGINAL ARTICLE

Developmental Assessment and Effect of Intervention in

Children with Global Developmental Delay
SHAZIA MAQBOOL, EHSAN ULLAH, TAYYABA KHAWAR BUTT, WAJEEHA ZAHRA, MIAN M SHARIFF

-----------------------------------------------------------------ABSTRACT
Authors affiliations
--------------------------------------------Correspondence to:
Shazia Maqbool
Department of Developmental
Paediatrics, The Childrens
Hospital & Institute of Child
Health, Ferozepur Road, Lahore
Email: drshazimaq@yahoo.com

Pak Paed J 2011;35(3):139-44

Background: The prevalence of childhood disabilities is up to 10% of the

total pediatric population and in a developing country like Pakistan this
figure is even higher. Health professionals use a range of different tools to
evaluate child development. An ideal screening tool should be cost
effective, easily administered and culturally relevant. Early intervention
programs when properly planned and introduced in time are helpful for
delayed children.
Objectives: To study the effect of intervention in developmental delay
children. To compare mental age and Developmental Quotient (DQ)
based on developmental profile.
Material & Methods: 42 children were selected to be enrolled in the study
of these 26 completed the study. Slosson Intelligence Test (SIT) was used
to assess the mental age and Portage Early Education Program (PEEP)
was used to assess the DQ. Early intervention therapy was given to these
children who were then reassessed after one year to see the effect of
intervention. Statistical analysis was done using SPSS 14 by applying
descriptive analysis, paired t-test and Pearson correlation coefficient. p
value of 0.05 or lower were taken as significant
Results: There was significant increase in mental age of these children
(p=0.000 t= 23.74). An improvement was seen in all developmental skill
areas p=0.000. The change in mental age correlated with the
improvement in cognition (p=0.000, r=0.780), language (p=0.000, r=0.642)
and self-help (p=0.026, r= 0.435). DQ was significantly correlated with
mental age (p=0.002, r=0.589)
Conclusion
Portage based assessment and therapeutic plans are useful to detect
developmental delay. DQ based on portage developmental profile is a
useful index of developmental assessment and it is comparable to
mental age. IQ may not be considered as a useful indicator of
improvement in young children.
Key Words: Global Developmental
Developmental Quotient (DQ)

Delay,

Early

Intervention,

Abbreviations: PEEP = Portage Early Education Programme, MA = Mental

Age, DQ = Developmental Quotient, IQ = Intelligence Quotient, SIT =
Slosson Intelligence Test, GDD = Global Developmental Delay, EIP = Early
Intervention Programme

www.ppa.org.pk

140
INTRODUCTION
Child development refers to the ordered
emergence of interdependent skills of sensorimotor, cognitive, language, and socialemotional functioning1. Many children in
developing countries are exposed to multiple risks
for poor development including poverty, poor
health and nutrition. According to a recent series
of reviews it is estimated that more than 200
million children under 5 years of age in
developing countries do not reach their full
potential. Sub-Saharan African countries have
the highest percentage of disadvantaged
children but the largest number live in South
Asia2.
Developmental disorder" and "developmental
disability" refers to a childhood mental or physical
impairment or combination of mental, physical,
behavioural and emotional impairments that
result in substantial functional limitations in major
Global Developmental Delay
life activities3.
(GDD) is a subset of developmental disabilities
defined as a significant delay in two or more of
the following developmental domains: gross/fine
motor,
speech/language,
cognition,
social/personal and activities of daily living4.
Developmental delay occurs in up to 15% of
children under 5 years of age5 while in the total
paediatric
population
childhood
disability
prevalence is up to 10%6. The prevalence of
disability in selected developing countries is as
follows:
Jamaica-15%,
Pakistan-15%
and
Bangladesh-8%7 with GDD as one of the major
contributors. The causes of GDD are many and
include genetic conditions like Downs syndrome,
Fragile X syndrome, Phenylketonuria, prenatal
problems like TORCH infections and maternal
malnutrition, perinatal problems like birth trauma,
hypoxia,
prematurity,
cerebral
ischemia,
hypothyroidism, and childhood problems like
intracranial infections, failure to thrive and lead
poisoning8. There is no universally accepted
approach to the etiological assessment of
developmental delay. Recommended tests used
to detect aetiology are cytogenetic studies and
molecular testing even in the absence of
dysmorphic features along with neuroimaging
preferably MRI. EEG and metabolic screening
should be done as and when indicated by history
and physical examination4. Besides biological

Khan QA, Iqbal H, Rehman RU

determinants, family and environmental factors

also play a major role in child development9.
Health professionals use a range of methods to
evaluate childrens development like checklist of
developmental milestones, clinical judgment,
parental recall of milestones and report of current
achievements, developmental screening tests
and assessment5. There are many standardised
tests used to evaluate GDD for example the
Griffiths Mental Developmental Scales (GMDS),
Schedule of Growing Skills II (SGS II), Denver
Developmental Screening Tool II (DDST II), Bayley
Mental & Motor Index etc. but finding an ideal
screening tool which is easily administered, cost
effective, demonstrates strong psychometric
qualities, and is culturally relevant remains a
challenge7. Although Portage is not a routine test
to
evaluate
developmental
delay
the
developmental functioning level assessed by
Portage portrays the degree of delay in different
skill areas also provides a baseline for a
therapeutic plan according to the level of
delay10. Portage is equally beneficial if a DQ is
derived from the given domains as was done in a
recent Chinese study where developmental
functions were assessed in all the children, using
the Chinese Child Development Inventory with
the updated norms and DQ was determined11.
Validity ofDQ with IQ has been successfully done
in another study12. Early recognition and
intervention is critical for all developmental, social
and behavioural problems. Interdisciplinary
coordination
provides
a
comprehensive
approach to screening, assessment and
intervention for developmental delays in infants
Early intervention
and young children13.
programs are helpful for these children, and the
addition of structured home activity programs
may augment the effects on developmental
progression14.

MATERIAL & METHODS

This was a one year prospective and descriptive
study at the Department of Developmental
Paediatrics, The Childrens Hospital, Lahore
Inclusion Criteria: Global Developmental Delay
children between 4 years -7 years of age
Exclusion Criteria: Degenerative brain disease; any

other chronic illness; Autistic Spectrum Disorders

www.ppa.org.pk

141

Developmental Assessment and Effect of Intervention in Children with Global Developmental Delay

An approval of institutional ethics committee of

The Childrens Hospital and Institute of Child
Health was obtained. Forty two (42) children were
diagnosed as having Global Developmental
Delay and were planned to be enrolled in the
study. After written consent, ten (10) parents
refused to participate because they were from
other cities and had logistic problems.
Intervention was initiated for thirty two children
but twenty six (26) children completed the study.
Their mental ages were assessed using the Slosson
Intelligence Test (SIT)15 which is a standardised
test to measure the Intelligence Quotient (IQ).
Their developmental profile was determined
using the Portage Early Education Program
(PEEP)10 to calculate the Developmental
Quotient (DQ) from the five domains assessed.
This DQ was determined as a percentage of the
developmental age divided by the chronological
age as was done in the Chinese studies using
Chinese Developmental scales11,16
An Early
Intervention
Program
(EIP)
including
developmental
therapy,
speech
therapy,
occupational therapy, sensory therapy, physical
therapy and behaviour modification therapy
were started and continued for one year. These
children were reassessed with SIT and PEEP to
study the effects of the intervention. Statistical
analysis was done using SPSS 14 by applying
descriptive analysis, paired t-test and Pearson
correlation co-efficient. p value of 0.05 or lower
was taken as significant17.

Quotient determined from the skill areas was also

significantly correlated with the mental age
(p=0.002, r=0.589) (Fig 2).
Although the increase in three skill areas
mentioned above resulted in improvement in the
mental age, no influence was seen on the
Intelligence Quotient (Table 3).

Fig 1: Change in Mental Age after Intervention

p= 0.000, t -22.74, Degree of Freedom 25 n-1

RESULTS
26 children with Global Developmental Delay
who completed one year of study were
reassessed after intervention.
There was a statistically significant increase in the
mental ages of these children (p=0.000, t=22.74)
(Fig 1). There was significant improvement in the
developmental skill areas including cognition
(p=0.000, t=-24.48), socialisation (p=0.000, t=18.20), language (p=0.000, t=-17.72), self-help
(p=0.000, t=-9.56) and motor (p=0.000, t= -9.04)
(Table 1). The change in mental age correlated
with improvements in cognition (p=0.000,
r=0.780), language (p=0.000, r=0.642) and self
help (p=0.026, r= 0.435) while the improvement in
motor (p=0.465, r=0.150) and socialisation
(p=0.115, r=0.317) had no influence on the
mental age (Table 2). The Developmental

Fig 2: Mental Age vs. Developmental Quotient

p = 0.002, r=0.589
TABLE I: Effect of Intervention on Developmental Profile

Skill Areas

Pre Mean
(In
Months )

Cognition
Socialization

37.60

Post
Mean
(In
Months )
61.40

-24.48

0.000

39.30

57.60

-18.20

0.000

Self Help

46.00

61.20

-9.56

0.000

Motor

36.60

61.90

-9.04

0.000

Language

36.62

61.92

-17.72

0.000

www.ppa.org.pk

Maqbool S, Ullah E, Butt TK, Zahra W, Shariff MM

142

TABLE 2: Correlation of Mental Age with Developmental

Profile after Intervention (n = 26)

Skill Area
Cognition
Socialization
Self Help
Motor
Language

r
0.780
0.317
0.435
0.150
0.642

p
0.000
0.12
0.026
0.47
0.000

TABLE 3: Correlation of IQ with Developmental Profile

after Intervention (n = 26)
Skill Area
Cognition
Socialization
Self Help
Motor
Language

r
0.310
0.024
0.021
0.034
0.228

p
0.123
0.907
0.921
0.867
0.262

DISCUSSION
Awareness of developmental delay and possible
interventions is very low in our part of the world.
An Indian study found that the mean age of
children referred for an early intervention
program was 4 years18 while in the west the mean
age of referral was 1.2 years19. The mean age of
referral in our study was 5.6 years with a mental
age of 3.5 years showing that the situation is
worse in our country. There is a dearth of research
on
early
intervention
studies
in
global
developmental delay and early intervention can
be better planned if developmental screening
and surveillance are done20. Portage was first
devised as a home based program to facilitate
early education in normal children and it soon
became a popular tool for developmental
assessment and therapy in children with special
needs. We compared the DQ of Portage with the
mental ages in addition to the IQ of SIT. In our
study DQ and mental age scores were
comparable both before and after intervention.
Developmental profile of DQ forms the basis of a
therapeutic plan and it gives an extra benefit to
use Portage both as an assessment and
therapeutic tool especially for age range less
than 6-7 years. Furthermore IQ at this age is not a
reliable index for measurement in children.
Early Intervention has been defined as a broad
array of activities designed to enhance a young
childs development21. These interventions are
intended to affect children directly via structured

www.ppa.org.pk

experiences and indirectly through influencing

the care giving environment and can be
provided in a variety of contexts, including home,
centre, hospital, and/or clinic.
The effects of early intervention on early child
development in infants with birth asphyxia in poor
countries have not been evaluated sufficiently to
determine if these interventions should become
standard practice22.
Out of various intervention programs available
we used developmental therapy including
speech therapy, sensory therapy, occupational
therapy and behavior modification therapy.
Developmental therapy was based on Portage
because of its simplicity, availability, and cross
cultural use as it is being widely used in
developed countries like the UK and USA as well
as in developing countries like Pakistan, India and
Bangladesh23,24. The improvement in all skill areas
was comparable to those in other studies25,-27.
The improvement in mental age was due to three
skill areas namely cognition,1 language12 and self
help while motor and socialization had no effect
on the mental age. This was also seen in another
study which showed that there was improvement
in cognition but there was little evidence of an
effect of early intervention on motor outcome in
the short, medium or long term basis28. In our
study the IQ was not influenced by the
intervention
though
in
another
study
improvement was reported both in DQ and IQ29.
A study done in Japan validated DQ as an
estimate of IQ12 and it is argued that IQ testing
should not be done30 in very young children so
DQ can be alternatively used as it is comparable
to mental age and this is reflected in our study.

CONCLUSIONS
Early intervention to improve skill areas is effective
and should be planned according to the need
within the resources available. DQ based on
Portage is a useful index of developmental
assessment as it is comparable to mental age. IQ
may not be considered a useful indicator of
improvement in skill areas in young children.

ACKNOWLEDGEMENTS
We are grateful to Mr. Muhammad Shakeel Azam
for typing of the manuscript and to all the staff of

Developmental Assessment and Effect of Intervention in Children with Global Developmental Delay

the Department of Developmental Paediatrics for

putting in long hours during this research.
We are also grateful to Mr. Muhammad Zaheer
for help with the statistical analysis of this study
and for being available whenever he was
needed.

Indian Pediatr 2010; 416(47): 415-22.

8.

McDonald L, Rennie A, Tolmie J, et al.

Investigation of global developmental
delay. Arch Dis Child 2006; 91(8): 70105.

9.

Sachdeva S, Amir A, Alam S, et al. Global

Developmental Delay and Its Determinants
Among Urban Infants and Toddlers: A Cross
Sectional Study. Indian J Pediatr 2010; 77(9):
975-80.

10.

White M, Cameron RJ. Portage Early

Education Programme: A practical manual.
Windsor: NFER-NELSON; 1987.

11.

Lee YC, Wu CY, Liaw MY et al.

Developmental
profiles
of
preschool
children
with
spastic
diplegic
and
quadriplegic cerebral palsy. Kaohsiung J
Med Sci 2010; 26(7): 341-49.

12.

Hiroshi K, Kirokazu O, Kaoru S, et al. Validity

of DQ as an estimate of IQ in children.
Psychiatry Clin Neurosci 2003; 57(2): 231-33.

13.

Mousmanis P, Watson W J. The 18-month

well-child visit in primary care: Clinical
strategies for early Intervention. Paediatr
Child Health 2008; 13(10): 845-849.

14.

Tang MH, Lin CK, Lin WH et al. The effect of

adding a home program to weekly
institutional-based therapy for children with
undefined developmental delay: A pilot
randomized clinical trial. J Chin Med Assoc
2011; 74(6): 259-66.

15.

Slosson. Manual Slosson Intelligence Test.

The Psychological Corporation, USA, 1960.

16.

Chen CM, Chen CL, Hou JW et al.

Developmental profiles and mentality in
preschool
children
with
Prader-Willi
syndrome: a preliminary study. Chang Gung
Med J 2010; 33(4): 436-42.

17.

Statistical Package for Social Sciences.

Version 14. SPSS Inc USA; 2006.

-------------------------------------------------------------Shazia Maqbool, Ehsan Ullah, Wajeeha Zahra,

Department of Developmental Paediatrics The
Childrens Hospital & Institute of Child Health, Lahore
Tayyaba Khawar Butt
Department of Paediatric Medicine, Institute
Medical Sciences & Services Hospital, Lahore

of

Mian M Shariff
Currently working as Consultant Haematologist,
Broomfield Hospital, Chelmsford, United Kingdom

REFERENCES
1.

Engle PL, Black MM, Behrman, JR, et al.

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million children in the developing world.
Lancet 2007; 369(9557): 229-42.

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McGregor SG, Cheung YB, Cuero S, et al.

Developmental potential in the first 5 years
for children in developing countries. Lancet
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Accardo PJ, Whitman BY, Behr SK, et al.

Dictionary of Developmental Disabilities
Terminology. 2nd ed. Baltimore, MD: Paul H.
Brookes Publishing Co; 2003.

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Shevell M, Majnemer A, Noetzel M et al.

Practice Parameter: Evaluation of the child
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the quality standards subcommittee of the
American Academy of Neurology and the
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Oberklaid F, Efron D. Developmental Delay:

Identification and management. Australian
Family Physician, Sept. 2005; 34(9): 739-42.

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Diseases and Related Health Problems. 10th
Revision. World Health Organization; 2007.

Kaur P, Chavan B S, Lata S et al. Early

Intervention in Developmental Delay. Indian
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7.

Poon JK, Larosa AC, Pai GH. Developmental

delay timely identification and assessment.

Bailey Jr. DB, Hebbeler K, Scarborough A et

al. First experiences with Early Intervention:
A national perspective. Pediatrics 2004;
113(4): 887-896.

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Maqbool S, Ullah E, Butt TK, Zahra W, Shariff MM

144

20.

Lipkin PH, Macias MM, Duncan P, et al.

Update on Developmental Surveillance and
Screening Recommendations. Pediatrics
[Internet]. 2009 Feb [cited 2011 May 18];
Available
from:
http://pediatriaappublications.org/
cgi/eletters/118/1/405.

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Brooks-Gunn J, McCarton CM, Casey PH, et

al. Early Intervention in low-birth weight
premature infants results through age 5
years from the infant health and
development
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1994;
272(16): 1257-62.

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Wallander JL, McClure E, Biasini F, et al.

Brain Research to Ameliorate Impaired
Neurodevelopment

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Based
Intervention Trail (Brain-HIT). Revista Romana
De Pediatrie 2010, 59(2): 137-145.

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Russell F. Portage in the UK: recent

developments. Child Care Health Dev 2007;
33(6):677-83.

24.

Sturmey P, Thorburn MJ, Brown JM, et al.

Portage guide to early intervention: crosscultural aspects and intra-cultural variability.
Child Care Health Dev 1992; 18(6):377-94.

25.

Carpenter B. The impetus for familycentered early childhood intervention.

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Child Care Health Dev 2007; 33(6):664-9.

26.

Nahar B, Hamadani JD, Ahmed T, et al.

Effects of psychosocial stimulation on
growth and development of severely
malnourished children in a nutrition unit in
Bangladesh. Eur J Clin Nutr 2009; 63(6):72531.

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Hamadani JD, Huda SN, Khatun F, et al.

Psychosocial Stimulation Improves the
Development of Undernourished Children in
Rural Bangladesh. J Nutr 2006; 136(10):
2645-52.

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Spittle A, Orton J, Doyale LW, et al. Early

developmental intervention programs post
hospital discharge to prevent motor and
cognitive impairments in preterm infants.
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CD005495.

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Ade A, Gupta SS, Maliye C, et al. Effect of

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and Development Quotient of Children.
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Moeschler JB, Shevell M. Clinical Genetic

Evaluation of the child with mental
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141

Khan QA, Iqbal H, Rehman RU

ORIGINAL ARTICLE

Is Lumbar Puncture Necessary among Children with First

Febrile Seizure?
MUHAMMAD SAEED, TAHIR NADEEM, SAMIR M. AL-NUFIEE

-----------------------------------------------------------------ABSTRACT
Authors affiliations
--------------------------------------------Correspondence to:

Muhammad Saeed,
Department of Pediatric
Neurologist, P.O.Box 6741.
Childrens Hospital Taif,
Kingdom of Saudi Arabia.
E mail:
muhammad964@hotmail.com

Pak Paed J 2011;35(3):145-48

Objective: The objective of this study was to find out the frequency of
meningitis among children who present with first febrile seizure.
Study design: A retrospective record review of the patients from 6
months to 5 years of age who presented with first febrile seizure and
evaluated for CSF at Childrens hospital Taif, KSA.
Methodology: All patients who presented to emergency department
with first febrile seizure, from January 2008 to May 2011, from 6 months
to 5 years age were studied. Lumbar puncture was performed in all
cases.
Results: A total of 272 patients were studied. 165 cases (61%) were male
and 107(39%) were female. All patients underwent lumbar puncture, of
whom 6(2%) had abnormal CSF findings suggestive of meningitis. Thus
meningitis was diagnosed in 2% of children with first febrile seizure.
Conclusions: Our results indicate that proportion of meningitis was very
low in children presenting with first febrile seizure. We suggest that by
practicing meticulous clinical examination and close monitoring, it is
possible to avoid unnecessary lumbar puncture in these patients.
Key words: Febrile seizures, lumbar puncture, clinical examination,
meningitis

INTRODUCTION
Febrile seizures (FS) are the most common
problem in pediatric neurology. The relation
between fever and seizures had been
documented by Hippocrates in the 5th century
B.C1.
Febrile seizures occur in 2- 5% of all children and,
thus make up the most common convulsive
event in children younger than 60 months. The
American Academy of Pediatrics (AAP) issued
practice
parameters
regarding
the
neurodiagnostic evaluation of children with first
simple febrile seizures in 19962. The term febrile
seizure is not intended for use among children

with evident central nervous system infections or

underlying seizures disorder3.
The prevalence of meningitis in children with
seizure and fever in North American pediatric
emergency wards was between 0- 2%4. The
revised AAP guidelines state that lumbar
puncture should be performed when a child with
a seizure and fever also has symptoms that
suggest meningitis.
The issue of whether a well appearing child
presenting with first febrile seizure is at increased
risk of meningitis has remained controversial5,6.
Probability of meningitis in children with febrile
seizures varies from 0 to 6.7%7.

www.ppa.org.pk

146
TThe study wa
as conducte
ed with the objectives to
t
find out the value of CS
SF analysis with
w
presume
ed
febrile seizures who ro
outinely und
dergo lumba
ar
p
puncture,
to
o find out the predictiv
ve factors for
m
meningitis
a
and
whethe
er lumbar puncture
p
wa
as
n
necessary
in
n children presenting with first febriile
s
seizure.

M
METHODOLO
OGY
TThis study was
w
hospita
al based, retrospectiv
ve
a
analysis,
co
onducted in
i
the de
epartment of
p
pediatric
neurology, Childrens Hosp
pital Taif, KSA
A,
from January
y 2008 to Ma
ay 2011.
A total of 27
72 children aged
a
from 6 months to 5
y
years,
who presented
p
wiith first febrile
e seizure were
in
ncluded in the study. These cases were
w
identifie
ed
b reviewing
by
g the admiission registe
ers and datta
w
was
collecte
ed from med
dical record
ds. The deta
ails
o
of
current illness an
nd investig
gations were
r
recorded.
Children witth other ne
C
eurological diseases lik
ke
c
cerebral
palsy, mental re
etardation, past
p
history of
m
meningitis
with sequel, other neurological
d
diseases,
and fever afte
er occurrenc
ce of seizure
es
o antibioticss for more th
or
han forty-eig
ght hours were
e
excluded
fro
om the study
y. Children having
h
axilla
ary
t
temperature
e 38oC (recorded in eme
ergency, OP
PD
o in the warrd), were considered as febrile. All th
or
he
p
patients
we
ere examin
ned in de
etail by th
he
p
pediatricians
s of the hospital. Lumb
bar puncture
es
w
were
perform
med after ta
aking written consent from
t
the
parents and
a
CSF was collected in three steriile
v
vials.
One viial was sent for total an
nd differentiial
c
cell
count, one
o
vial for sugar and protein, an
nd
t
third
one forr culture. Ab
bnormal CSF results were
la
abeled in a child with fever and seizure if CSSF
h
had
a comb
bination of tw
wo of the folllowings:
A Cells gre
A.
eater than 5//mm3, prote
ein more tha
an
40mg% and sugar less than 2/3
2
of bloo
od
sugar.
B Positive smear
B.
s
on Grrams stain and
a
growth of
bacteria in CSF.

R
RESULTS
TThere were a total of 272
2
cases th
hat presente
ed
w
with
first feb
brile episode of seizure
e between 6
m
months
to 5 years of age
e. One hund
dred and sixxty
five cases (6
61%) out of 272 were male
m
and 10
07
p
patients
(39
9%) were fe
emale. The duration of
s
seizures
rang
ged from 0.2
20 minutes to
t 40 minute
es

w
www.ppa.org
.pk

Saee
ed M, Nadeem T, Samir M. Al-Nufiee

o five minu
utes. The ma
ajority of
with a median of
patients (96%) ha
ad seizures lasting less than or
equal to 15 minutes; 12(4%) patients
p
had
d seizures
lasting
g greater th
han 30 min
nutes. There were a
total of
o 89 patien
nts in 6 -12 months
m
age group,
g
95
in 12-18 months and
a
88 abov
ve 18 month
hs age. 6
m
childrren (2%) werre diagnosed to have meningitis
and other cause
es of seizure
es associate
ed fever
mentiioned in tab
ble 1.
Two hundred an
nd sixty six cases (98%
%) of our
nd only six (2%)
(
had
patients had norrmal CSF an
raised
d CSF protein and pleoc
cytosis. 4 ca
ases were
male and 2 were
e female. None
N
of the patients
had cutaneous
c
signs, neck sttiffness or otther signs
of me
eningeal irritation. CSF culture
c
was negative
in all cases. Am
mong casess of mening
gitis, the
duration between
n the onset of fever and
d seizures
was more than 24 hours and seizurres were
recurrrent, but in remaining cases, seizures
occurrred within th
he first 24 ho
ours of fever. No case
of me
eningitis cam
me with status epilepticuss.
All pa
atients who presented with fever,, seizures
and abnormal
a
CSSF appeared
d extremely ill or had
febrile
e seizures witth complex features.
f
300
250
200
150
100
50
0
Total Patie
ents

Male
e

Fem
male

Fig 1: Sex distributtion among study cases

Table 1: causess of febrile
e illness and their
ency
freque
Cause
es of febrrile
illness
URTI
Bronch
hiolitis/
Pneum
monia
Gastro
oenteritis
Menin
ngitis
Urinary
y tract infectio
on

Number of
ents
patie
214
4
30
0
20
0
6
2

Perc
centage
79.0
00
11.0
00
7.0
00
2.0
00
0.7
73

USSION
DISCU
Febrile
e seizures are
a
the mosst common form of
seizure
es seen in children. The prevalence of

Is Lumbar Puncture Necessary among Children with First Febrile Seizure?

meningitis among children with seizures and fever

in North American Pediatric ED is between 1%
and 2% and through selective referral, may be as
high as 7% in an European country8-9.
An evidence based review from Unitedstats
America suggested that the probability of
bacterial meningitis presenting as fever and
seizures was 0.45-1.2510. These figures are in
accordance with our findings of 2% CSF
pleocytosis in study cases. It also indicated that
perhaps large number of unnecessary lumbar
punctures was done.
It was seen that in younger age group, there was
significant probability of having meningitis without
signs of meningeal irritation, compared to older
children11.
Over the past 20 years, there have been
significant changes in the incidence of meningitis
in pediatric population. Several authors have
confirmed a dramatic reduction in the incidence
of meningitis since the addition of new vaccines
to the primary course of childhood immunization
in 199212. Bacterial meningitis in the absence of
associated signs (irritability, lethargy, and/ or
bulging fontanalle) is extremely uncommon. In
case series, where this information was recorded,
only four out of a total 30 cases had no
associated meningeal signs at the time of
presentation13.
The hospital management of febrile seizures has
changed dramatically over the past 20 years.
However, there is still a wide variation in practice
between
departments
and
individual
pediatricians in the management of this common
childhood condition. A significant proportion will
undergo lumbar puncture because of perceived
risk of occult meningitis under 1 year of age. Is this
justified? The available data would not support
this practice anymore. The risk of meningitis in the
absence of other clinical signs is extremely small
(less than one in two hundred), even in this age
group. Furthermore, early lumbar puncture is not
a sensitive predictor of meningitis in this group of
patients, missing over 40% of cases if performed
routinely on admission to hospital14.
Recent evidence shows that considering
meningitis in children with convulsions and fever
in the absence of other symptoms and signs is
now questionable.

www.ppa.org.pk

147

The updated AAP guidelines state that lumbar

puncture should be performed when a child with
seizure and fever also has symptoms that suggest
meningitis. These symptoms include neck stiffness
and Kernigs signs and /or Brudzinkskis signs. A
lumbar puncture is an option if an infant aged 6
to 12 months has a seizure and fever but has not
received the recommended immunizations for
Hemophilic
influenza
type
b
(Hib)
or
streptococcus pneumonia or if his or her
immunization status can not be determined.
Lumbar puncture also should be considered
when a child with a seizure and fever has been
pretreated with antibiotics, because antibiotics
can mask the signs and symptoms of meningitis
but may not be sufficient to eradicate it. If it has
been decided to perform a lumbar puncture,
blood culture and serum glucose testing should
be conducted concurrently to determine
whether the hypoglycorrhachia characteristics of
bacterial meningitis is present. Measuring serum
electrolytes,
calcium,
phosphrous,
and
magnesium or complete blood count or blood
glucose should not be routinely performed for
determining the cause of simple febrile seizures.
Likewise, neuroimaging is not necessary when
evaluating a simple febrile seizure in a child15.

CONCLUSION
To conclude, considering the complications of
lumbar puncture in children, if the children do not
have any signs indicating meningitis (decrease in
consciousness
level,
headache,
irritability,
nausea, vomiting), pediatricians could possibly
avoid unnecessary lumbar punctures from being
performed, by observing and monitoring these
patients and regularly examining them in the
early stages, except when other signs of
meningitis are seen.
---------------------------------------------------------------------------Muhammad Saeed, Tahir Nadeem, Samir M. Al-Nufiee
Department of Pediatric Neurologist, P.O.Box 6741.
Childrens Hospital Taif, Kingdom of Saudi Arabia.

REFERENCES
1.

Shinner S. Febrile Seizures. In: Swaiman KF,

Ashwal S, Ferriero DM, editors. Pediatric
neurology; principles and practice. 4th ed.
Vol 1. Philadelphia: Mosby Elsevier; 2006.
p.1078-86.

148

Saeed M, Nadeem T, Samir M. Al-Nufiee

2.

Practice parameters: the neurodiagnostic

evaluation of the child with first simple
febrile seizures. Pediatrics 1996; 97(5): 76972.

9.

Offringa M, Beishuizen A,Derksen-Lubsen G,

et al. Seizures and fever: Can we rule out
meningitis on clinical basis alone? Clinc
Pediatr 1992; 31(9): 514-22.

3.

Nelson KB, Ellenberg JH. Predictors of

epilepsy in children who have experienced
febrile seizures. N Engl J Med 1997;
295(19):1029-33.

10.

Carrol W, Brookfield D. Lumbar puncture

following febrile seizures- a painful pointless
procedure? Arch Dis Child 2002; 87(3): 23840.

4.

Toach SJ, Geil PA. Incidence of bacterimia,

urinary tract infections and unsuspected
bacterial meningitis in children with febrile
seizures. Pediatr Emerg Care 1999; 15(1):912.

11.

Joshi Batajoo R, Rayamajhi A, Mashaseth C.

Children with first febrile seizures. Is Lumbar
puncture necessary? J Nepal Med Assoc
2008; 47(171): 109-12.

5.

Nozicka L. Lumbar puncture and first febrile

simple seizure. Pediatrics 1997; 99(2): 306-07.

12.

6.

Rosenberg NM, Simon JE, Felter R, et al.

Lumbar puncture for first febrile seizure?
Pediatr Emerg Care 1992; 8(5): 300-01.

Petola H, Kipli T, Annttila M. Rapid

disappearance of Haemophilus influenza
type b meningitis after routine childhood
immunizations with conjugate vaccines.
Lancet 1992; 340(8819): 592-94.

13.

Mclntyre PB, Gray SV, Vance JC.

Unsuspected bacterial meningitis in febrile
convulsions. Med Aust 1990; 152(4): 183-86.

14.

Invasive Haemophilus Influenzae. Royal

College of pediatrics and child health.
British Pediatric Surveillance unit. 15th Annual
Report 2000-2001. London; 2001: p.23-25 .

15.

Neurodiagnostic evaluation of the child

with simple febrile seizure. Pediatrics 2011;
127(2): 389-94.

7.

8.

Armon K, Stephen T, MacFaul R, et al. An

evidence and consensus based guidelines
for the management of a child after first
febrile seizure. Emerg Med J 2003; 20(1):1320.
Wears RL, luten RC, Lyons RG. Which
laboratory tests should be performed on
children with apparent febrile seizures? An
Analysis and review of literature. Pediatr
Emeg Care 1986; 2(3):191-96.

www.ppa.org.pk

149

Khan QA, Iqbal H, Rehman RU

ORIGINAL ARTICLE

Pattern of Neonatal Diseases in Special Care Baby Unit

(SCBU) Khyber Teaching Hospital, Peshawar
QAMAR ALI KHAN, HAMID IQBAL, HABIB UR REHMAN

-----------------------------------------------------------------Pak Paed J 2011; 35(3): 149-53

ABSTRACT
Objective: To document the number, disease pattern and outcome of
patients admitted to Neonatal Unit.
Study Design: Descriptive study.
Place and Duration of Study: The study was conducted in the Neonatal
Unit of Department of Child Health, Peshawar, Pakistan from 1st January
2009 to 31st December 2009.
Material and Methods: The data of all Neonatal admission was
recorded and analyzed for age, weight, sex, duration of stay, cause of
admission and outcome.
Authors affiliations
-------------------------------------------Correspondence to:
Qamar Ali Khan,
Department of Child Health,
Khyber Teaching Hospital
Peshawar.

E-mail: ppa.nwfp@hotmail.com

Results: A total of 3203 neonates were admitted from 01-01-2009 to

31-12-2009. Out of these 2142 (66.87%) were male and 1061 (33.1%).
were females. Full term babies were 20414 (75.43%) and premature low
birth weight were 787 (24.57%) of the total admissions. Neonatal
jaundice, neonatal sepsis, prematurity/ low birth weight and birth
asphyxia (HIE) were the main causes of neonatal admissions to the
SCBU. Neonatal jaundice accounted 799 (24.9%) of the total admission
to the unit. Neonatal infections were the next most common cause of
admission 790 (24.66%), followed by birth asphaxia contributed 676
(24.7%). Other causes responsible for admission to our neonatal unit
were infants of diabetic mother 14 (0.43%) congenital heart diseases 12
(0.37%), meningitis 18 (0.56%), pneumonia 50 (1.56%), dysmorphic
features 10 (0.31%), congenital hypothyroidism 02 (0.31%), surgical cases
25 (0.78%) Criglar Najar syndrome 02 (0.06 %). Out of total admission
2717(84.82%) were discharged. and 473(14%) expired. There were
292(9.1%) males and 181(5.6%) female. The common cause of death
was birth asphyxia 148 (21.89%) and prematurity 141 (17.9%), while sepsis
126 (15.4%) and jaundice 47 (5.88% were the other common causes.
Most of the babies 1909 (59.6%) were referred from KTH obstetric ward
labor room and operation theatre while 509(15.8%) were referred from
other hospitals / private maternity and 785 (24.5%) were referred from
other hospitals/private maternity homes and 785 (24.5%) were home
deliveries. Discharge on will was 31 (0.96%) and leave against medical
advice was in 16 (0.49%). Large number of the babies i.e. 1420 (44.2%)
were admitted in first 24 hours of birth.
Conclusion: Birth asphyxia, Low birth weight (LBW), neonatal sepsis were
the major causes of neonatal admission.
Key Words: Disease pattern, outcome, Neonates.

www.ppa.org.pk

150
INTRODUCTION
Neonatology is a part of pediatrics which is
coming up now as a sub-specialty and in near
future will expand more and more as a result of
neonatal screening programs, the availability of
resources for diagnosing different metabolic as
well as congenital problems. Neonatal period
(0 to 28 days of life) is the most dangerous period
of life because of various problems it has to come
across. Most of them may not have any serious
problem or difficulty and will need only minimal
care, which can be provided by the mother if
properly counseled by a health worker. Preterm /
low birth weight babies born to high risk mother
are more prone to have problems1. Most of the
causes of neonatal morbidity in our country are
preventable2. Some of the newborns in
developing countries have an impaired growth
during their intrauterine life, reflecting the
nutritional status of the mother3. Almost half of the
infant deaths in our country occur within first 28
days of life4. Prematurity accounts for majority of
high risk newborns as they face a large number
of problems.5 The prognosis of these neonates
depends upon their underlying condition and its
severity, management and their outcome. For
this purpose neonatal audits are carried out in
Pakistan from time to time in order to create an
awareness regarding the preterm babies and
other neonatal problems which they face and
are managed in an effective way6-8. Neonatal
morbidity and mortality has not decreased due
to the lack of the available resources in
developing countries. This can be decreased by
proper and timely intervention9. For better
neonatal
care
and
prevention
of
the
preventable diseases leading to high neonatal
morbidity and mortality, there should be a proper
and continuous system for audit of neonatal
admission all over the country. The purpose
behind such types of audits in neonatal units
should be the identification of various
deficiencies in the management of these
neonates and also to assist the health workers
especially those at the community level for the
better
understanding
and
effective
management of various neonatal problems in
Pakistan. Inequalities in the provision of health
care are one of the reasons for differences in
neonatal morbidity and mortality. These can be
reduced by proper intervention9. The neonatal
disease pattern changes between different

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Khan QA, Iqbal H, Rehman RU

places, time to time and even of the same

place10-12. Thus, it is necessary for better neonatal
status that we continue to report causes of
neonatal disease from time to time13. The
objective of this study was to document the
number, disease pattern and outcome of
patients admitted to Neonatal unit.

MATERIALS AND METHODS

This was a descriptive study. The data of all the
admitted neonates in Special Care Baby Unit
(SCBU), Khyber Teaching Hospital was recorded
from 1st Jan 2009 to 31st Dec.2009 and analyzed
for age and weight at the time of admission, sex,
duration of stay, cause of admission and final
outcome. The SCBU admits all the babies from
Community and our labour ward. We analyzed
the admission and discussed the data of the year
2009. The following variables were analyzed: age,
weight, sex, duration of stay, reason of admission,
pace of delivery and outcome.
Following terminologies were used in defining
data.
a)
b)

c)
d)
f)
g)
h)
i)

Diagnosis: indication for admission or final

diagnosis.
Preterm: according to WHO definition new
born baby delivered before completed 37
weeks of gestation, from 1st day of last
menstrual period.
Low birth weight: weight < 2500 gm.
Neonatal jaundice: diagnosed by assessing
of serum bilirubin level, blood grouping and
estimation of G6PD.
Sepsis: diagnosed on clinical sign symptom
and positive blood culture.
Congenital heart disease: diagnosed on the
bases of clinical signs, ECG, Echo
cardiography and chest x ray.
Birth asphyxia: diagnosed clinically on the
basis of APGAR scoring in hospital delivery,
history, physical examination, cranial U/S.
Tracheoesphagel
atresia
with
fistula:
diagnosed by passing radiopaque dye
through nasogastric tube followed by x-ray.

RESULTS
A total of 3203 neonates were admitted
from 01-01-2009 to 31-12-2009. Out of these 2142

Pattern of Neonatal Diseases in Special Care Baby Unit, Khyber Teaching Hospital, Peshawar

(66.87%) were male and 1061 (33.1 %) were

females (table 1). The table 2 gives the ratio of
the full term and low birth weight babies. Full term
babies were 2416 (75.43%) and premature/low
birth weight were 787 (24.57%) of the total
admissions. Table 3 shows the age at admission.
Most of the babies were admitted in first 24 of
age. The numbers of babies of age less than 24
hour were 1420 (44.20%), 24 to 96 hours were 660
(20.20%), 4 to 7 days were 593 (18.51%) and 14 to
28 days were 129 (4.02%). The babies admitted
below 1000gm were 15 (1.56%), 1000 to 1500 gm
were 228 (10.22%), 1500 gm to 2500 gm babies
were 567 ((17.70%), 2500 to 3500 gm were 2100
(65.80%) and having weight >3500 gm were
(6.02%) (table 4). The table 5 indicates duration of
hospital stay of the admitted babies. It was less
than 24 hours in 893 cases, 24 to 48 hours in 1183,
72 to 96 hour in 387, 4 to 7 days in 195 and 7 to 14
days were 26. Table 6 indicates the causes of
admission to the unit during the study period.
Neonatal
jaundice,
neonatal
sepsis,
prematurity/low birth weight and birth asphyxia
with hypoxic ischemic encephalopathy were the
main causes of admissions to the SCBU. Neonatal
jaundice accounted for 799 (24.9%) of total
admission to the unit. Neonatal infections were
the next commonest cause of admission and
cases having sepsis were 790 (24.66%). It was
followed by birth asphyxia which contributed to
676 (24.7%) cases. Other causes responsible for
admission to our neonatal unit were infant of
diabetic mother 14 (0.43%), congenital heart
disease 12 (0.37%), meningitis 18 (0.56%),
pneumonia 50 (1.56%), dysmorphic babies 10
(0.31%), hypothyroidism 02 (0.31%), surgical
conditions 25 (0.78%) and Criglar Najar syndrome
02 (0.06 %). The table number 7 shows the
outcome of the major neonatal diseases. Out of
total admission 2717 (84.82%) were discharged
and 473 (14%) expired (there male were 292
(9.1%) male babies and 181 (5.6%) female
babies). The common cause of death was birth
asphyxia 148 (21.89%) and prematurity 141
(17.9%), while sepsis in 126 (15.4%) and jaundice
in 47 (5.88%) were the other common causes.
Most of the babies 1909 (59.6%) were referred
from Khyber Teaching Hospital obstetric ward
labor room and operation theatre while 509
(15.8%) were referred from other hospitals/private
maternity homes and 785 (24.5%) were home
deliveries. Discharge on will was in 31(0.96%)

151

cases and those who left against medical advice

were 16 (0.49%) in number.
TABLE 1:- Male: Female (n=3203)
Sex

Number

Percentage

2142
1061

66.87
33.10

Male
Female

TABLE 2:- Term: Preterm/ Low birth (n=3203)

Gestation
Term
Preterm

Number
2416
787

Percentage
75.43
24.57

TABLE 3:- Age at time of admission (n=3203)

Percentage
Age
Number
<24 h
1420
44.20
24-96 hour
660
20.20
4-7 days
593
18.51
7-14 days
401
12.50
14-28 days
129
4.02
TABLE 4:- weight at time of admission (n=3203)
Weight in gm
<1000 gm
1000-1500gm
1500-2500gm
2500-3500gm
3500-400 gm and above

Number
15
228
567
2100
193

Percentage
1.56
10.2
17.70
65.56
6.02

TABLE 5:- Hospital Stay of the admitted Babies (n=3203)

Duration of stay
<24 hour
24-48 hour
72-96 hour
4-7 day
7-14 day

Number of patients
893
1183
387
195
26

TABLE 6:- Causes of admission in SCBU (n=3202)

Disease
NNJ
Neonatal Sepsis
Low birth wt/premature
Birth asphyxia HIE
Infant of Diabetic mother
IDM
Surgical
Congenital heart Disease
Meningitis
Dysmorphism Features
Hypothyroidism
Criglar najar syndrome
Pneumonia

Number
799
790
787
676
14
25
12
18
10
02
02
50

Percentage
24.94
24.66
24.57
21.10
0.43
0.78
0.37
0.56
0.31
0.06
0.06
1.56

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Khan QA, Iqbal H, Rehman HU

152
TABLE 7:- Out come of the admitted cases (n=3203)
Disease
Neonatal Jaundice
Sepsis
Premature/low birth weight
Birth Asphyxia
Surgical
Congenital heart Disease
IDM
Meningitis
Pneumonia
Dysmorphism
Hypothyroids
Criglar najar

Total Number
799
790
787
676
25
12
14
18
50
10
02
02

DISCUSSION
In our study most of the babies were admitted
with in 1st 24 hours of life (44.1 %). The other study
conducted at different cities of the country shows
that 33.61% admitted during first 24 hour at NIH
Karachi10, 44.7% in Chandka Medical College
Larkana8 and 75% at Childrens Hospital Lahore11.
These figures show the majority of neonatal
problems occur in the 1st 24 hours of life, the male
predominance at admission is consistent with
other studies from different cities of the country.
Low birth wt and very low birth wt are the major
contributor to neonatal mortality and morbidity.
In our study 24.57 % were low birth wt/preterm
which seems to be high when compared to other
studies, Chandka Medical College Larkana8 36%,
children hospital Lahore11 39% and NIH Karachi10
55.4% while much less were reported in
Bangladesh14 13.2%, Ethiopia 13.25%15 and India16
20%.. LBW admission may possibly be due to poor
maternal nutrition and poor access to antenatal
care because majority of the mother are severely
anemia, short stature and malnourished10. These
factors were also reported in Ethiopia15. In our
study 84.82% neonates were discharged
satisfactorily after receiving the necessary
treatment. This high percentage could be due to
increase awareness among heath workers and
provision of all possible management in spite of
limited resources. 0.96% neonates were sent
whom on request of their attendants/parents
while 0.49% left against medical advice (LAMA).
This low percentage shows increase awareness
among parents to aware the opportunities of
hospital stay for the better management of their
babies.5 9.6% were refer from hospitals,15.8% in

www.ppa.org.pk

Discharge
Expired
Percentage
752 (94.11%
47
5.88
664 (84.05%)
126
15.94
646(82.08%)
141
17.91
528(78.10%)
148
21.89
All were return to surgical and could not follow
10 (83.3%)
02
16.60
11(78.78%)
03
21.00
16 (88.8%)
02
11.11
46 (92%)
04
8.00
9 (90%)
01
10.00
02 (100%)
0
0.00
02 (100%)
0
0.00

private maternity while home delivery were

24.5%. Infection remains one of the major
problems in neonatal period. It is the leading
cause of neonatal admission after jaundice at
SCBU. It also contributes to morbidity and
mortality17 in the developing countries. In our
study 24.66% babies were admitted with sepsis as
compare to 45.21% reported from NIH Karachi10,
47.3% in Peshawar6 and 21.10% from Mayo
Hospital, Lahore18. Predisposing factors were due
to poor obstetric care, delivery by untrained
persons and poor access to health facilities.
Unhygienic delivery and poor neonatal care18.
The increased ratio of infection may be one of
the major contributing factors for Low Birth
Weight and can result from an infection the
mother had a poor blood flow to the uterus. The
strong co-existence among Low Birth Weight and
sepsis in our study is also reported from other
cities9,13.
Neonatal jaundice was responsible for the 24.4%
neonatal admission in our series as compare to
13.15% from NIH Karachi10 8.33% from Childrens
Hospital Lahore11 and 3.5% Chandka Medical
College Larkana8. It was reported high (30.71%)
from Bangladesh14. In 1983 Jaundice was
reported, was the leading cause of neonatal
admission in Pakistan19 and it was about 30%. This
change in percentage of neonatal admission to
jaundice could be due to the changing pattern
of neonatal disease with geographical variation
from time to time8. The average Pakistani women
are anemic, malnourished, short stature,
contributing to increased chances of cephalic
pelvic disproportion and prolong labour leading
to birth asphyxia. In our study birth asphyxia was

Pattern of Neonatal Diseases in Special Care Baby Unit, Khyber Teaching Hospital, Peshawar

the 3rd major cause of admission 676(21.10%)

while it was 40.66% at Chandka Medical College
Larkana8, 31% at Children Hospital Lahore11 and
18.85% NIH Karachi10. Our results are slightly better
when compared with the above studies. This
could be due to timely referral and resuscitation
at the time of birth. In our study 84.82 % baby
were discharged home satisfactory after
receiving necessary treatment. This high
percentage could be due to increased
awareness among health workers specially LHWs
and provision of all possible management in spite
of our limited resources. Neonatal mortality in our
study is 14% and it was high i.e. 25.85 % at NIH
Karachi10, 34% at Children Hospital Lahore11 and
38 % at Chandka Medical College Larkana10. The
neonatal mortality could be contributed to their
critical condition at the time of admission. The
commonest cause of death was birth asphyxia
148 (21.89%) followed by low birth wt/Prematurity
141-(17.91%) and sepsis 126(15.94%), while sepsis
was the major cause of death in NIH Karachi10
(46.4%). Mortality from birth asphyxia and pre
maturity with the similar figure reported from
India16. The highest neonatal death due to birth
asphyxia and prematurity in our study reflects the
increase work load, lack of staff, equipment and
also poor antenatal care. The antenatal care,
monitoring of fetus during delivery and in time
referral may reduces the high mortality rate.
Mortality from birth asphyxia reported from
Childrens Hospital Lahore11 is 40%, antenatal
monitoring of high risk pregnancy, timely referrer
and resuscitation at the time of birth at all level is
mandatory to reduce high case fatality and
morbidity related to birth asphyxia 20.

CONCLUSION
Neonatal jaundice, low birth weight, asphyxia
and sepsis were the major causes of admission in
our study. Therefore it should be a part of overall
preventive strategy towards reducing neonatal
morbidity and mortality. This goal can be
achieved by proper and affective intervention by
community mobilization and participation.

2.

Bhutta ZA. Priorities in newborn care and

development of clinical neonatology in
Pakistan: where to now? J Coll Physician
Surg Pak 1997; 7: 231-34.

3.

Yinger NV, Ransom EI. Why invest in

newborn health? Policy perception on
newborn Health 2003. Washington DC: Save
the children; 2003.

4.

Chaudhry IJ, Chaudhry NA, Hussain R, et al.

Neonatal septicemia. Pak Postgrad Med J
2003; 14(1):18-22.

5.

William W. Current pediatric diagnosis and

treatment.
Sixteen
Ed.
McGrawHill/Appleton
&
Lange:
McGrawHill/Appleton & Lange; 2003; 1-63 (2a).

6.

Roghani MT, Mohammad T. Neonatal

disease profile in NWFP. An analysis of four
years admissions. Pak Pediatr J 1983; 7: 1722.

7.

Haneef SM, Tabssum S, Qureshi Z, llahi S.

Pattern of neonatal disease, Pak Pediatr J
1985; 9: 42-50.

8.

Abbasi KA. Neonatal disease profile in

Larkana before and after establishment of
neonatal Ward. J Pak Med Assoc 1995; 45:
235-36.

9.

Jamal M, Khan N. Neonatal morbidity and

mortality in high risk pregnancies. J Coll
Physician Surg Pak 2002; 12(11): 657-61.

10.

Parkash J, Das N. Pattern of admission to

neonatal unit. J Coll Physician Surg Pak
2005; 15(6): 341-44.

11.

Chishti AL, Iqbal MA, Anjum A, et al. Risk

factor analysis of birth asphyxia at the
Childrens hospital, Lahore. Pak Pediatr J
2002; 26(2): 47-53.

12.

Wu Z, Viisainen K, Wans Y, et al. Perinatal

mortality in rural China:
retrospective
cohort study. BMJ 2003; 327 (7427):: 1319.

13.

Butt TA, Kazir MY, Bhatti MT, et al. Evaluation

of risk factor and Supportive investigation in
the diagnosis of neonatal sepsis. Ann KE
Med Coll 2002; 8(4): 292-94.

14.

Islam MN. Situation of neonatal health in

Bangladesh. The Orion [Internet]. 2000 May
[cited 2011 May 20]; 6: Available from:

REFERENCES
1

Parthasarathy A. Text book of Pediatrics,

2nd Edition 2002; 42-73p.

153

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Khan QA, Iqbal H, Rehman HU

154
http://www.orion-group.net/journals/
Journals/Vol6_May2000/start.htm

south-Eastern Nigeria. J Perinat Med 2006;

34(2): 166-72.

15.

Gebremariam A. Factors predisposing to

low birth weight in Jammu Hospital South
Western Ethiopia. East Afr Med J 2005;
82(11): 554-58.

18.

Ejaz I, Khan HI, Baloch GR. Neonatal

mortality reports from a tertiary hospital in
Lahore/causes and outcome. Pak Pediatr J
2001; 25: 35-38.

16.

Thora S, Awadhiya S, Chansoriya M, Kaul KK.

Perinatal and infant mortality in urban
Slums under IUCD scheme. Indian Pediatr
1996; 33: 19-23.

19.

Arif MA, Jaundice in newborn. Pak Pediatr J

1983; 7: 37-43.

20.

Shah GS, Singh R, Das BK. Outcome of

newborn with birth asphyxia. J Nepal Med
Assoc 2005; 44(158):44-6.

17.

Ojukwu JU, Abonvi LE, Ugwn J, et al.

Neonatal septicemia in high risk babies in

www.ppa.org.pk

PAKISTAN PAEDIATRIC FORUM

DENGUE FEVER GUIDELINES: ITS CONTROVERSIES

ABDUL REHMAN, HUMAYUN IQBAL KHAN

-----------------------------------------------------------------Authors affiliations
-------------------------------------------Correspondence to:
Abdul Rehman,
Department of Paediatrics,
Quaid-E-Azam Medical,
College, Bahawalpur.
E-mail:
drarehman100@yahoo.com

Pak Paed J 2011; 35(3): 155-62

ABSTRACT

Pakistan is confronting increasing incidence of dengue infection. The

Government of the Punjab (Pakistan) published guidelines for the
management of dengue fever in September 2011. These guidelines
resemble those published by World Health Organization, Regional Office
for South-East Asia in 2011 but are not the same as those recommended
by World Health Organization, Geneva 2009. The purpose of this review
is to discuss the scientific justifications of these guidelines and disease
classification in the light of available research.
Key Words: Dengue fever; Dengue hemorrhagic fever; Dengue Shock
Syndrome; Severe dengue; Crystalloids: Dextran; Hydroxyethyl starch;

INTRODUCTION
Pakistan, like other countries especially of South
East Asia, is confronting increasing incidence of
dengue infection. Dengue virus is now endemic
in Pakistan, circulating throughout the year with a
peak incidence in the post-monsoon period.
Median age of dengue patients has decreased
and younger patients may have become more
susceptible1. The Government of the Punjab
(Pakistan) in collaboration with the Sri Lanka
College of Pediatricians published guidelines for
the management of dengue fever in September
20112 which are nearly the same as those
published in Sri Lanka in December 20103 and
those published by World Health Organization,
Regional Office for South-East Asia in 20114. These
are not the same as those recommended by
World Health Organization, Geneva 20095. The
reasons of these controversies include; lack of
animal model for research, most of the studies
are conducted in low resource countries, and
there is very limited knowledge available which is
based on personal experience and is not
evidence based. In addition there are ethical
issues due to research on humans. The purpose of
this review is to discuss the scientific justifications

of guidelines and disease classification published

by the Government of the Punjab (Pakistan) in
the light of available research.

CLASSIFICATION
Many dengue cases are self-limiting but
complications such as hemorrhage and shock
can be life-threatening. If untreated, mortality
from the complications of dengue is as high as
20%, whereas if recognized early and managed
properly, mortality is less than 1%6; hence, it will
be useful if certain symptoms, signs, and
laboratory parameters associated with the
development of complications are identified so
that such cases may receive more attention.
The World Health Organization (WHO) case
classification of dengue into dengue fever
(DF)/dengue haemorrhagic fever (DHF)/dengue
shock syndrome (DSS) was formulated by the
Technical Advisory Committee at its meeting in
Manila, Philippines in 1974 and updated in 1997
(shown in fig 1). Several criticisms have been
raised against the case definition of DHF. It is
argued that the case definition of DHF is too rigid
and too difficult to apply in primary care or

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Rehman A, Khan HI

resource limited settings. The application of WHO

1974 classification of dengue fever in children in
various countries like India showed that all the
four features of DHF may not be present and
such cases might be fatal as well. So this case
definition failed to identify a significant proportion
of DF/DHF7-10. Moreover severe manifestations,
such as encephalopathy and hepatic failure,

were not included in the DHF case definition. It

was questioned whether the case definitions,
which were developed primarily on the basis of
data derived from pediatric cases in southeast
Asia, were applicable to other regions and
populations11. Consequently, a new clinical
classification of dengue disease was published in
the most recent WHO guideline3.

The WHO Classification

(1975, 1997)

Asymptomatic
Dengue

Dengue
Infection
Symptomatic
Dengue Infection

Undifferentiated
Fever

Dengue Fever

Fever with 2 of the

following:
Headache
Arthritis
Retro-orbital pain
Rash
Myalgia
Hemorrhage
Manifestations
Leukopenia and
Supportive
Serology
or
Occurrence of the
same location
and time as other
confirmed
dengue cases

Without
Hemorrhage

With
hemorrhage

Without
Shock

Dengue
Hemorrhage Fever

All 4 components must

be met
Fever
Hemorrhage
Manifestations
Thrombocytopenia
Evidence of
plasma leakage

Dengue
Shock
Syndrome

4 criteria for
DHF
Evidence of
circulatory
failure
Rapid and
weak pulse
Narrow pulse
pressure (<20
mm/Hg) or
hypotension for
age
Cold clamy skin

Fig 1:- The WHO classification 1975, 1997

The new WHO 2009 guidelines classified dengue
as dengue (without or with warning signs) and
severe dengue as shown in fig 2. The 2009 clinical
classification represents a significant departure
from the prior classification. In contrast to the

www.ppa.org.pk

previous classification, which defined DHF as a

clinical entity with plasma leakage as the
cardinal feature that differentiated it from DF, the
2009
classification
lists
several
clinical
manifestations as qualifiers for severe dengue.

DENGUE + WARNING SIGNS

SEVERE DENGUE

With warning

Without

1.
2.

sings

3.

CRITERIA FOR DENGUE + WARNING SIGNS

Probable dengue
Live in/travel to dengue endemic
area.
Fever and 2 of the following
criteria:

Nausea, vomiting

Rash

Aches and pains

Tourniquet test positive

Leukopenia

Any warning sing

Laboratory confirmed dengue
{important
no
sing
plasma
leakage}

Severe plasma leakage

Severe hemorrhage
Severe organ impairment

CRITERIA FOR SEVERE DENGUE

Warning signs*
Abdominal pain or tenderness

Severe plasma leakage

Leading to:

Persistent vomiting
Clinical fluid accumulation
Mucosal bleed
Lethargy, restlessness
Liver enlargement >2 cm
Laboratory: increase in HCT
concurrent with rapid decrease
in platelet count

Shock (DSS)
Fluid
accumulation
with
respiratory distress
Severe bleeding
As evaluated by clinician
Severe organ involvement
Liver: AST or ALT>=1000
CVS: Impaired consciousness
Heart and other organs

*{requiring strict observation and

medical intervention}

Fig 2:- The Who classification 2009

The improvement in dengue-associated mortality
over the past decades has been based on the
understanding of the natural history of plasma
leakage in DHF, which occurs around the time of
defervescence and coincides with the nadir of
the platelet count and a 20% rise in hematocrite.
Delayed detection and treatment of plasma
leakage is the major cause of organ failure, listed
as severe manifestations in the 2009 classification.
The presence of severe organ involvement as a
criterion for severity separate from plasma
leakage in the revised classification places
emphasis on isolated organ failure as a common
and significant cause of dengue severity. With
the exception of liver failure severe organ
impairment in the absence of plasma leakage is
very rare. This may reduce the emphasis on the
most important aspect of dengue disease and
the major factor contributing to fatality. Moreover
it seems 2009 classification is less specific as
compared to previous one resulting in over
diagnosis especially in areas where it is
uncommon11. A recent multicentre study in 18

countries on usefulness and applicability of the

revised dengue case classification showed that
13.7% of dengue cases could not be classified
using
the
DF/DHF/DSS
classification
by
experienced reviewers as compared to only 1.6%
with the revised classification. Moreover,
acceptance and perceived user-friendliness of
the revised system was high, particularly in
relation to triage and case management12.
Basuki et al showed in 2010 that revised dengue
classification system was better in detecting
severe dengue infections than the previous WHO
classification system13. In brief, none of the
classification is ideal but revised classification is
better than previous one especially in areas
where Dengue infection is endemic.

DENGUE
FEVER
VERSUS
HAEMORRHAGIC FEVER

DENGUE

The pathogenesis of dengue is complex and

multifactorial14. During the acute phase of illness

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158
the virus is present in the blood and its clearance
from this compartment generally coincides with
defervescence. Humoral and cellular immune
responses are considered to contribute to virus
clearance via the generation of neutralizing
antibodies and the activation of CD4+ and CD8+
T lymphocytes. In addition, innate host defence
may limit infection by the virus. After infection,
serotype specific and cross-reactive antibodies
and CD4+ and CD8+ T cells remain measurable
for years5,15. The hypothesis of antibody-mediated
enhancement is not sufficient to explain the
development of severe disease (DHF). The
pathogenesis of severe dengue is not well
understood and more than one mechanism may
be involved. It is the interplay between virus
factors and genetically determined host factors
that determine the disease outcome in the
individual patient14. It has been observed that the
risk of severe disease is increased at least 15-fold
during secondary
compared to primary
infections. Various mechanisms have been
suggested,
including
antibody-dependent
enhancement, complement activation by virusantibody complexes and T-cell mediated
immunopathology. Differences in virulence of
viral genotypes have also been suggested to
explain the pathogenesis of severe dengue5,16-17.
It has been extremely difficult to measure the
contribution of viral genetics to dengue disease
presentation in humans mainly because there
have been no adequate models of disease. It is
very difficult to say that DF and DHF are two
different clinical conditions2 or the same clinical
condition with varying severity5,18. The endothelial
cell activation may mediate plasma leakage
which seems to be functional rather than
destructive
effects
on
endothelial
cells.
Thrombocytopenia may be associated with
alterations in megakaryocytopoieses by the
infection and increased peripheral consumption.
Hemorrhage
may
be
due
to
the
thrombocytopenia and associated platelet
dysfunction
or
disseminated
intravascular
coagulation. These changes are mostly transient
and reversible and occur in severe dengue4,5.

PHASES OF DENGUE INFECTION

The natural history of dengue infection should be
understood for proper management of the
disease. There are three phases of dengue

www.ppa.org.pk

Rehman A, Khan HI

infection febrile phase, critical or leaking phase

and convalescent phase.
Febrile phase: This phase is seen both in DF and
dengue DHF. It lasts for 2 to 7 days and is
characterized by fever, headache, retrorbital
pain, myalgia, arthralgia, nausea, vomiting and
rash. There may be mild hemorrhagic
manifestations,
leucopenia
and
mild
thrombocytopenia.
Presence
of
tender
hepatomegaly favours the diagnosis of DHF.
Critical phase: This is seen only in DHF and is
characterized by evidence of plasma leakage.
Its onset is around 5th or 6th day of illness (may be
as early as 3rd day of fever). There is
defervescence, sudden drop in platelet count
and rise in hematocrit (> 20% of the baseline).
There may be ascities and/or pleural effusion
(more commonly on right side). These features
are indicative of plasma leakage. In addition
there may be decrease in serum alburm less than
3.5 mg/dL and non-fasting serum cholesterol less
than 100 mg/dl. The phase generally last for 24 to
48 hours with gradually increasing plasma leak in
the first half of the phase and decreasing plasma
leak in the second half. Some patients may
develop shock (Dengue Shock Syndrome DSS)
which manifests by sweating, abdominal pain,
persistent
vomiting,
restlessness/altered
consciousness level, postural dizziness, decreased
urine output (< 0.5 ml/kg/hour), cold extremities,
prolonged capillary refill time > 2 seconds,
unexplained tachycardia, tender hepatomegaly
> 2cm, increasing diastolic pressure, narrowing of
pulse pressure < 200 mmHg, postural drop > 20
mmHg of systolic blood pressure, hypotension
(from patients baseline).
Convalescent or recovery phase: This phase lasts
for 2 to 5 days after the critical phase in DHF and
febrile phase in DF. There is improved general
wellbeing,
improved
appetite,
dieresis,
stabilization of hematocrit, and rise in white cell
count and latter platelet count. There may be a
generalized
convalescent
rash
which
is
erythamatous with clear areas (islet of white in
sea of red) with marked itching.

FLUIDS
Fluid management in dengue is difficultthe
balance between too much and too little is
critical and getting it wrong can be life-

159

Dengue Fever Guidelines: Its Controversies

threatening. Fluid resuscitation is not without risk

and fluid overload in the recovery phase can
cause acute respiratory distress syndrome.
Type of Fluid: The published studies comparing
fluid resuscitation with crystalloid or colloidal
solutions in dengue hemorrhagic shock in
children were conducted in settings with poor
resources. The studies are poorly designed19.
There are four studies including three trials
conducted in children with DSS in Vietnam20-22
while the fourth trial in the Philippines23. The trials
reported a superior efficacy of colloids over
crystalloids for resolution of severe shock, with
faster restoration of cardiac index and
normalisation of packed cell volume or blood
pressure, or both. Cifra et al 200323 compared 6%
hydroxyethyl starch (Haes-Steril) with Ringers
lactate. Dung et al 199920 and Ngo et al 200121
compared between dextran 70, 3% gelafundin,
Ringers lactate and normal saline in a bolus of
20ml/kg over1 hour and10ml/kg over 2nd hour
while Wills in 200522 compared the group with
moderate shock (pulse pressure >10 and 20 mm
Hg) with dextran 70, 6% hydroxyethyl starch or
Ringers lactate while in other group with severe
shock (pulse pressure <10 mm Hg) compared
with dextran 70 or starch. The first bolus given was
15ml/kg over1 hour and 2nd 10ml/kg over 2nd
hour. In children with dengue who received
dextran 70 developed signs of severe reactions
(which included fever and rigors without
cardiorespiratory compromise) in 8% cases, while
0.5% children who received starch (6%
hydroxyethyl starch) developed an afebrile event
with an urticarial rash22. In another dengue trial
9% children who received gelatin polymer
(gelafundin) and one (1/70) who received
dextran developed allergic reactions but without
signs of cardiovascular compromise21.
Kalayanarooj in 2008 showed that 10% Haes-steril
was as effective as dextran-40 in the treatment of
DHF patients who have severe plasma leakage.
Both colloidal solutions were safe in DHF patients
with no allergic reaction observed and no
interference in renal functions and hemostasis
and the average drop in hematocrit after the
bolus dose of both colloid i.e. dextran or HaesSteril was 7.9 and 8.5% (p = 0.381)24. Wills et al
(2005) showed that dextran 70 and 6%
hydroxyethyl starch perform similarly in children
with severe shock22.

There is substantial evidence indicating that

colloids are better than crystalloids for treating
severe shock (defined as pulse pressure
10mmHg) in dengue septic shock, but both
have similar efficacy in moderate shock. As
severe shock in dengue septic shock is much less
common than moderate shock, crystalloids
remain the mainstay for treatment of this
condition (20-22,25. All the three types of colloids
may be used but preference should be given
either to 6% hydroxyethyl starch or dextran. The
dextran 40 as colloid of choice by the
Government of the Punjab (Pakistan) guidelines
for the management of dengue fever2 is not
evidence based. There is no clinical data
available that can discuss the maximum amount
of colloid to be given in DSS.
Commonly available artificial colloids in Pakistan
include dextran 70 (Plasmax-70), succinylated or
modified fluid gelatins (Gelofusine 4%, Gelofundin
3%) or urea-crosslinked gelatins (polygeline in the
form of Haemaccel or Plasma Plus 3.5%) and
hydroxyethyl starch (Haes-Steril 2000/0.5 as 3%,6%
and 10%). There is need to study the best type of
fluid tested by randomized control trials recruiting
patients with severe DSS who have already
developed third space fluid accumulation26.
Amount of Fluid:
There are no clinical studies available to
calculate amount of fluid required during the
critical period. The Government of the Punjab
(Pakistan) guidelines2 calculates total fluid as
maintenance + 5% to given during critical
period (24 to 48 hours). This is based on Sri Lankan
guidelines (Fig 3). These recommendations may
be used in most of the cases but clinical studies
are needed. The best methods for titrating fluid
therapy and detecting early signs of hemorrhage
are repeated, meticulous, clinical evaluation in
conjunction with analysis of serial hematocrit
trends by experienced caregivers. The end
points/targets of fluid administration are
normalization of the systolic BP (if low) and
obtaining a pulse pressure of 30 mm Hg, a urine
output of 0.51 mL/kg/hr with stable vital signs,
and a gradual decrease in the elevated baseline
hematocrit level avoiding fluid overload22,27-28.
Monitoring hourly urine output serves two
important goals: an output of 0.51.0 mL/kg/hr
with stable vital signs indicates shock reversal and
ensures a minimal acceptable circulating

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160

Rehman A, Khan HI

and clinical features of dengue fever in

Pakistan from 2003-2007: a retrospective
cross-sectional study. PLoS One [Internet].
2010 Sep 13 [cited 2011 Aug 14]; 5(9):
12505.
Available
from:
http://www.
plosone.org/article/info%3Adoi%2F10.1371%
2Fjournal.pone.0012505.

volume, whereas an output of >1.52 mL/kg/hr

may be the earliest indicator of over hydration
with the potential risk of respiratory insufficiency28.
Total fluids for 48 hrs (oral + intravenous)
Maintenance + 5% deficit.
Maintenance
For 1st 10 kg = 100 ml/kg
For 2nd 10 kg = 50 ml/kg
From 20 kg to 50kg = 20 ml/kg
5% Deficit

2.

Guidelines on Management of Dengue

Fever and Dengue Haemorrhagic Fever in
Children and Adolescents, Government of
the Punjab (Pakistan) - The Children Hospital
& the Institute of Child health. Lahore;
September 2011.

3.

Guidelines on Management of Dengue

Fever and Dengue Hemorrhagic Fever in
Children and Adolescents, Ministry of Health
- Sri Lanka in Collaboration with the Sri
Lanka College of Paediatricians. December
2010

4.

Comprehensive guidelines for prevention

and control of dengue and dengue
hemorrhagic fever. Revised and expanded
edition, Delhi: World Health Organization,
Regional Office for South-East Asia; 2011.
SEARO Technical Publication Series No. 60.

5.

Dengue: guidelines for diagnosis, treatment,

prevention and control. 2nd edition,
Geneva: World Health Organization; 2009.
Report No.: WHO/HTM/NTD/DEN/2009.1.

6.

WHO report on global surveillance of

epidemic
prone
infectious
diseases.
Geneva: World Health Organization; 2005.

7.

Gupta P, Khare V, Tripathi S, et al.

Assessment of World Health Organization
definition of dengue hemorrhagic fever in
North India. J Infect Dev Ctries 2010; 4(3):
150-55.

8.

Phuong CX, Nhan NT, Kneen R, et al. Clinical

diagnosis and assessment of severity of
confirmed dengue infections in Vietnamese
children: is the world health organization
classification system helpful? Am J Trop
Med Hyg 2004; 70(2): 172-79.

9.

Setiati TE, Mairuhu AT, Koraka P, et al.

Dengue disease severity in Indonesian
children: an evaluation of the World Health
Organization classification system. BMC
Infect Dis [Internet]. 2007 March 26 [cited
2011Aug 22]; 7: 22. Available from:
http://www.biomedcentral.com/content/p
df/1471-2334-7-22.pdf

50 ml/kg upto 50 kg

Fig 3:- Fluid calculation in critical phase of

D.H.F. (Based on Sir Lanka Guidelines3)
Glucose in the intravenous fluids: Both
hyperglycaemia and hypoglycaemia may occur.
These may be transient or may persist. The study
conducted in Bangladesh in adults during
dengue fever showed that 21.1% had diabetes
while 54.1% had impaired glucose tolerance.
These findings warrants for avoidance of dextrose
infusions as fluid replacement in dengue fever29
Correction of acidosis: There are no clinical
studies available to answer when to correct
acidosis with sodium bicarbonate in dengue
fever. The Government of the Punjab (Pakistan)
recommends
to
use
sodium
guidelines2
bicarbonate if blood pH is <7.35 together with
HCO3 level < 15mmol/l but WHO guidelines 200934
recommends its use if pH is <7.15. There is
standard teaching to avoid sodium bicarbonate
for metabolic acidosis in most of the critical
conditions if pH 7.15 as it is not a safe drug. It is
better to avoid sodium bicarbonate if pH 7.15
unless we have evidence against it.
CONCLUSION:
There is need in the modification of guidelines
published by the Government of the Punjab
(Pakistan) for the management of dengue fever
and establishment of research center.
------------------------------------------------------------------------Authors affiliations
Abdul Rehman
Department of Paediatrics, Quaid-E-Azam Medical
College, Bahawalpur.
Prof. Humayun Iqbal Khan
Department of Paediatrics, Postgraduate Medical
Institute/Lahore General Hospital, Lahore

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Alexander N, Balmaseda A, Coelho IC, et

al. Multicentre prospective study on
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Ngo NT, Cao XT, Kneen R, et al. Acute

management of dengue shock syndrome:
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Comparison of three fluid solutions for
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Engl J Med 2005; 353(9): 877-89.

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of the efficacy of 6% Haes-Steril and
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solutions in dengue hemorrhagic fever
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replacement in infants with dengue
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hemodynamic, clinical, and laboratory
variables: A pilot study. Pediatr Emerg Care
2007; 23(3): 36875.

29.

Hasanat MA, Ananna MA, Ahmed MU, et al.

Testing blood glucose may be useful in the
management of dengue. Mymensingh
Med J 2010; 19(3): 382-85.

www.ppa.org.pk

PAKISTAN PAEDIATRIC FORUM

Pakistan Cardiac Society Guidelines for Prevention of

Rheumatic Fever and Rheumatic Heart Disease
NAVEED AKHTAR, MASOOD SADIQ, FAIZ UL HASSAN RIZVI, Haseena Chagani, Asad Hafeez,

Adnan Gul, Madeeha Hina

-----------------------------------------------------------------Pak Paed J 2011;35(3): 162-68

INTRODUCTION
Rheumatic fever (RF) is an inflammatory disease
mediated by humoral and cellular auto-immune
response that occurs as delayed sequelae of
group A beta-hemolytic streptococcal infection
of the throat1. It affects the connective tissue
particularly in the heart, joints, skin and nervous
system2. Rheumatic Heart Disease (RHD) is a
crippling disease and is the most common
cardiovascular disease in children and young
adults and remains a major public problem in
developing countries3. Poor housing conditions
and over-crowding remain major contributing
factors in facilitating the spread of group A betahemolytic streptococci4.
RF and RHD cannot be separated from each
other from epidemiological point of view. Recent
data from Pakistan has shown a very high
prevalence of RHD in both urban and rural
population. In a large cross-sectional survey,
conducted on more than 25000 urban school
going children from inner Lahore using
echocardiography to confirm the cardiac lesion,
has estimated a prevalence of 22/10005. A study
from Rahim Yar Khan from a rural area showed a
prevalence rate of 5.7/1000. Less than 20% of the
patients were aware of their diagnosis and only
8% were taking rheumatic fever prophylaxis6.
Programs ensuring intense secondary prophylaxis
and primary prevention, have attained relevant
decrease in mortality, prevalence, incidence,
hospital admission and severity of RF/RHD in the
developing world7.
The Scientific Council of Pakistan cardiac Society
has extensively reviewed the current evidence
based data on Rheumatic Fever to update the
guidelines for Pakistan. The main objective of

www.ppa.org.pk

these guidelines is to identify and present the best

evidence for practice of ARF diagnosis and
prophylaxis.

DIAGNOSIS OF RHEUMATIC FEVER

There is no specific clinical or laboratory test for
the diagnosis of Acute Rheumatic Fever (ARF)8.
The Jones criteria for the diagnosis of ARF first
introduced in 19449 divides the clinical features of
ARF into major and minor manifestations and has
been periodically modified and updated10.
It has been proposed that two levels of Jones
Criteria may be appropriate: the present or
perhaps, even stricter version for countries where
Rheumatic Fever is uncommon, and separate
criteria for countries, with high rates of Rheumatic
Fever.
Recent Advance in Echocardiographic Diagnosis of RF:

In 2004 World Health Organization Expert

Consultation
Report
stated
that
echocardiographically diagnosed, clinically silent
rheumatic
valve
involvement
should
be
managed as rheumatic heart disease until
proved otherwise. Since then large scale land
mark studies have been performed looking at
prevalence
of
RHD
detected
by
the
echocardiography including Pakistan5,6,11. The
study by Eloi Merijon et al showed comprehensive
echocardiographic
screening
identified
approximately 10 times as many children with
rheumatic heart disease as were identified by the
traditional strategy of clinical screening11.
The newly published Australian and New Zealand
guidelines on prevention of Rheumatic Fever
have already accepted echocardiographic
subclinical carditis as a major criterion in
diagnosis of rheumatic heart disease. Keeping in

Pakistan Cardiac Society Guidelines for Prevention of Rheumatic Fever and Rheumatic Heart Disease

view of the above data and very high

prevalence of RHD in Pakistan and now with the
availability of echocardiography and trained
personnel at least in major teaching and DHQ
hospitals
we
have
included
the
echocardiographic evidence of carditis as major
manifestation in diagnosis of rheumatic fever.
The main modification made in 2004 guidelines
by Pakistan Cardiac Society is the acceptance of
echocardiographic evidence of carditis as a
major manifestation (table 1).
Major Manifestations8:
Carditis: The rheumatic etiology can usually be
confirmed by a typical appearance on
echocardiography. Valvulitis usually presents
clinically as an apical holosystolic murmur with or
without a mid-diastolic flow murmur (CareyCoombs murmur) or an early diastolic murmur at
the base of the heart (aortic regurgitation).

Although pericarditis and myocarditis may

occur, cardiac inflammation in ARF almost
always affects the valves especially the mitral
and aortic valves12. The natural history of valve
regurgitation is a 25-50% improvement by one
year13. The diagnosis of carditis is particularly
difficult in rheumatic recurrence. Undue
tachycardia is in the absence of fever,
pericardial rub and a new regurgitant murmur
are clues towards possible carditis. Evidence of
heart failure not responding to standard antifailure treatment shall also point to possible
recurrence indicating need for anti-inflammatory
drugs.
It is the most common presenting
symptom of ARF (occurring in up to 75% of first
attacks) in which large joints are usually affected,
especially knees and ankles. Typically, the arthritis
of ARF is extremely painful. Monoarthritis may be
a presenting feature if there is a history of NSAID
use early in the course of the illness (prematurely
aborting the manifestation of polyarthritis).
Polyarthritis is usually asymmetrical and migratory.

Arthritis:

chorea: Chorea has a strong

association with carditis. Even in the absence of
echocardiographic evidence of carditis, patients
with chorea should be considered at risk of
subsequent cardiac damage14. Therefore, they
should all receive secondary prophylaxis, and be
carefully
followed
up
for
subsequent
Sydenhams

163

development of RHD. Chorea is the ARF

manifestation most likely to recur and is often
associated with pregnancy or oral contraceptive
use. The vast majority of cases resolve within 6
months (usually within 6 weeks) although rare
cases lasting as long as 3 years have been
documented14-15. Chorea may occur after a
prolonged latent period following GAS infection15
therefore no additional manifestations are
required in order to make a diagnosis of ARF.
Subcutaneous nodules: It is rare (less than 2% of
cases) but highly specific manifestation of ARF16.
It tends to appear 1-2 weeks after the onset of
other symptoms, last only 1-2 weeks (rarely more
than 1 month) and strongly associated with
carditis.
Erythema marginatum: It is rare as well as difficult to

detect (especially in dark-skinned people) and is

rarely seen as the sole major criterion in ARF and
should be accompanied by additional major
criteria in order to make the diagnosis.
Minor Manifestations

Arthralgia: It may suggest ARF if the arthralgia

occurs in the same pattern as rheumatic

polyarthritis
(migratory,
asymmetrical
and
affecting large joints) but if polyarthritis is present
as a major manifestation, polyarthralgia cannot
be considered an additional minor manifestation.
Fever:
Most
manifestations
of
ARF
are
accompanied by fever (with the exception of
chorea). It is an important consideration in the
absence of no other cause of fever.

Elevated acute phase reactants: A serum ESR of

50mm/h meets this diagnostic criterion. The ESR
in ARF is typically >80mm/hr, usually remains
elevated for >4 weeks, and may remain elevated
for 3-6 months despite a much shorter duration of
symptoms. The serum CRP concentration rises
more rapidly than the ESR and also falls more
rapidly with resolution of the attack.
Prolonged P-R interval: An electrocardiogram
(ECG) should be performed in all cases of
suspected ARF. The P-R interval increases
normally with age therefore needs to be ageadjusted. The following upper limits of normal are:

Age 3-12 years: 0.16 seconds

Age 12-16 years: 0.18 seconds
Age 17+ years: 0.20 seconds

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164

Akhtar N, Sadiq A, Rizvi FUH, Chagani H, Hafeez A, Gul A, Hina M

When carditis is present as a major manifestation

(clinical and/or echocardiographic), prolonged
P-R interval cannot be considered an additional
minor manifestation in the same person.

PRIMARY PREVENTION
Primary prevention of acute rheumatic fever is
accomplished by proper identification and
adequate antibiotic treatment of group A
B-hemolytic
streptococcal
(GAS)
tonsillopharyngitis. The aim of the primary
prevention is to promptly recognize and treat all
the patients with group A beta-hemolytic
streptococcal tonsillopharyngitis. While this
approach is therapeutically simple, in practice, it
is difficult to achieve. In order to prevent a single
case of RHD, several thousand cases of
streptococcal throat infection must be identified
and treated17.
At least, one third of acute RF results from inapparent streptococcal throat infection17-18. In
addition, not all symptomatic patients seek
medical care. Therefore, in these instances, RF is
not preventable. Primary prevention is difficult
even if strict management of sore-throat is
followed on scientific lines18. Benzathine Penicillin
G is the anti-microbial agent of choice for the
treatment of GAS, except in patients with history
of penicillin (PCN) allergy. There has been
concern raised that recurrent Group A betahemolytic (GABH) infections occur more
frequently after PCN treatment than with other
anti-microbial therapy, indicating emergence of
resistant strains against penicillin PCN19. However,
Benzathine PCN still is the drug of choice as it has
narrow spectrum of activity and long standing
proven efficacy and is the least expensive
regimen. PCN may be administered IntraMuscularly (IM) or orally, depending on the
patient`s likely adherence to an oral regimen20.
In many countries resistance to macrolide
antibiotics has reached more than 15%. This must
be taken into account when considering a
macrolide therapy for Group A streptococcal URT
infection21. There have been no controlled studies
showing that tonsillectomy is effective in reducing
the incidence of RF and it is not recommended
for the primary prevention of RF22. Treatment of
streptococcal
tonsillopharyngitis.
The
oral
antibiotics of choice are penicillin and amoxicilli .
The recommended dosage of intramuscular

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Benzathine penicillin G is 600 000 U IM for patients

who weigh 27 kg (60 lb) or less and 1 200 000 U for
patients who weigh more than 27 kg.
A strategy consisting of educating health
personnel to recognize bacterial sore throat using
simple clinical algorithms (instead of relying on a
bacteriologic diagnosis), followed by a single
injection of Benzathine PCN for the treatment of
suspected cases, has been shown to be
effective. The implementation of such a strategy
through the existing healthcare infrastructure
may be efficient and cost-effective and has the
potential to reduce the burden of RF/RHD23.

SECONDARY PROPHYLAXIS
Due to impossible logistics and financial
constraints associated with primary prevention,
focus has been to prevent the recurrence of
Rheumatic Fever (secondary prevention). This
approach is more practical and has shown to be
effective in developing countries24. An individual
with previous attack of RF, in whom
streptococcal pharyngitis develops, is at higher
risk for developing recurrent attacks of RF. A
group A beta hemolytic streptococcal (GAS)
infection need not to be symptomatic and can
trigger recurrence, even if optimally treated.
Further, with each recurrence of RF, the chances
of acquiring carditis increase exponentially.
Duration of Prophylaxis: Risk of recurrence depends

on several factors. It increases with multiple

previous attacks, whereas the risk decreases as
the interval since the most recent attack
lengthens25-26. The data on the recurrence of
rheumatic fever in Pakistan is limited27. By
extrapolating this information and the current
evidence from Australia, New Zealand, South
Africa and American Heart Association`s
guidelines on secondary prophylaxis, we
recommend the following program which
depends on a number of factors. These include:

Age (ARF recurrence is less common after the

age of 25 and uncommon after the a age
of 30)27-28.

Clinical pattern (presence or absence of

carditis or RHD and severity of carditis or RHD)

Environment (particularly the likelihood of

ongoing exposure to GAS)

Time elapsed since last episode of ARF (ARF

recurrences are less common greater than

165

Pakistan Cardiac Society Guidelines for Prevention of Rheumatic Fever and Rheumatic Heart Disease

five years since last episode).

duration of secondary prophylaxis is outlined in

Table 3.

Based on these factors, the recommended

TABLE 1: Criteria for the Diagnosis of Rheumatic Fever and Rheumatic Heart Disease (Pakistan Cardiac Society 2010)
Diagnosis Categories

Criteria

Primary Episode of RF

Two major* or one major and two minor** manifestations plus

evidence of preceding group A streptococcal infection***

Recurrent attack of RF in a patient with

established rheumatic heart disease

Two major* or one major and two minor** manifestations plus

evidence of preceding group A streptococcal infection
OR
Two minor manifestations plus evidence of preceding group A
streptococcal infection

Rheumatic Chorea

Other major manifestations or evidence of preceding group A

streptococcal infection not required

Insidious onset rheumatic carditis

Major Manifestations*
Carditis
(including
evidence
of
subclinical rheumatic valve disease on
echocardiogram)
Polyarthritis
Chorea
Erythema marginatum
Subcutaneous nodules
***

Minor Manifestations**
Fever
Raised ESR or CRP
Polyarthralgia (When arthritis is present as major criteria,
arthralgia can not be considered as minor)

Prolonged P-R interval (When carditis is present as a major

manifestation, a prolonged P-R interval cannot be
considered an additional minor manifestation in the same
person)

Supporting evidence of preceding group A streptococcal infection within last 45 days:

All the cases of suspected ARF should have elevated serum streptococcal serology demonstrated. If the
initial titer is below the upper limit of normal, testing should be repeated 10-14 days later.

TABLE 2: Secondary Prevention of Rheumatic Fever (Prevention of Recurrent Attacks)

Agent

Dose

Mode

Benzathine penicillin G

600,000 U for children <27 kg (60 lb), 1,200,000 U for those

>27 kg (60 lb) every 3 wk

Intramuscular

Penicillin V

250 mg twice daily

Oral

Sulfadiazine

0.5 g once daily for patients <27 kg (60 lb), 1.0 g once daily
for patients

Oral

>27 kg (60 lb)

For individuals allergic to
penicillin and sulfadiazine

40mg/kg per day (children)(2 divided doses ,maximum

1g/day)

Macrolide or Azalide

400mg (adolescents and adults) twice daily

Oral

TABLE 3: Recommendations for the Duration of Secondary Prophylaxis

Category

Duration of Prophylaxis

All persons with Acute Rheumatic

Fever

Minimum of 10 years after most recent episode ARF or until age 21 years
(whichever is longer)

All persons with ARF with Carditis

and established RHD

Minimum of 10 years after most recent episode ARF or until age 30 years
and then specialist review for consideration of the need for continuation of
prophylaxis.

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166

Akhtar N, Sadiq A, Rizvi FUH, Chagani H, Hafeez A, Gul A, Hina M

TABLE 4: Measures that may reduce the pain of Benzathine Penicillin

Use a 23 gauge needle.

Apply pressure with thumb for 10 seconds
before inserting needle

Use of ethyl-chloride spray prior to injection.

Distraction
techniques
conversation)

Warm syringe to room temperature before

using

Good rapport with the case, assisted by having a designated

nurse for each case, is a significant aid to injection comfort,
compliance and understanding.

Allow alcohol from swab to dry before

inserting needle.
Recurrent

Intramuscular Benzathine Penicillin G: An injection of

Choice of Regimen for

Rheumatic Fever (Table 2):

Prevention

of

1,200,000 U of this long-acting penicillin

preparation every 3 weeks is the recommended
regimen for secondary prevention in most
circumstances in Pakistani population.
Oral Agents: Oral agents are more appropriate for
patients at lower risk for rheumatic fever
recurrence. Accordingly, some physicians may
consider switching patients to oral prophylaxis
when they have reached late adolescence or
young adulthood and have remained free of
rheumatic attacks for at least 5 years. The
recommended oral agent is penicillin V and
dosage for children and adults is 250 mg twice
daily. For patients allergic to penicillin,
sulfadiazine
is
recommended
and
the
recommended dose of sulfadiazine is 0.5 g once
per day for patients weighing 27 kg (60 lb) or less
and 1 g once per day for patients weighing>27
kg. For the patient who is allergic to both
penicillin and sulfisoxazole, an oral macrolide
(erythromycin
or
clarithromycin)
orazalide
(azithromycin) is recommended.

Reducing the pain of the BPG injection

The formulation of intramuscular penicillin G is
painful. Methods for reducing the pain are given
in the table 4.

ACKNOWLEDGMENTS
We would like to thank the following for their
support and encouragement in formulating the
guidelines on prevention of rheumatic fever and
rheumatic heart disease.

A. Hafeez Akhtar ,Pakistan Cardiac Society.

Prof. Abdus Samad, Pakistan Cardiac Society.
Prof. Azhar Masood A.Faruqui, Pakistan
Cardiac Society.

www.ppa.org.pk

during

injection

(e.g.

with

Prof. Kaleemuddin Aziz, Pakistan Paediatric

Cardiology Society.
Prof. Azhar Mehmud Kayani, President
Pakistan Cardiac Society.
Prof. Khan Shah Zaman, Secretary Pakistan
Cardiac Society.
Prof. M Ashraf Sultan Chairman Infectious
disease
group
of
Pakistan
Pediatric
Association.
Dr. Khalif Bile Mohamud, World Health
Organization Representative.
Prof. Shahryar A. Sheikh, President World Heart
Federation.

-------------------------------------------------------------------------------Authors affiliations
Naveed Akhtar,
Chairperson Scientific Council of Pakistan Cardiac
Society on Valvular Heart Diseases, Associate Professor
of Cardiology, Shifa International Hospital, Islamabad.
Prof. Masood Sadiq,
Department of Paediatrics Cardiology, The Children`s
Hospital/The Institute of Child Health & Punjab Institute
of Cardiology, Lahore. drmasoodsadiq@hotmail.com
Faiz ul Hassan Rizvi,
Department of Paediatrics Cardiology, Sheikh Zayed
Medical College, Rahim Yar Khan.
Haseena Chagani,
Department of Pediatrics Cardiology, Dow University of
Health Sciences Karachi.
Asad Hafeez,
Health Services Academy of Islamabad.
Adnan Gul
Department of Paediatrics Cardiology, Lady Reading
Hospital, Peshawar.
Madeeha Hina,
Penicillin Clinic Pakistan Cardiac Society Islamabad.

REFERENCES:
1.

Guilherme L, Kalil J. Rheumatic Fever: From

Sore-throat to Autoimmune Heart Lesions.
Int Arch Allergy Immunol 2004;134: 56-64.

Pakistan Cardiac Society Guidelines for Prevention of Rheumatic Fever and Rheumatic Heart Disease

2.

Stollerman GH, Lewis AJ, Schultz I, Taranta

A. Relationship of immune response to
group A streptococcus to the course of
acute, chronic and recurrent rheumatic
fever. AM J Med 1956; 20:163.

3.

Rheumatic fever and rheumatic heart

disease. Report of a WHO study group.
Technical report series No. 764, World Health
Organization, Geneva (1988).

4.

Gordish, Lilienfield A, Rodriguez R. Studies in

the epidemiology and preventability of
rheumatic fever.II. socioeconomic factors
and the incidence of acute attacks. J
Chron Dis 1969; 21: 655.

5.

Sadiq M, Islam K, Abid R, Latif F, Rehman

AU, Waheed A, Azhar M, Khan JS.
Prevalence of rheumatic heart disease in
school children of urban Lahore. Heart 2009;
95: 353-57.

12.

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Marijon E, David S., Celermajer et al.

Rheumatic heart disease screening by
Echocardiography: The inadequacy of
World Health Organization Criteria for
Optimizing the Diagnosis of Subclinical
Disease. Circulation 2009; 120: 663-68.

EdwardsWDetal.Activevalvulitisassociatedwith
chronicrheumaticvalvulardiseaseandactive
myocarditis.Circulation.1978;57:181185.
13.

Bland EF. Chorea as a manifestation of

rheumatic fever: a long-term perspective.
Trans Am Clin Climatol Assoc, 1943; 73: 20913.

14.

Lessof M. Sydenhams chorea. Guys Hosp

Rep. 1958; 107: 185-206.

15.

Carapetis JR, Currie BJ. Rheumatic fever in

a
high
incidence
population:
the
importance of monoarthritis and low grade
fever. Arch Dis Child. 2001; 85: 223-27.

6.

Rizvi SF, Khan MA, Kundi A, Marsh DR,

Samad A, Pasha O. Status of rheumatic
heart disease in rural areas. Heart 2003;

16.

Dajani AS. Current status of non-suppurative

complications of group A streptococci.
Pediatr Infect Dis J 1991; 10: 525-27.

7.

World Health Organization. Report of

consultation review progress and develop
future activities. The WHO global program
for prevention of rheumatic fever and
rheumatic
heart
disease.
Geneva,
Switzerland: World Heart organization
(1999).

17.

Ebell MH et al. The rational clinical

examination: Does this patient have strep
throat? Journal of American Medical
Association, 2000, 284(22): 2912-18.

18.

Markowitz M, Gerber MA, Kaplan EL.

Treatment
of
streptococcal
pharyngotonsillitis: Reports of penicillin`s
demise are premature. J Pediatr 1993; 123:
679.

19.

Dajani AS, Taubert K, Ferrieri P. Treatment of

streptococcal pharyngitis and prevention of
rheumatic fever. Pediatrics 1995; 96: 758.

20.

Denny FW, Waunmaker IW, Brink WR.

Prevention of rheumatic fever: Treatment of
preceding streptococcal infection. JAMA
1950; 143: 151.

21.

Matanoski GM. The role of tonsils in

streptococcal infections: A comparison of
tonsillectomized
children
and
sibling
controls, American Journal of Epidemiology,
1972, 95(3): 278-91.

22.

Michael A. Gerber, Robert S. Baltimore,

Charles B. Eaton et al. Prevention of
rheumatic fever and diagnosis and
treatment
of
acute
streptococcal

8.

Lennon D, Wilson N, Atatoa-Carr P, et al.

New Zealand Guidelines for Rheumatic
Fever,
Diagnosis,
Management
and
Secondary Prevention, June 2006.

9.

Jones TD. Diagnosis of rheumatic fever.

JAMA. 1944; 126: 481-84.

10.

Special Writing Group of the Committee on

Rheumatic Fever and Kawasaki Disease of
the Council on Cardiovascular Disease in
the young of the American Heart
Association, Guidelines for the Diagnosis of
Rheumatic Fever. Jones criteria 1992
update. JAMA. 1992; 268: 2069-73.

11.

Marijon E, Phalla Ou, David S. Celermajer et

al. Prevalence of rheumatic heart disease
detected by Echocardiographic screening.
N Engl J med 2007; 357: 470-76.

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168

Akhtar N, Sadiq A, Rizvi FUH, Chagani H, Hafeez A, Gul A, Hina M

pharyngitis: A scientific statement from the

American Heart Association Rheumatic
fever, Endocarditis, and Kawasaki disease
committee of the council on cardiovascular
disease in the young, the Interdisciplinary
council on functional genomics and
translational
biology,
and
the
interdisciplinary council on quality of care
and outcomes research: Endorsed by the
American
Academy
of
Pediatrics.
Circulation 2009;119: 1541-51.
23.

Ganesan Karthikyan, Bongani M. Mayosi. Is

primary prevention of rheumatic fever the
missing link in the control of rheumatic heart
disease in Africa? Circulation 2009;120;709713.Allergic
reactions
to
long-term
Benzathine
penicillin
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for
rheumatic fever: International Rheumatic
Fever Study Group. Lancet. 1991;337:1308
1310.

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24.

Bland EF, Duckett Jones T. Rheumatic fever

and rheumatic heart disease: a twenty year
report on 1000 patients followed since
childhood. Circulation. 1951; 4: 83643.

25.

Wilson MG, Lubschez R. Recurrence rates in

rheumatic fever: evaluation of etiologic
concepts and
consequent preventive
therapy. JAMA. 1944;126: 47780.

26.

Chagani, Aziz KU. Clinical profile of acute

rheumatic fever in Pakistan. Cardiol Young
2003; 13: 2835.

27.

Gordis L, Lilienfeld A, Rodriguez R. Studies in

the epidemiology and preventability of
rheumatic fever, I: demographic factors
and the incidence of acute attacks. J
Chronic Dis. 1969; 21: 64554.

CASE REPORT

Nephrogenic Diabetes Insipidus

SHAAFIA FATIMA, HAFSA MUHAMMAD, AYESHA ARIF

-----------------------------------------------------------------Authors affiliations
------------------------------------------Correspondence to:Shaafia Fatima
Department of Paediatrics, Sir
Ganga Ram Hospital, Lahore.
E-mail:
shaafia1986@hotmail.com

ABSTRACT

Pak Paed J 2011;35(3): 169-70

Congenital nephrogenic diabetes insipidus is a rare disorder in which the

kidney is insensitive to antidiuretic hormone. It is mostly because of
mutation in vasopressin type 2 receptor gene. Few cases have been
reported with incidence of 3 in 100,000. We report here a case of an 11
month old infant who presented in emergency with dehydration,
excessive cry, polyuria, polydipsia and constipation. During hospital stay
detailed history, clinical examination and laboratory investigations
suggest diagnosis of nephrogenic diabetes insipidus. He was administered
on thiazide diuretics after which infant showed improvement.

INTRODUCTION
Nephrogenic Diabetes Insipidus is a rare disorder
of water metabolism characterized by an inability
to concentrate urine even in presence of
Antidiuretic hormone1. Mostly congenital but can
be acquired (secondary) due to disorders
affecting renal tubular functions1,2. Incidence of
Diabetes Insipidus in general population is 3 in
100,000 with a slightly higher incidence among
males (60%)2. We report here a case because of
its rarity3.

CASE REPORT
A male baby weighting 2.6 kg, who was born
following a normal pregnancy and delivery. He
could not gain height and weight according to
his age. He was second issue of a cousin
marriage, was breast fed and appeared healthy
otherwise. Weaning started at 5 months of age
but was not tolerated by him; he began to vomit
several times a day, cried unless given milk and
soaked 10-12 diapers daily. He also had
constipation passing hard pebble like stools every
5th day and sometimes after giving suppository.
History of repeated hospital admissions due to
dehydration was also there. Now at 11 months of
age he presented to our emergency with
dehydration and irritability. He had dry skin,
sunken eyes, slow skin pinch and slightly moist

mucous membrane. Vitals were normal at

presentation. Weight and length were below 5th
percentile. He was developmentally delayed
with neck holding at 7 months of age. During
hospital stay his dehydration was corrected and
various investigations were performed. His serum
electrolytes
showed:
sodium
176
mEq/l,
potassium 4.2 mEq/l, chloride 140 mEq/l,
bicarbonate 21 mEq/l.
Serum electrolytes again showed similar readings
when repeated after 4 days. Serum calcium was
10.3 mg/dl. Complete blood examinations
showed low hemoglobin for which blood was
transfused. Renal function tests were normal.
Intake output record showed output about 8-10
cc/kg/hr. Complete urine examination showed
pH 8.0 and specific gravity 1.005. Urine osmolality
was 154 and serum osmolality was 347.
Abdominal ultrasound was normal. MRI of brain
was done to exclude central diabetes insipidus
which was normal. Both serum and urine
osmolality along with history suggested diagnosis
of Nephrogenic Diabetes Insipidus. He was
started on thiazide diuretics5 and after one week
of treatment his constipation and vomiting were
settled. He was not dehydrated. Now he was
soaking 7-8 diapers daily. His serum electrolytes
were
performed which
showed:
sodium
156 mEq/l, potassium 4.4 mEq/l, and chloride
130 mEq/l. The baby is still on follow up.

www.ppa.org.pk

170
DISCUSSION
Congenital Nephrogenic Diabetes Insipidus (NDI)
is a rare disease the most common pattern of
inheritance is an X-linked recessive disorder which
occurs from mutation in antidiuretic arginin
vasopressin V2 receptor gene (AVPR 2).
Autosomal dominant or recessive pattern is due
to mutation in gene designated AQP21,4.
Hypercalcaemia and hypokalemia can also
cause partial Nephrogenic Diabetes Insipidus.
Diagnosis is suspected in a male infant with
polyuria, hypernatremia and dilute urine. Serum
osmolality >290mOsm/kg and urine osmolality
<290mOsm/kg is suggestive of Nephrogenic
Diabetes Insipidus1

Fatima S, Muhammad H, ARIF A

proximal tubule reabsorption of water. The

antidiuretic action of thiazides in diabetes
insipidus is secondary to increased renal sodium
excretion. This sodium loss causes extracellular
volume contraction, resulting in reduced GFR
and increased sodium and water reabsorption at
the proximal tubule. Hence, less sodium and
water are delivered to the distal tubule and
collecting duct and less of these are lost in
urine5,6.

CONCLUSION
Main differential diagnosis is central diabetes
insipidus which can be excluded by doing water
deprivation test and administration of vasopressin
intranasally. Prevention of recurrent dehydration
and hypernatremia in patients with congenital
Nephrogenic Diabetes Insipidus has significantly
improved the neurodevelopmental outcome.
-------------------------------------------------------------------------------Authors affiliations
Shaafia Fatima, Hafsa Muhammad, Prof. Ayesha Arif
Department of Paediatric, Sir Ganga Ram Hospital,
Lahore.

REFERENCES

Knowledge Of Mothers Regarding Nutritional

Care Of Child Having Cerebral Palsy
Treatment of NDI includes (1) maintenance of
adequate fluid intake and access to free water;
(2) minimizing urine output by limiting solute load
with a low-osmolar, low-sodium diet; and (3)
administering
medications
directed
at
decreasing urine output. Thiazide diuretics
effectively induce sodium loss and stimulate

www.ppa.org.pk

1.

Dell KM, Avner ED. Nephrogenic Diabetes

Insipidus. In: kleigman RM, Behrman RE,
Jenson HB, Stanton BF, editors. Nelson
textbook of pediatrics. 18th edition.
Philadelphia: Elsevier; 2007: 2200-01.

2.

Saborio P, Tipton GA, Chan JC. Diabetes

Insipidus. Pediatr rev 2000; 21(4): 122-29.

3.

Linshaw MA. Back to basics: congenital

nephrogenic diabetes insipidus. Pediatr
rev 2007; 28(10): 372-80.

4.

Chan JCM, Kemp S. Pediatrics Diabetes

Insipidus: Medscape [Internet]. Updated
2010 Feb 23 [cited 2010 Dec12]. Available
from: http://emedicine.medscape.com /
article/919886-overview#a0104

5.

Loffing J. Paradoxical antidiuretic effect of

Thiazides in Diabetes insipidus: another
piece in puzzle. J Am Soc Nephrol 2004;
15(11): 2948-50.

6.

Takemura N. Successful long term

treatment of congenital nephrogenic
diabetes insipidus in a dog. J Small Anim
Pract1998; 39(12): 592-94.

CASE REPORT

Histiocytosis Syndromes of Childhood

JOVARIA MANNAN, MUHAMMAD NAVEED, ATTIA KALIM

-----------------------------------------------------------------Authors affiliations
---------------------------------------------Correspondence to
Muhammad Naveed
Department of Pediatrics
Medicine Fatima Memorial
Hospital Lahore.
Email:
naveed_khaleeque@hotmail.
Com

ABSTRACT

Pak Paed J 2011; 35(3): 171-74

This is the case report of three babies age 4 months, 21/2 months and
2 months who presented to us. Case 1 and 3 as sepsis, whereas case 2 as
anemia without visceromegaly. Appropriate treatment failed and bone
marrow biopsy revealed malignant histiocytosis in case 1 and
hemophagocytosis in case 2 and 3.
Keyword: histiocytosis, Hemophagocytic Lymphohistiocytosis, Langerhans
cell.

INTRODUCTION
These disorders are grouped together because
they have in common a prominent proliferation
or accumulation of cell of the monocytemacrophages and dendritic cell in affected
tissues. These disorders sometime are difficult to
distinguish clinically and usually treated as sepsis.
Hence Histiocytosis syndrome should be kept in
mind with differential of sepsis
Case1: A 3rd issue of consanguineous marriage,
3 months old baby boy presented with history of
fever for 1 week, which was low grade to start
with became high grade intermittent without any
constitutional symptoms. Two days later he
developed cough and breathing difficulty
followed by loose motion, 6-7 episode/day,
grade 4 without blood and mucous .Child was
breast and formula fed, immunized according to
EPI, programme. He had one healthy sister 3
years old, where as one brother died at age of 30
day due to prematurity and its complications.
On examination baby had no dysmorphism,
growth parameter were at 50th percentile, looked
sick was tacypneic, dyspneic maintained O2>
90% at Fio2 of 0.40. There was good bilateral air
entry without added sound. Abdomen was
distended, with liver 5 cm, spleen 4 cm palpable
below costal margin. Rest of the examination was
normal.
Initial CBC showed Hb 9.9 gm/dl, WBC count
6.0x103, neutrophils. 30%, lymphocytes 60%,

platelets count 113x103 /L. ABGs at Fio2 of 0.40

showed > 90% O2 saturation had no significant
CO2 retention. X-ray chest, blood sugar, serum
electrolytes, renal function, and liver function
were normal. At this moment provisional diagnosis
of sepsis was made. Antibiotics, antimalarial and
IV fluids were started but no response was seen
after 48 hours. Case was reviewed, CBC and Xray chest was repeated.
This time CBC showed Hb 8.5 gm/dl, WBC count
6.6x103, neutrophils, 40%, lymphocytes, 60%,
platelets count 35x103/L,X-ray chest showed
middle lobe consolidation. Hemophagocytosis
was suspected and bone marrow requested
.Report came as malignant histiocytosis (Fig 1).
Child was referred to Department of Oncology,
Childrens Hospital for chemotherapy and further
management.
Case 2: A baby girl 11/2 month old presented with
history of pallor since 20 days of age. She was
transfused at local health facility for a Hb of 6.5
gm/dl. She remained well for 4 weeks but again
developed progressive pallor, this time complete
blood count was done.
Hb 1.5 gm/dl, RBC count 0.42x106/l, WBC 9.5x103,
neutrophils, 40%, lymphocytes, 60%, platelets
count 60x103/L. Child was referred to Fatima
Memorial Hospital for further management. At
presentation there was no history of fever, rash,
cough, loose motion, vomiting, weight loss,
feeding difficulty, drug intake and radiation

www.ppa.org.pk

Mannan J, Naveed M, Kalim A

172
exposure. She was born normally at home, no
history of maternal fever, rash and jaundice.
Father and mother were not cousins. She was
active, pale baby with no dysmorphic features.
All growth parameter at 50th percentile. Pallor was
positive rest of examination was unremarkable.
On basis of history and examination provisional
diagnosis was Blackfan Diamond anemia so
bone marrow biopsy requested. On bone
marrow
biopsy
impression
was
Hemophagocytosis with megaloblastic bone
marrow. Serum folic acid, Vit B12, fibrinogen and
serum cholesterol were normal. Antimalararial,
antiviral started and blood transfused. This patient
refused chemotherapy and is still on follow up.
On follow up at 2 month of age she developed
hepatomegaly. At 3 month of age she reported
with chest infection and thrombocytopenia.
Currently she requires packed cell and platelets
transfusions repeatly.
Case 3: A male baby, 2 month old, presented
with history of high grade intermittent fever for 15
days along with respiratory difficulty and
reluctance to feed. Antibiotics and antimalarial
were given at local health facility but fever did
not settle and child was referred to Fatima
Memorial Hospital. At presentation fever was
persistent but respiratory difficulty and feeding
problems were improved.
On examination he was irritable baby with no
dysmorphic feature, growth parameter at 50th
percentile, maintaining O2 saturation at room air.
He had hepatomegaly and splenomegaly; 8cm
and 6 cm respectively. CVS, respiratory and CNS
examination were normal.

Fig 1: Case 1 Malignat histiocytosis

www.ppa.org.pk

Fig 2: case 2 Haemophaocytosis

DISCUSSION
The childhood histiocytoses constitute a diverse
group of disorders, which, although individually
rare, may be severe in their clinical expression.
These disorders are grouped together because
they have in common a prominent proliferation
or accumulation of cells of the monocytemacrophage and dendritic in affected tissues.
Although these disorders sometimes are difficult
to distinguish clinically, are usually treated as
sepsis. Accurate diagnosis is essential and
needed for facilitating progress in treatment. A
systematic classification of the childhood
histiocytoses is based on histopathologic findings
immunostaining that may require special sample
processing. WHO proposed classification of
histiocytic and dendritic cell is as follow (Table 1)1.
Three classes of childhood histiocytosis are
recognized, based on histopathologic findings.
The most well-known childhood histiocytosis,
previously known as histiocytosis X, constitutes
class I and includes the clinical entities of
eosinophilic granuloma Hand-Schller-Christian
disease, and Letterer-Siwe disease. The name
Langerhans' cell histiocytosis (LCH) has been
applied to the class I histiocytoses. Birbeck
granule, a tennis racketshaped bilamellar
granule that, when seen in the cytoplasm of
lesional cells in LCH, is diagnostic of the disease2.
Langerhans cell histiocytosis (LCH) can be local
and asymptomatic, as in isolated bone lesions, or
can involve multiple organs and systems, with
clinically
significant
symptoms
and
consequences.
The
clinical
manifestations

173

Histiocytosis syndromes of Childhood

depend on the site of the lesions and on the

organs and systems involved and their functions.
The definitive diagnosis of LCH also can be
established by demonstrating CD1a-positivity of
lesional cells. The clinical course of single-system
disease (usually, bone, lymph node, or skin)
usually is benign, with a high chance of
spontaneous remission. Therefore, treatment
should be minimal and should be directed at
arresting the progression of a bone lesion that
could result in permanent damage before it
resolves spontaneously. Multisystem disease, in
contrast, should be treated with systemic
multiagent chemotherapy3.class II histiocytoses
are nonmalignant proliferative disorders that are
characterized by accumulation of antigenprocessing cells (macrophages). Hemophagocytic lymphohistiocytoses (HCH) are the result
of
uncontrolled
hemophagocytosis
and
uncontrolled
activation
(upregulation)
of
inflammatory
cytokines
similar
to
the
macrophage
activation
syndrome.
Tissue
infiltration by activated CD8 T lymphocytes and
activated
macrophages
as
well
as
hypercytokinemia are classic features4. With the
characteristic
morphology
of
normal
macrophages by light microscopy, these
phagocytic cells lack the two markers (Birbeck
granules and CD1a-positivity) characteristic of
the cells found in LCH.1 The two major diseases
among
the
class
II
histiocytoses
have
indistinguishable pathologic findings. One is
familial
hemophagocytic lymphohistiocytosis
(FHLH),
previously
called
familial
erythrophagocytic lymphohistiocytosis FEL, which
is the only inherited form of histiocytosis and is
autosomal
recessive.
Various
mutations,
deletions, or insertions that cause frameshift or
missense mutation in perforin genes (PRF1 and
PRF2), MUNC 13-4, and syntaxin 11 have been
reported5. The other is the infection-associated
hemophagocytic syndrome (IAHS), also called
secondary hemophagocytic lymphohistiocytosis.
The major forms of HLH, familial hemophagocytic
lymphohistiocytosis (FHLF) and secondary HLH,
have a remarkably similar presentation consisting
of a generalized disease process, most often with
fever, maculopapular and/or petechial rash,
weight loss, and irritability. FHLH also is
characterized by severe immunodeficiency.
Children with FHLH always are <4 yr of age,
whereas children with secondary HLH may

present at an older age. Physical examination

often
reveals
hepatosplenomegaly,
lymphadenopathy, respiratory distress, and
symptoms of CNS involvement, unlike that of
aseptic meningitis in which the cerebrospinal fluid
cells are the same phagocytic macrophages as
found in the peripheral blood or bone marrow
(Table 2)2.
TABLE 1: WHO Classification of Histiocytosis
Class

Syndromes

LCH

Letters Siwe Disease

Hand Schuller-christian disease

Eosinophilic Granuloma

Congenital
self-healing
reticulohistiocytosis

II

Histiocytosis
of
mononuclear
phagocytes other than Langerhans
cells
Familial
and
reactive
hemophagocytic lymphohistiocytosis
(HLH)
Sinus histiocytosis with massive
lymphadenopathy (SHML, RosaiDorfman disease)
Reticulohistiocytoma
Juvenile xanthogranuloma (JXG)

Malignant histiocytic disorders

Acute monocytic leukemia (FAB M5)
Malignant histiocytosis
True histiocytic lymphoma

III

TABLE 2: Diagnostic
Lymphohistiocytosis

criteria

for

Hemophagocytic

Fever >38.5C and lasting 7 days

Splenomegaly >3 cm
Two of the following hematologic abnormalities:
Anemia (<9 g/dL hemoglobin)
Thrombocytopenia (<100,000 cells/L)
Neutropenia (<1000 neutrophils/L)
ONE OF THE FOLLOWING ABNORMALITIES:
Hypertriglyceridemia >2.0 nmol/L
Hypofibrinogenemia <150 mg/dL
And
Hemophagocytosis in bone marrow, spleen, or lymph
node
No evidence of marrow hyperplasia or malignant
neoplasia

www.ppa.org.pk

Mannan J, Naveed M, Kalim A

174
The diagnostic distinction between FHLH and
secondary HLH sometimes can be based on the
acute onset of secondary HLH in the presence of
a documented infection. In this case, treatment
of the underlying infection, coupled with
supportive care, is critical. If the diagnosis is made
in a setting of iatrogenic immunodeficiency,
immunosuppressive
treatment
should
be
withdrawn and supportive care should be
instituted along with specific therapy for
underlying infection. When FHLH (gene mutations
in perforin or Munc 134 proteins) is diagnosed or
suspected and when an infection cannot be
documented,
therapy
currently
includes
etoposide, corticosteroids, and intrathecal
methotrexate. Some recommend antithymocyte
globulin and cyclosporine for maintenance
therapy. Nevertheless, even with chemotherapy,
FHLH remains ultimately fatal, often after a
relapse of the disease2. Allogeneic stem cell
transplantation
is
effective
in
curing
approximately 60% of patients with FHLH. In
contrast, in secondary HLH, when an infection
can be documented and effectively treated, the
prognosis is good without any other specific
treatment. When a treatable infection cannot be
documented, which the case in most patients is
presumed to have secondary HLH, the prognosis
may be as poor as that of FHLH, and an identical
chemotherapeutic
approach,
including
etoposide, is recommended2.
Acute monocytic leukemia and true malignant
histiocytosis are included among the class III
histiocytoses, because they are unequivocal
malignancies of the monocyte-macrophage
lineage. These patients present with sudden onset
of generlized symptoms that include fever,
sweating, weight loss, enlarged lymph nodes,
heptospleenomegaly,
anemia,
leukopenia,

www.ppa.org.pk

thrombocytopenia and skin, bone or gut

involvement in half of the patients. Treatment is
chemotherapy with stem cell transplantation
-------------------------------------------------------------------------------Authors affiliations
Prof. Jovaria Mannan, Muhammad Naveed, Attia Kalim
Department of Pediatrics Medicine Fatima Memorial
Hospital Lahore.

REFERENCES
1.

Harris NL, Jaffe ES, Diebold J, et al. World

Health
Organization
classification
of
neoplastic diseases of the hematopoietic
and lymphoid tissues: report of the Clinical
Advisory Committee meeting-Airlie House,
Virginia, November 1997. J Clin Oncol 1999;
17(12): 3835-49.

2.

Ladish
S.
Histiocytosis
Syndrome
of
Childhood. In: Kleigman RM, Behrman RE,
Jenson HB, Stanton BF, editors. Nelson
textbook of pediatrics. 18th edition.
Philadelphia: Elsevier; 2007: 2159-61.

3.

Nathan DG, Orkin SH, Ginsburg D, et al.

Nathan and Oski's Hematology of Infancy
and Childhood. 6th ed. Philadelphia, WB
Saunders, 2003: 1379.

4.

Kogawa K, Lee SM, Villanueva J, et al.

Perforin expression in cytotoxic lymphocytes
from
patients
with
hemophagocytic
lymphohistiocytosis
and
their
family
members. Blood 2002; 99(1): 61-66.

5.

Arico M, Danesino C, Pende D, et al.

Pathogenesis
of
haemophagocytic
lymphohistiocytosis. Br J Haematol 2001;
114(4): 761-69.

CASE REPORT

Pseudohypoaldosteronism,
Hypothyroidism
Hypoparathyroidism in a Two-Year-Old Boy

and

ABDULMONEIM AL-AGHA

-----------------------------------------------------------------ABSTRACT
Authors affiliatios
-------------------------------------------Correspondence to:Abdulmoein Al-Agha
Department of Pediatrics, King
Abdulaziz University Hospital,
P.O.Box 80215, Jeddah 21589,
Saudi Arabia
E-mail: aagha@kau.edu.sa

Pak Paed J 2011;35(3): 175-77

A two-year-old boy, found to have a persistent hyperkalemia,

hyponatraemia with metabolic acidosis in addition to repeated
episodes of apnoeic attacks secondary to low serum calcium. Except
for failure to thrive, his physical examination was within normal.
Laboratory
values
confirmed
the
unusual
combination
of
pseudohypoaldestronism,
hypoparathyroidism
and
congenital
hypothyroidism. Renal function was normal. Hormonal evaluation
revealed normal cortisol, as well as 17- hydroxyl progesterone which
were done to exclude the possibility of congenital adrenal hyperplasia
as the cause of electrolyte disturbance. In the absence of aldosterone
deficiency or renal dysfunction, it was assumed that this infant had
primary
renal
resistance
to
aldosterone,
known
as
pseudohypoaldestronism.
We attempted to report an unusual
combination of persistent yet 3 endocrinopathies in closely related
parents.
Key words: Aldosterone, thyroid, hypocalcaemia, hypoparathyroidism.

INTRODUCTION
Pseudohypoaldosteronism (PHA) is a rare
condition of salt wasting in infancy with renal
tubular resistance to the actions of aldosterone.
The disease is divided into 2 forms: primary and
secondary (transient) PHA. The primary form is
further divided into type 1 and type 2. Type 1 is
subdivided into renal type 1 (also known as
Cheek and Perry syndrome), Multiple Target
Organ Defect type 1 (MTOD) and Early
Childhood Hyperkalemia. Type 2 is subdivided
into Gordon Syndrome (also known as Chloride
Shunt syndrome), and adolescent hyperkalemic
syndrome. The underlying pathology differs
according to the types and subtypes of PHA,
which is due either to a defect in the quantity
and functions of aldosterone receptors, the
epithelial sodium channels or the sodium-chloride
co-transporters.

The first case of primary PHA was reported in 1958

by Cheek and Perry1. Signs and symptoms vary
according to the types of PHA. It is a state of
hyponatermic, hyperkalemic metabolic acidosis,
which might occur at early infancy but can also
be present in utero; (polyurea leading to
polyhydramnios, which was presented in our case
or during adolescence (hypertension). Anorexia
and vomiting usually develop after birth with signs
of dehydration and failure to thrive. Short stature
is seen in children as they get older. Blood
pressure varies according to type. Furthermore,
there is a higher incidence of lower respiratory
tract infections in children with MTOD. Death may
occur from cardiac arrhythmia due to severe
hyperkalemia. Investigations usually reveal a
hyponatremic, hyperkalemic metabolic acidosis.
Aldosterone levels maybe low, normal or high,
according to the type of PHA and volume status.
Plasma renin levels are usually high. Cortisol levels

www.ppa.org.pk

176
and renal function should be normal. Renal
ultrasound is usually indicated to rule out any
urinary tract malformations, urinalysis and urine
culture should be done to rule out urinary tract
infection. Management includes rehydration,
correction of acidosis and hyperkalemia with
alkalinizing
agents
(sodium
bicarbonate).
Potassium binding resins (sodium resonium) are
usually prescribed to control hyperkalemia. High
sodium and low potassium diets are advised, in
addition to the supplementation of sodium
(sodium chloride). The use of exogenous
mineralocorticoids has no role in correcting the
abnormalities of this disorder. During outpatient
care serum electrolytes, height, weight and
blood pressure should be closely monitored. We
present a case illustrating the unusual association
of pseudohypoaldosteronism, hypothyroidism
and hypoparathyroidism in a two-year-old boy.

CASE REPORT
A two-year-old male patient, product of 34
weeks of gestation, with a birth weight of 1.8 kg
presented to the emergency room of King AbdulAziz University Hospital, Jeddah, Saudi Arabia, a
few days after birth. He had a two-day history of
frequent attacks of apnea, associated with bluish
discolouration of his lips (each lasted for a few
seconds), poor activity, reduced oral intake and
poor weight gain since birth. His vital signs were
stable except for an oxygen saturation of 88% on
room air. He was lethargic and irritable, in
addition to being underweight for his age but
with no dysmorphic features.
Regarding family history; his parents were first
degree cousins, and his brother died during
infancy at the age of 3 months in another
hospital secondary to hypocalcemic convulsions
and electrolyte imbalance. There was no
medical record of the brother's case. During his
first admission, the laboratory investigations
revealed severe hyponatraemia of 125 mmol/L
(136-145), hyperkalemia of 6.4 mmol/L (3.5-5.1)
and moderate metabolic acidosis pH: 7.22 (7.377.45), a serum bicarbonate level of 18.5 mmol/L
(21-26). A hormonal study was done showing a
normal serum cortisol level of 170.6 nmol/L (138636), normal levels of 17- hydroxyprogesterone of
3.2 ng/ml (0.6-7), normal ACTH level of 18.76

www.ppa.org.pk

Al-Agha A

pmol/L (9-52), and a normal aldosterone level of

129 ng/dl (5-132).
During hyponatremia, (a sample was taken when
sodium levels were low) and we found a high
serum rennin level of 104 pg/ml (6-80). Renal
ultrasound
revealed
no
urinary
tract
malformations, urinalysis and culture revealed no
urinary tract infection. Based on the previous
findings
the
diagnosis
of
pseudohypoaldosteronism
was
established.
Regarding the investigations of the repeated
attacks of hypocalcemia, patient total serum
calcium was 1.32 mmol/L (2.12 - 2.5), his serum
phosphate levels were high, 2.5 mmol/L (0.811.58), with a normal serum alkaline phosphatase
level of 231 U/L (136 - 325). The diagnosis of
hypoparathyroidism was made because of low
parathyroid hormone level of 0.35 Pmol/L (1.6 6.9) during the hypocalcaemic attacks. Also, low
levels of free T4 11.7 Pmol/L (12 - 22), and a high
TSH level of 8.7 IU/L (0.27 - 4.2) with the diagnosis
of hypothyroidism were reported as well. Series of
investigations were done during the repeated
attacks and admissions that showed similar
values. No genetic analysis has been done due
to unavailability of genetic testing. The patient
has been following up in the pediatric
endocrinology clinic till now. Currently, the
patient is on oral medications that include
sodium bicarbonate, potassium binding resins
(sodium resonium), one-alpha drops, calcium
carbonate, sodium chloride solution and Lthyroxine. The patients last visit was at the age of
3 years and it showed TSH level of 3.1 IU/L, T4 14.6
Pmol/L, PTH 0.41 Pmol/L, serum calcium 2.1
mmol/L, potassium 3.6 mmol/L and sodium 136
mmol/L. Our patient's maintenance therapy
improved his electrolyte disturbances and thyroid
function; however, due to his permanent
endocrinopathies his hormone levels did not
improve.

DISCUSSION
A thorough literature review regarding the topic
at
hand
(pseudohypoaldosteronism,
hypothyroidism and hypoparathyroidism) that
extended to the past decade revealed no
reported cases with similar associations. The
cases
we
found
were
of
transient
pseudohypoaldosteronism with urinary tract
malformations,
i.e.
vesicoureteral
reflux2

Pseudohypoaldosteronism, Hypothyroidism and Hypoparathyroidism

obstructive uropathy and posterior urethral

There
were
reported
cases
of
valve3.
pseudohypoaldosteronism with pustular miliaria
rubra4 and a case associated with right renal
duplication anomaly with poorly functioning
upper pole moiety which was resolved due to
surgical intervention.
Many studies were conducted on the association
of hypothyroidism5 and hypoparathyroidism6 with
thalassemia major due to iron overload. Such
studies focused on the means of prevention
through good chelation therapy. There were
reported cases of hypothyroidism in ANA positive
Juvenile Rheumatoid Arthritis and Systemic Lupus
Erythematosus which showed a connection
between thyroid disease and autoimmune
diseases7. One such case reported the onset of
neonatal hypothyroidism after trophoblastic
disease during pregnancy in a hyperthyroid
mother8. Other cases revealed the association of
autoimmune
hypothyroidism
with
Down
syndrome and Celiac disease. Hypothyroidism
was also seen in those patients with Williams
syndrome.
Several
cases
of
transient
neonatal
hypoparathyroidism born to hyperparathyroid
mothers were reported9. There was one case of
hypoparathyroidism associated with Pallister-Hall
Syndrome10. Our literature review revealed no
similar cases that could be linked to ours. We
believe this is the first reported case that reveals
the
association
between
pseudohypoaldosteronism, hypothyroidism and
hypoparathyroidism.

pyelonephritis as a cause of hyponatremia /

hyperkalemia in young infants with urinary
tract malformations. Pediatr Infect Dis J.
1995; 4(1): 56-59.
3.

Blchmann G, Schuster T, Heger A, et al.

Transient
pseudohypoaldosteronism
secondary to posterior urethral valves--a
case report and review of the literature. Eur
J Pediatr Surg 2001; 11(4): 277-79.

4.

Argoubi H, Fitchner C, Richard O, et al.

Pustular miliaria rubra and systemic type 1b
pseudohypoaldosteronism in a newborn.
Ann Dermatol Venereol 2007; 134(3 Pt 1):
253-56.

5.

Karamifar H, Shahriari M, Sadjadian N.

Prevalence of endocrine complications in
betathalassaemia major in the Islamic
Republic of Iran. East Mediterr Health J 2003;
9(1-2): 55-60.

6.

Toumba M, Sergis A, Kanaris C, et al.

Endocrine complications in patients with
Thalassaemia Major. Pediatr Endocrinol Rev
2007; 5(2): 642-48.

7.

Aleem A, Al-Momen AK, Al-Harakati MS, et

al.
Hypocalcemia
due
to
hypoparathyroidism in beta-thalassemia
major patients. Ann Saudi Med 2000; 20(56): 364-66.

8.

True DK, Thomsett M, Liley H, et al. Twin

pregnancy with a coexisting hydatiform
mole and liveborn infant: complicated by
maternal hyperthyroidism and neonatal
hypothyroidism. J Paediatr Child Health
2007; 43(9): 646-48.

9.

Tseng UF, Shu SG, Chen CH, et al. Transient

neonatal hypoparathyroidism: report of four
cases. Acta Paediatr Taiwan 2001; 42(6):
359-62.

10.

Bacchetta J, Ranchin B, Brunet AS, et al.

Autoimmune hypoparathyroidism in a 12year-old girl with McKusick cartilage hair
hypoplasia. Pediatr Nephrol 2009; 24(12):
2449-53.

ACKNOWLEDGMENT
I would like to thank Mrs. Joy Almeda De Silva for
her secretarial assistance.

REFERENCES
1.

Cheek DB, Perry JW. A salt wasting

syndrome in infancy. Arch Dis Child 1958;
33(169): 252-56.

2.

Melzi ML, Guez S, Sersale G, et al. Acute

177

www.ppa.org.pk

ABSTRACT

Abstract Service
-----------------------------------------------------------------Pak Paed J 2011 35(3): 178-79

Acute Tc-99m DMSA scan for identifying

dilating vesicoureteral reflux in children: a
meta-analysis

cannot be recommended as replacement for

VCUG in the evaluation of young children with a
first febrile UTI.

by

Pediatrics. 2011 Jul; 128(1):e169-79.

Department of Pediatrics, Democritus University of

Thrace
and
University
General
Hospital
of
Alexandroupolis, Thrace, Greece.

A randomized controlled trial of propranolol

for infantile hemangiomas.

Mantadakis E, Vouloumanou EK, Georgantzi GG,

Tsalkidis A, Chatzimichael A, Falagas ME.

Controversy exists regarding the type and/or

sequence of imaging studies needed during the
first febrile urinary tract infection (UTI) in young
children. Several investigators have claimed that
because
acute-phase
Tc-99m
dimercaptosuccinic acid (DMSA) renal-scan
results are abnormal in the presence of dilating
vesicoureteral reflux, a normal DMSA-scan result
makes voiding cystourethrography (VCUG)
unnecessary in the primary examination of infants
with UTI. To evaluate the accuracy of acutephase DMSA scanning in identifying dilating
(grades III through V) vesicoureteral reflux
documented by VCUG in children with a first
febrile UTI, we performed a meta-analysis of the
accuracy of diagnostic tests as reported from
relevant studies identified through the PubMed
and Scopus databases. Patient-based and renal
unit-based analyses were performed. Overall, 13
cohort studies were identified. Nine studies
involved patients younger than 2 years, 3
involved children aged 16 years or younger, and
1 involved exclusively neonates. Girls constituted
22% to 85% of the involved children. Pooled (95%
confidence intervals) sensitivity and specificity
rates of DMSA scanning were 79% and 53%,
respectively, for the patient-based analysis (8
studies) and 60% and 65% for the renal unit-based
analysis (5 studies). The respective areas under
the hierarchical summary receiver operating
curves were 0.71 and 0.67. Marked statistical
heterogeneity was observed in both analyses, as
indicated by I(2) test values of 91% and 87%,
respectively. Acute-phase DMSA renal scanning

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by

Hogeling M, Adams S, Wargon O.

Source FRCP, Sydney Children's Hospital, High Street,
Randwick, New South Wales 2031, Australia.
hogelingm@yahoo.ca.

Objective: Propranolol hydrochloride is a safe

and effective medication for treating infantile
hemangiomas (IHs), with decreases in IH volume,
color, and elevation.
Methods: Forty children between the ages of 9
weeks and 5 years with facial IHs or IHs in sites
with the potential for disfigurement were
randomly assigned to receive propranolol or
placebo oral solution 2 mg/kg per day divided 3
times
daily
for
6
months.
Baseline
electrocardiogram,
echocardiogram,
and
laboratory
evaluations
were
performed.
Monitoring of heart rate, blood pressure, and
blood glucose was performed at each visit.
Children younger than 6 months were admitted
to the hospital for monitoring after their first dose
at weeks 1 and 2. Efficacy was assessed by
performing blinded volume measurements at
weeks 0, 4, 8, 12, 16, 20, and 24 and blinded
investigator scoring of photographs at weeks 0,
12, and 24.
Results: IH growth stopped by week 4 in the
propranolol group. Significant differences in the
percent change in volume were seen between
groups, with the largest difference at week 12.
Significant decrease in IH redness and elevation
occurred in the propranolol group at weeks 12
and 24 (P = .01 and .001, respectively). No
significant
hypoglycemia,
hypotension,
or

179

Abstract Service

bradycardia occurred. One child discontinued

the study because of an upper respiratory tract
infection. Other adverse events included
bronchiolitis,
gastroenteritis,
streptococcal
infection, cool extremities, dental caries, and
sleep disturbance.
Conclusion:
Propranolol
hydrochloride
administered orally at 2 mg/kg per day reduced
the volume, color, and elevation of focal and
segmental IH in infants younger than 6 months
and children up to 5 years of age.
Pediatrics. 2011 Aug; 128(2):e259-66.

Manifestations of severe vitamin d deficiency

in adolescents: effects of intramuscular
injection of a megadose of cholecalciferol
by

Soliman AT, Adel

Aziz Bedair EM.

A,

Wagdy

M,

Alali

M,

Department of Pediatrics, Hamad Medical Center, PO

Box 3050, Doha, Qatar

We recorded the manifestations of severe

vitamin D deficiency (VDD) in 40 adolescents
before and 3 and 6 months after treatment with
a mega dose of cholecalciferol (10 000 IU kg(-1),
max 600 000 IU). Significant improvement of
symptoms related to VDD was reported in 34/40.
Three months after the injection, serus calcium,
phosphate,
alkaline
phosphatase
and
parathormone were normal in all adolescents
with VDD with 25-hydroxyvitamin D (25OHD) level
= or >20 ng ml(-1). After 6 months, the majority
had 25OHD level <20 ng ml(-1). Two patterns of
radiological changes have been recorded with
complete healing achieved in all patients after a
year of therapy. A mega dose of cholecalciferol
is an effective therapy for treatment of VDD in
adolescents for 3 months but not for 6 months.
Radiographs of the ends of long bones are still
valuable tool for diagnosis and follow-up of these
patients.
J Trop Pediatr. 2011 Aug; 57(4):303-6.

The utility of an interferon gamma release

assay for diagnosis of latent tuberculosis

infection and disease in children:

systematic review and meta-analysis

by

Machingaidze S, Wiysonge CS, Gonzalez-Angulo

Y, Hatherill M, Moyo S, Hanekom W, Mahomed H
SourceSouth
African
Tuberculosis
Vaccine
Initiative, Institute of Infectious Diseases and
Molecular Medicine, University of Cape Town,
Cape Town, South Africa.
Background: The utility of interferon gamma
release assays (IGRAs) has been assessed in
adults, but remains unclear in children. We
reviewed the literature on the use of a
commercial IGRA in immunocompetent children
for the diagnosis of both latent tuberculosis
infection (LTBI) and TB disease.
Methods: We searched PubMed for studies
published before January 2010 on the diagnosis
of TB in children using an IGRA. We compared the
specificity and sensitivity of the tuberculin skin test
(TST) and the IGRA for LTBI and conducted a
random effects meta-analysis on sensitivity of the
IGRA for TB disease.
Results: Of 68 studies identified, 20 were included
in this review. There was increased specificity of
the IGRA for LTBI in children compared with TST,
but varying sensitivities. Sensitivity of the IGRA in
detecting TB disease in children also varied when
compared with TST (mean score, 0.57). For all TB
cases, the pooled sensitivity was 66% (95%
confidence
interval
[CI],
53%-78%)
with
heterogeneity (I = 74.8%). Stratification by
background
TB
incidence
highlighted
a
significantly reduced IGRA sensitivity of 55% (95%
CI, 37%-73%) in high incidence settings when
compared with low incidence settings, 70% (95%
CI, 53%-84%).
Conclusions: There was no clear evidence that
IGRAs should replace TST for detecting LTBI in
children. Sensitivity of the IGRA for TB disease was
no different from TST, and a significantly reduced
IGRA sensitivity was found in high-burden TB
settings compared with low-burden TB settings.
Further studies are needed to determine the
value of IGRAs in LTBI and TB disease diagnosis in
children.
Pediatr Infect Dis J. 2011 Aug; 30(8):694-700.

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NEWS AND VIEWS

-----------------------------------------------------------------Pak Paed J 2011; 35(3): 180-81

The Measles Initiative vaccinates one billion

children in first decade
WASHINGTON D.C., 4 August 2011 The Measles
Initiative today announced it has helped
vaccinate one billion children in more than 60
developing countries since 2001, making
significant gains in the global effort to stop
measles.
With
accelerated
immunization
activities spearheaded by governments and the
Measles Initiative, global measles mortality has
decreased by an impressive 78 percent
worldwide from 733,000 deaths in 2000 to 164,000
in 2008. Reductions in measles-related deaths
during that same time period accounts for nearly
a quarter (24 percent) of the overall decrease in
childhood mortality, representing significant
progress toward Millennium Development Goal 4
(MDG4). Since 2009, widespread outbreaks
affecting 30 countries in sub-Saharan Africa,
including the Democratic Republic of the Congo
and Ethiopia, have resulted in more than 320,000
new measles cases and more than 2,400
measles-related deaths. In the past year, several
European nations have faced their worst measles
outbreaks in more than 10 years, with more than
30,000 estimated cases across the region. The U.S.
is also experiencing its largest measles outbreak
since 1996, with more than 150 reported cases.
The rise in outbreaks, especially in Africa, can be
attributed in large part to the decrease in
financial support to the Measles Initiative, said
Andrea Gay, executive director of childrens
health with the United Nations Foundation.
Funding decreased from a high of $150 million in
2007 to $68 million in 2010. Due to inadequate
funding, measles vaccination campaigns have
been delayed and the target age groups have
been narrowed, resulting in outbreaks and in less
children being vaccinated overall, she said. The
WHO estimates that waning support could result
in half a million more deaths each year and erase
the Measles Initiatives gains by 2013. Because it
costs less than $1 per child to vaccinate against
measles, the real stumbling block is the lack of
political commitment in many countries. The

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Measles Initiative continues to advocate with

governments and appeal to donors around the
world to maintain an aggressive vaccination
schedule, and improve routine immunization and
surveillance in developing countries. The support
of other nations, paired with financial and
technical support from the Measles Initiative, has
proven to be influential among those countries
whose immunization programs have not kept
pace. Looking ahead to its second decade, the
Measles Initiative will focus on achieving a series
of interim targets toward the eventual
eradication of measles. The first of these
milestones will be to reduce measles mortality by
95 percent by 2015 (compared to 2000). The
Measles Initiative estimates it will need
approximately $212 million between 2012 and
2015 to reach the targets.
Reference:
UNICEF.
Available
from:
http://www.unicef.org/media/media_59466.html
downloaded on August 30, 2011.

Childhood ADHD Prevalence Rises By 28% In

Ten Years In USA
Over a ten-year period, the prevalence of
children diagnosed with ADHD (attention deficit
hyperactivity disorder) rose from 7% to 9% of all
children, an increase of 28%, according to a
report issued by the National Center for Health
Statistics, part of the CDC. The period studied was
from 1998-2000 through 2007-2009. The authors
are not yet sure whether the statistics represent a
real increase, or reflect more aggressive
diagnosis and reporting. They believe it is
probably mainly due to the latter. They added
that this report concentrated on children aged
between 5 and 17 years.
Reference: Akinbami LJ, Liu X, Pastor PN, Reuben CA.
Attention deficit hyperactivity disorder among children
aged 517 years in the United States, 19982009. NCHS
data brief, no 70. Hyattsville, MD: National Center for
Health
Statistics.
2011.
Available
at
http://www.cdc.gov/nchs/data/databriefs/db70.pdf

News and Views

181
Society. Their policy statement will be published in
Pediatrics, September 2011 issue.

Boxing Is Not A Good Sports Option For

Children And Teenagers, Says American
Academy Of Pediatrics

Reference: "Policy StatementBoxing Participation by

Children and Adolescents" American Academy of
Pediatrics, Council on Sports Medicine And Fitness,
Canadian Paediatric Society, Healthy Active Living and
Sports Medicine Committee. Pediatrics August 28th,
2011.

A sport where the main objective is to

deliberately hit someone on the head is not
appropriate for children and teenagers, says the
American Academy of Pediatrics in a new Policy
Statement, along with the Canadian Paediatric

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