Professional Documents
Culture Documents
CONTENTS
FROM THE EDITOR'S DESK 79
Journal Office: Indian Journal of Practical Pediatrics, IAP-TNSC Flat, F Block, Ground Floor, Halls Towers,
56, Halls Road, Egmore, Chennai - 600 008. INDIA. Tel.No. : 044-28190032 E.mail : ijpp_iap@rediff mail.com
Address for ordinary letters: The Editor-in-Chief, Indian Journal of Practical Pediatrics, Post Bag No.524,
Chennai 600 008.
Address for registered/insured/speed post/courier letters/parcels and communication by various authors:
Dr. A. Balachandran, Editor-in-chief, Indian Journal of Practical Pediatrics, F Block, No. 177, Plot No. 235,
4th Street, Anna Nagar East, Chennai - 600 102. Tamil Nadu, INDIA.
1
Indian Journal of Practical Pediatrics 2005; 7(2) : 78
- Editorial Board
Published and owned by Dr. A. Balachandran, from Halls Towers, 56, Halls Road, Egmore,
Chennai - 600 008 and printed by Mr. D. Ramanathan, at Alamu Printing Works,
9, Iyyah Mudali Street, Royapettah, Chennai - 600 014. Editor : Dr. A. Balacnadran.
2
2005; 7(2) : 79
Greetings from the Journal Committee of pediatric age group and may serve as a marker for
IJPP! In this issue we are focusing on Pediatric underlying immune deficiency state.
Dermatology. We profusely thank Dr.Jayakar
Thomas, Guest Editor for this issue who has Dr.Shabhaz A Janjua from Pakistan has
carefully chosen the topics and authors for this written in detail about Pediculosis and scabies in
issue. We also thank Dr.Vijayabhaskar, children, which are the most common causes for
Dr.V.Anandan and Dr.R.Madhu the office bearers itchy skin disorders in tropics. The author has given
of IAP Dermatology Group for coordinating with a vivid picture on the parasites, clinical features
the Guest Editor and Journal Committee for and the management of these itchy disorders. With
meticulously going through the manuscript in his vast experience and clinical knowledge on
detail. We all know that Pediatric Dermatology is dermatology Dr.Jayakar Thomas has dealt in detail
very interesting subject and it varies distinctly from about the Emergencies in pediatric dermatology.
adult skin disorders. Thus, these topics will He has stressed the need for intensive care for these
definitely enrich the knowledge of practicing conditions and we have to start thinking of intensive
pediatrician on practical dermatological problems. skin care unit in the near future. The differentiating
Dr.Jayakar Thomas in his note on Guest Editor features between SSSS, SJS and TEN will serve as
mentioned that the pediatric dermatology is now a ready reckoner for the practitioners.
advancing at a greater speed and more and more Under the management update the article on
information will come in the near future. Bacterial meningitis in the post neonatal period
Collagen vascular disorders in children written by Nagabhushana Rao P, et al will be an
written by Dr.Ian McColl from Australia is a good academic feast to the young postgraduates and
review on some of the conditions like lupus pediatricians who are dealing with very sick
erythematosus, dermatomyositis, scleroderma, etc, children in the hospital settings. He has written
which will be very useful for the postgraduates and extensively on the current trends in the management
the practicing pediatrician. Uricaria in children of this dreadful clinical condition. Under the
is the common skin condition encountered in the popular heading on Radiologist talks to you,
clinical practice. Dr.Sandipan Dhar has given a Vijayalakshmi G, et al has written on Evaluation
clear account on the causes of urticaria, the of neonatal jaundice. They have mentioned the
management and review on current literature. role of imaging in an infant with neonatal jaundice
to decide the surgical intervention.
Drug reaction in children is very alarming
for the parents as well to the practitioners. DM The Journal Committee profusely thanks our
Thappa, et al has written in detail the epidemiology, Guest Editor and the Pediatric Dermatology Group
pathogenesis and the clinical features of various for their effort in bringing out this special issue.
drug eruptions. We hope this article will bring more We also thank all the authors for contributing
light on this controversial subject. Dr.Sangeeta interesting articles in this issue.
Amladi has contributed the article on Childhood Dr. A.Balachandran
bacterial skin infections. She has mentioned that Editor-in-Chief
bacterial skin infections are the most common in
3
Indian Journal of Practical Pediatrics 2005; 7(2) : 80
INSTRUCTIONS TO AUTHORS
General
Print the manuscript on one side of standard size A4, white bond paper, with margins of at least 2.5 cm (1)
in double space typescript on each side. Use American English using Times New Roman font 12 size.
Submit four complete sets of the manuscript.
They are considered for publication on the understanding that they are contributed to this journal solely.
All pages are numbered at the top of the right corner, beginning with the title page.
All manuscripts should be sent to: The Editor-in-Chief, Indian Journal of Practical Pediatrics
Manuscript
1st Page
Title
Name of the author and affiliation
Institution
Address for correspondence (Email, Phone, Fax if any)
Word count
No. of figures (colour / black and white)
No. of references
Authors contribution
2nd Page
Abstract (unstructured, not exceeding 100 words) with key words (not exceeding 4)
3rd Page -
Acknowledgement
Points to remember (not more than 5 points)
Text
References
Tables
Legends
Figures should be good quality, 4 copies black & white / colour,*
(4 x 6 inches Maxi size) Glossy print
* Colour images will be charged separately
Text
Only generic names should be used
Measurements must be in metric units with System International (SI) Equivalents given in parentheses.
References
Recent and relevant references only
Strictly adhere to Vancouver style
Should be identified in the text by Arabic numerals in parentheses.
Type double-space on separate sheets and number consecutively as they appear in the text.
Defective references will entail rejection of article
Tables
Numbered with Roman numerals and typed on separate sheets.
Title should be centered above the table and explanatory notes below the table.
Figures and legends
Unmounted and with figure number, first authors name and top location indicated on the back of each
figure.
4
2005; 7(2) : 81
Declaration by authors **
I/We certify that the manuscript titled . represents valid work and that neither
this manuscript nor one with substantially similar content under my/our authorship has been published or is
being considered for publication elsewhere. The author(s) undersigned hereby transfer(s), assign(s), or otherwise
convey(s) all copyright ownership, including any and all rights incidental thereto, exclusively to the Indian
Journal of Practical Pediatrics, in the event that such work is published in Indian Journal of Practical Pediatrics.
I / we assume full responsibility for any infringement of copyright or plagiarism.
5
Indian Journal of Practical Pediatrics 2005; 7(2) : 82
Pediatric dermatology is a fascinating concern to the reader and to the child patient.
speciality. Needless to say that the pediatric skin Bacterial dermatoses, Scabies and Pediculoses,
differs in more than one way from its adult Urticaria, Collagen Vascular Disorders and
counterpart anatomically, physiologically, Adverse Cutaneous Drug Reactions are seen
pathologically and in response to treatment. every day in a busy out-patient department and
More of it is described in the pages to follow. these topics have been written by authorities in
the respective subjects. For this I acknowledge
As one practicing pediatric dermatology, it
my colleagues Drs, Sangeeta Amladi, Shahbaz
is indeed my pleasure to be the Guest Editor of
Janjua, Sandipan Dhar, Ian McColl and Devinder
this issue of the Indian Journal of Practical
Thappa. The article on Emergencies in Pediatric
Pediatrics (IJPP) that deals with Pediatric skin
Dermatology is added for academic reasons and
disorders. At the very outset, I must thank the
for the inhouse physicians.
Editor-in-Chief, Dr. A. Balachandran for giving
me this opportunity. My special thanks to our overseas
contributors Dr. Shahbaz Janjua from Pakistan
Given the speed at which pediatric and Dr.Ian McColl from Australia for their instant
dermatology is now advancing and the interest acceptance to send in their articles.
shown by pediatricians and dermatologists alike,
Finally, I have to immensely thank my wife
I am forced to humbly accept the fact that the
Dr. Nirmala Thomas for the cooperation and help
utility of this issue is likely to get outdated
rendered by her in compiling this work.
rapidly. However my colleagues who have
contributed to this issue have made every attempt Dr. Jayakar Thomas
to highlight the fundamentals, which will never Senior Consultant Dermatologist,
change. Readers may add on subsequently. The Apollo Hospitals and
topics are of importance in day-to-day practice Kanchi Kamakoti CHILDS Trust Hospital,
and have been dealt with the utmost care and Chennai, India
RESPICON 2005
Organized by
IAP Respiratory Chapter & IAP Environment & Child Health Group
Hosted by
IAP Respiratory Chapter, Karnataka State Branch
Co-Sponsors: IAP-BPS, Bangalore Branch.
Venue: Jnana Jyothi Convention Hall, Central College Campus, Bangalore, Karnataka.
Date: 10th and 11th September 2005
Address for correspondence: Dr.S.Nagabhushna, Organizing Secretary, RESPICON 2005, Ashwini
Health Centre, I main II cross, Sundar Nagar, Gokula Post, Bangalore 560 054.
Email:nagabhushana_s@rediffmail.com
6
2005; 7(2) : 83
DERMATOLOGY
CLINICAL FEATURES OF discoid lupus and the annular lesions more typical
COLLAGEN VASCULAR of subacute lupus3. Most cases are female with
DISORDERS IN CHILDREN an 8:1 ratio to males. This is the same ratio that
is seen in systemic lupus. More chronic lesions
* Ian McColl will show the features of discoid lupus with
scaling, atrophy and hypo or hyperpigmentation.
Abstract: Collagen vascular diseases encompass
Infants with neonatal lupus are typically born to
a group of diseases that are seen both in adults
mothers with systemic lupus, rheumatoid arthritis
and in children. In this review, emphasis is on
or some other type of mixed connective tissue
certain findings that differentiate the conditions
disease.
between children and adults. The diseases
considered include lupus erythematosus, Infants with neonatal lupus have also shown
dermatomyositis, scleroderma, mixed connective thrombocytopenia4, aplastic anaemia, mild liver
tissue disease and Sjogrens syndrome involvement and rarely CNS vasculopathy. Skin
lesions of neonatal cutaneous lupus may be
Key words: Scleroderma, Lupus Erythematosus, present at birth so sunlight is not necessarily a
Dermatomyositis, Mixed Connective Tissue prerequisite for the development of the rash3.
Disease However most cutaneous lesions occur within a
few days of birth and can occur on any part of
Lupus erythematosus
the body, including the scalp, but they are seen
Lupus erythematosus can present very early most frequently around the eyes. The lesions are
in childhood as neonatal lupus. This condition often annular with slightly scaly plaques similar
is seen in the children of mothers who are Ro to those seen in subacute lupus. Telangiectasia
antibody positive1. The children present with may persist at sites of previous lesions and this
annular lesions in sun exposed areas and with telangiectasia can last for some years3. The skin
increased photosensitivity. Cardiac involvement lesions themselves usually disappear by about
occurs in 75% of cases with congenital heart 7 months of age but may rarely persist for as long
block seen in 15% to 30% of affected infants2. as 15 months. This is usually related to the
This heart block is irreversible. However the disappearance of the mothers Ro antibody from
cutaneous changes are reversible. These infants the childs bloodstream. The differential
initially show increased sun sensitivity diagnosis of these lesions include atopic eczema,
developing into diffuse erythema in sun exposed seborrhoeic dermatitis, psoriasis, tinea faciei and
areas particularly around the periocular skin. photosensitive genodermatoses such as Blooms
However they may also develop the lesions of syndrome, Rothmund-Thomson and Cockayne
syndrome.
* Dermatologist
John Flynn Medical Centre, Lupus erythematosus in childhood usually
Tugun, Gold Coast, presents as systemic lupus rather than as localised
Australia. benign cutaneous discoid lupus. The peak
7
Indian Journal of Practical Pediatrics 2005; 7(2) : 84
incidence of the disease is around the age of 12 Unlike normal urticaria the hive like lesions last
years and the condition is usually more acute and longer than 24 hours and often have haemorrhage
severe than that found in adults. Morphologically left after the lesion has cleared, particularly at
the classic discoid lupus lesions are the the peripheries of the hives. Urticarial vasculitis
commonest skin manifestation of systemic lupus may be associated with hypo complementemia.
erythematosus in childhood. The classic features
of discoid lupus lesions are scaling with follicular Telangiectasia of the nail folds is common
plugging, telangiectasia and hypopigmentation. to scleroderma, dermatomyositis and lupus
The cutaneous lesions may be the presenting erythematosus, but a papular telangiectasia of the
feature of systemic lupus in childhood in about palms and fingers is more common in lupus.
25% of cases. The butterfly rash consists of Occasionally the vasculitis of lupus can give rise
erythema and scaling particularly over the nose to small peripheral cutaneous infarcts, but this
and cheek areas. Crusting and scaling of the phenomenon is more commonly seen in
lower lip is an additional feature because it is the scleroderma than in lupus.
most sun exposed site. Children with systemic
lupus also develop a diffuse sunburn like rash Chilblains or perniosis are tender purplish
and may also develop plaques. These may show nodules at the peripheries particularly of the
the typical features of discoid lupus being annular fingers and toes. This may also be a presenting
with thick carpet tack like scale, atrophy and both feature of both systemic and discoid lupus.
hypo and hyperpigmentation. The hyperpigmen-
Lupus profundus characterised by facial
tation is particularly common on the outside of a
depressions due to loss of subcutaneous fat with
lesion representing a lesser degree of basal layer
associated hypo and hyperpigmentation may be
damage than the hypopigmented area. Mucous
seen with associated discoid lupus but also in
membrane lesions comprising of erosions,
systemic lupus. Around 50% of patients with
gingivitis and mucosal haemorrhage may be seen.
lupus profundus will eventually develop systemic
Scarring alopecia is also a feature of lupus. lupus. These lesions are usually seen on the
Increased fragility of the hair results in hair forehead, cheeks and buttocks.
broken off at different levels, with the patient
developing a receding hairline. Dermatomyositis
Livedo reticularis, reticulated bluish red
The clinical features of dermatomyositis are
discolouration of the skin with a net like pattern,
much the same in children as in adults except for
is more particularly seen in other connective
calcinosis which is much more common in
tissue diseases such as scleroderma, but it is also
children. Unlike dermatomyositis in adults,
a feature of systemic lupus. It is made worse by
children do not show an association with
exposure to cold. Raynauds phenomenon
underlying malignancy. In a child, look for the
characterised by a stark white digit that
heliotrope periocular rash involving the upper and
subsequently goes blue on exposure to cold is a
lower eyelids, photosensitivity and other diffuse
feature of lupus, but perhaps a more common
erythema particularly over the extensor surfaces
feature in scleroderma. It may precede the onset
of the knees and elbows. On the hands this
of the condition by months to years.
erythema is prominent over the interphalangeal
Urticarial vasculitis is another cutaneous joints in contradistinction to lupus erythematosus
manifestation of systemic lupus in children. where it is the area of skin between the joints
8
2005; 7(2) : 85
that is more usually inflamed. Generally in The muscle weakness in children is the same
dermatomyositis in children, the skin features will as in adults involving particularly the large
precede the joint weakness by three to six months. muscles of the thighs and arms known as the limb
The condition is more common in females than girdle muscles. The rash in dermatomyositis
males, but the ratio is only 2:1. In children the usually gives a history of being worse after sun
commonest age for this condition is between five exposure and may precede the development of
and 12 years. The other clinical features that are muscle weakness by some months, sometimes
different in children compared to adults are that years. However the dermatitis over the knuckles
they rarely have Raynauds phenomenon and and the eyelid rash are usually the first
have more muscle weakness and involvement. manifestations of the condition. The presenting
Gottrons papules are seen on the dorsal clinical characteristics of children with
interphalangeal joints and extensor surfaces of dermatomyositis were described by Pachman
the elbows and knees. They present as indicating that 100% of the children had a rash
erythematous and violaceous flat top papules but and proximal muscle weakness with reducing
are seen in both adults and children. Facial frequencies for other clinical features, but with
oedema can also be seen. The cuticles at the base 23% showing calcinosis6. A periocular facial rash
of the nails show fairly typical changes in is a common feature in dermatomyositis but facial
dermatomyositis. The cuticles themselves are oedema is also seen. Scarring and non-scarring
thickened, rough and scaly as if they have been alopecia can also be seen. Calcinosis that
traumatised. Under the dermatoscope the develops in dermatomyositis in children generally
capillary loops show linear telangiectasia and appears late in the course of the illness. Cutaneous
loop drop out, but this does not allow you to calcinosis is a feature of childhood
differentiate between dermatomyositis, lupus and dermatomyositis that is not seen to the same
scleroderma. As in lupus and scleroderma there extent in adult onset dermatomyositis, being seen
may be infarcts of the tips of the fingers due to in about 70% of cases of the juvenile variant but
angiitis. Facial hypertrichosis and hyper- in only about 5% of adult cases The calcium
pigmentation is more common in children with deposits are usually seen on the buttocks,
dermatomyositis than in adults. This is shoulders and elbows and may be extruded from
independent of the use of steroid therapy. the skin causing chronic ulceration.
Cutaneous erythema and dermatomyositis Paradoxically children showing this complication
fluctuate from day to day. It is certainly have a more favourable prognosis.
exacerbated by sun exposure and is more
common over the elbows, knees and shoulder tips The worse the initial inflammation of the
as well as the face, but in some cases the myositis skin in dermatomyositis, the more likely the child
may be much more marked than the dermatitis. is to develop severe calcinosis, but nowadays with
Late in the chronic stages of juvenile good treatment this inflammation is shut off early
dermatomyositis, poikiloderma can be seen. This and calcinosis is less likely to be seen. The
is characterised by hypo and hyperpigmentation calcinosis in dermatomyositis can take a variety
with telangiectasia and white atrophy. As many of patterns including superficial plaques or
as 40% of children can get oral lesions, with nodules in the extremities, calcinosis
involvement of the palate and buccal mucosa and circumscripta which is deeper and usually seen
the gum margin with lichen planus like whitish in the proximal muscles, calcinosis universalis
patches on the tongue and buccal mucosa5. and mixtures of these forms7.
9
Indian Journal of Practical Pediatrics 2005; 7(2) : 86
Telangiectasia usually occurs on the face Mixed connective tissue disease is again a
and is described as being mat like. These lesions rare condition in childhood. The cutaneous
are larger and more diffuse than those of the linear findings in children are an amalgam of the
telangiectasia seen in other collagen diseases. findings that are seen in the other collagen
They are often macular or square shaped and disorders described in this article. It can contain
hence are known as telangiectatic mats. The combinations of lupus, dermatomyositis,
CREST syndrome is seen in both children and scleroderma and Sjogrens syndrome so that
adults and describes Calcinosis, Raynauds sclerodactyly may been seen with a heliotrope
phenomenon, Esophageal dysfunction, rash, but generally these patients present with
Sclerodactyly and Telangiectasia. The features similar to lupus and with some
10
2005; 7(2) : 87
Raynauds and associated joint problems.9 There 3. Weston WL, Morelli JG, Lee LA. The clinical
are some clinical differences between adult and spectrum of anti-Ro-positive cutaneous
childhood forms of mixed connective tissue neonatal lupus erythematosus. J Am Acad
disease. Thrombocytopenia is usually only seen Dermatol 1999;40(5 Pt 1 ):675-681.
in childhood forms and renal and cardiac 4. Watson RM, Kang JE, May M et al.
problems are much higher in children than in Thrombocytopenia in the neonatal lupus
adults with the same condition. syndrome Arch Dermatol 1988; 124:560.
Points to remember 5. Hamlin C, Shelton JE. Management of oral
findings in a child with an advanced case of
1. Collagen vascular diseases are not common dermatomyositis. Pediatr Dent 1984; 6:46.
in children.
6. Pachman LM, Hayford JR, Chung A et al.
2. An unusual persisting skin rash with fever
Juvenile dermatomyositis at diagnosis:clinical
and joint pains are clues to suspect this characteristics of 79 children. J Rheum 1998;
group of conditions. 25(6):1198.
3. Renal parameters are to be closely
7. Blane CE, White SJ, Braunstein EM et al.
monitored.
Patterns of calcification in childhood
References dermatomyositis. Am J Radiol 1984;142:397.
1. Lee LA, Frank MB, McCubbin VR, et al. The 8. Chudwin DS, Daniels TE, Wara DW et al.
autoantibodies of neonatal lupus Spectrum of Sjogrens syndrome in children.
erythematosus. J Invest Dermatol 1994; J Pediatr 1981;98:213.
102:963-966. 9. Singsen BH, Bernstein BH, Kornreich HK
2. Korkij W, Soltani K. Neonatal lupus et al. Mixed connective tissue disease in
erythematosus: a review. Pediatric Dermatol childhood: a clinical and serological survey.
1984; 1( 3):189-195 J Pediatr 1977;90:893.
MAHAPEDICON-2005, AMRAVATI
XVI, Maharashtra State Conference of IAP, Maharashtra State Branch
Date: November 11,12 & 13th 2005
Contact:- Dr. Satish Tiwari / Dr. Satish Agrawal / Dr. Manoj Rathi, Org. Secretaries.
Secretariat:- Yashodanagar No. 2 Amravati Maharashtra 444606Ph. (0721) 2672252, 5612680
E-mail : ati_drtiwari@sancharnet.in ati_drsva99@sancharnet.in dr_manojr@yahoo.com
11
Indian Journal of Practical Pediatrics 2005; 7(2) : 88
DERMATOLOGY
infestations in chronic urticaria in adults is is particularly common in children who had been
negligible. In children, parasitic infestations are operated for spina bifida or other congenital
often implicated in cases of urticaria, although, malformations. Subsequently such cases of
may be overestimated at times 7 . Another urticaria can get aggravated in children while
important cause of urticaria in paediatric age eating chewing gum etc.
group is insect bites.
Vaccination and urticaria: The conventional
Inhalants, contact allergens and urticaria: belief is that urticaria can develop as a part of
Various inhalants, contact allergens are often anaphylaxis and serum 10 sickness following
associated with development of urticaria in vaccination because of sensitization by foreign
children mostly having personal and/or family proteins from serum and egg proteins on which
history of atopy. Various pollens from plants, viruses are grown. However, now it has been
ragweed and grass, various animal danders from established beyond doubt that children allergic
cats, dogs, horses, often cause urticaria in to eggs can be immunized safely with viruses
predisposed children. Contact with caterpillars grown on eggs11. There are only occasional
can cause urticaria in children. Prolonged contact reports of serum sickness due to horse/rabbit
with latex can cause urticaria in children8,9. This
antiserum.
13
Indian Journal of Practical Pediatrics 2005; 7(2) : 90
VI. In cases of chronic urticaria in adults, often and children below 8 years of age are supposed
in search of an etiology, one lands up in to suffer less as compared to their older
either collagen vascular disease or counterparts. Overall prognosis is, however,
lymphoreticular malignancy viz, lymphoma, favourable in children as compared to adults16,17.
leukemia etc. In children, however, such
causes are rare13. Management of urticaria and
angio-oedema in children
Natural history and prognosis
Natural history of urticaria in children is In majority of the cases of urticaria in
extremely variable. Course of most of the cases children, no investigation is required.
of ordinary urticaria/angio-odema is benign and Examination of peripheral blood and estimation
resolve on its own in a short span of time. The of absolute eosinophil count may be done.
duration of an acute attack on an average is few Estimation of total and specific serum IgE may
hours (particularly in cases of urticaria caused be carried out in chronic cases of urticaria.
by food and/or insect bites). In severe cases, the Oral antihistamines form the mainstay of
duration may be several days e.g., urticaria treat ment of urticaria. Classical H1 blockers have
caused by infections or cases of serum sickness. sedative and anticholinergic effects. However,
By and large two thirds of the cases of acute sedation is usually not a problem below 3-4 years
urticaria may become symptom free within two of age. There has been few pharmacokinetic
months1,6,8,14. Contrary to the popular belief, studies of antihistamines in children. Most of the
incidence of chronic urticaria was found to be prescribing patterns are empirically based upon
fairly common to the tune of 79.50% in children clinical experience18. By and large the onset of
in an Indian study15. It has been found that one action of most antihistamines is 30-60 minutes
third of newly affected children have symptoms after ingestion. However, full action is not
of chronic urticaria even 1 year after an acute reached for 2-3 hours. Various antihistamines
attack. Recurrent attacks mostly occur during used in children for urticaria are highlighted in
acute episodes of infections and their drug Table 4.
therapy. On an average mean duration of chronic
urticaria is 16 months in children. Higher There is little reason to choose one
incidence of resolution has been found in girls antihistamine over another except for avoidance
Table 4 : Antihistamines used in the For cases of anaphylaxis, acute urticaria with
treatment of urticaria in infants and angio-oedema, adrenaline (epinephrine) is the
children drug of choice. It is to be given subcutaneously
Sedative at a dose of 0.05 mg/kg/day in two divided doses.
Promethazine 0.5 mg/kg/dose Alternatively hydrocortisone, methyl-
Pheniramine 1.5 mg/kg/day prednisolone or dexamethasone, can be given
Chlorpheniramine 0.35 mg/kg/day intramuscularly or intravenously in single or two
Clemastine 0.125-0.25 mg bd 2-6 yrs, divided doses 1,18,19. Once the severity of the
0.5-1.0 mg bd 6-12 yrs, disease is brought under control, the maintenance
1 mg bd > 12 yrs therapy for 7-14 days can be done by institution
Hydroxyzine 1-2 mg/kg/day of oral prednisolone at a dose of 1mg to 3mg/kg/
Ketotifen 1 mg/day day or equivalent dose of betamethasone in single
Cyproheptadine 0.25 mg/kg/day or two divided doses. Cases of hereditary angio-
Mild Sedative oedema (HAE) show poor response to
Cetrizine 0.25 mg/kg/day conventional treatment modalities. Parenteral or
Non Sedative oral antihistamines, corticosteroids or even
Fexofenadine 30 mg bd 6-12 yrs adrenaline is of little/no help in such cases20,21.
Loratadine 5 mg/day <30 kg (to be However, all patients with HAE do not require
used only above 2 yrs of treatment. Treatment strategy can be planned as
age short term prophylaxis and long term
prophylaxis. For acute attacks before or after
surgery, infusion of purified inhibitor helps.
of adverse effects, including sedation in school Long-term control of the disease can be achieved
going children18. However the usually chosen by any one of the drugs e.g. danazol, fresh frozen
H1 blockers are chlorpheniramine, hydroxyzine plasma concentration, stanozolol, epsilon amino
and diphenhydramine. They are to be advocated caproic acid (EACA) or tranexamic acid20,21.
orally twice daily in syrup or tablet form. However, their potential toxicities limit their
On an average, for cases of acute urticaria 5 long-term safe use.
to 10 days antihistamine therapy is required; for Urticaria in infants and children,
cases of chronic urticaria the duration of particularly when recurrent and chronic, causes
treatment varies between 3 to 6 months. For cases lots of anxiety and apprehension in their parents.
not responding to oral antihistamine, H2 receptor Explaining the benign nature of the disease,
blocker e.g., ranitidine may be added. For school presumptive precipitating factors and their
going or older children, a combination of non avoidance help to allay anxiety of the parents.
sedating antihistamine during day time and Hence, reassurance and counseling of the parents
sedating antihistamine at night time is preferred. form the cornerstone of management of
In general antihistamines are extraordinarily urticaria and angio-oedema in infants and
safe 18 . New born babies sometime develop children1,22.
paradoxical CNS excitation and convulsions to Points to remember
some sedative antihistamines viz., promethazine,
hydroxyzine etc. This is thought to be due to 1. Aetiological factors are more readily
anticholinergic effect of these drugs. identifiable in infants and children.
16
2005; 7(2) : 93
2. Mostly acute urticaria is seen in children 9. Hamann CP. Natural rubber latex protein
as compared to frequent occurence of sensitivity in review. Am J Contact Derm 1993;
chronic urticaria in adults. 4 : 4-21.
10. McMahon BJ, Helminiak C, Wainwright RB.
3. Infections are very important cause of
Frequency of adverse reaction to hepatitis B
urticaria in paediatric age group.
vaccine in 43618 persons. Am J Med 1992; 92
4. Various food articles e.g., cow milk, fish, : 254-256.
egg, peanuts are commonly implicated as 11. James JM, Burks W, Roberson PK, Sampson
compared to food additives playing more HA. Safe administration of the measles vaccine
important role in adult urticaria. to children allergic to eggs. N Engl J Med 1995;
332 : 1262-1266.
5. In children, drugs are not that important a
cause for urticaria. 12. Sharma VK, Dhar S. Clinical pattern of
cutaneous drug eruptions among children and
References adolescents in North India. Pediatr Dermatol
1. Warin RP, Champion RH. Urticaria and 1995; 12 : 178-183.
angioedema. In : Ruiz Maldonado I Parish LC, 13. Kauppinen K, Juntunen K, Lanki H. Urticaria
Beare JM, eds. Textbook of Pediatric in children. Allergy 1984; 39 : 469-472.
Dermatology. Philadelphia, Grune & Stratton,
14. Legrain V, Taib A, Sage T et al. Urticaria in
1989: pp 600-611.
infants : a study of 40 patients. Pediatr Dermatol
2. Hannuksela M. Urticaria in children, Semin 1990; 7 : 101-107.
Dermatol 1987; 6 : 321-325. 15. Ghosh S, Kanwar AJ, Kaur S. Urticaria in
3. Champion RH, Roberts SOB, Carpentier RG, children. Pediatr Dermatol 1993; 10 : 107-110.
Roger JH. Urticaria and angioedema: a review 16. Harris A, Twarog FJ, Geha RS. Chronic
of 554 patients. Br J Dermatol 1969; 81 : 588- urticaria in childhood : natural course and
597. etiology. Ann Allergy 1983; 51 : 161-165.
4. Black AK, Champion RH. Urticaria, In : 17. Juhlin L. Recurrent urticaria: clinical
Champion RH, Burton JL, Burns JL, et al (eds). investigation of 330 patients. Br J Dermatol
Textbook of Dermatology, 6th edn. Oxford : 1981; 140 : 369-380.
Blackwell Science, 1998 : pp 2113-2139.
18. Kennard CD, Ellis CN. Pharmacologic therapy
5. Champion RH. Urticaria : then and now. Br J for urticaria. J Am Acad Dermatol 1991; 25 :
Dermatol 1988 : 427-436. 176-189.
6. Hamrick HJ, Moore GW. Giardiasis causing 19. Bochner BS, Lichtenstein LM. Anaphylaxis. N
urticaria in a child. Am J Dis Child 1983; 137 : Eng J Med 1991; 324 : 1785-1790.
761-763. 20. Agostini A, Cicardi M. Hereditary and acquired
7. Twarog FJ. Urticaria in childhood : C1-inhibitor deficiency : biological and clinical
pathogenesis and management. Pediatr Clin N characteristics in 235 patients. Medicine 1992;
Am 1983; 30 : 887-898. 71 : 206-215.
17
Indian Journal of Practical Pediatrics 2005; 7(2) : 94
DERMATOLOGY
18
2005; 7(2) : 95
11 (22%) fixed drug eruption (FDE), 10 (20%) 3. Generalized eruption is often pruritic.
erythema multiforme (EM), 6 (12%) toxic 4. Eruption is bilateral and symmetrical;
epidermal necrolysis (TEN), 5 (10%) Stevens- exception to this is fixed drug eruption.
Johnson syndrome (SJS), 3 (6%) urticaria, and 2
5. Regression of eruption occurs on withdrawal
(4%) erythroderma. The incubation period for
of drug.
maculopapular rashes, SJS and TEN due to
commonly used antibiotics and sulfonamides was 6. Similar type of rash recurs on re-exposure
short, a few hours to two to three days, reflecting to the same or similar drug.
reexposure, and for drugs used sparingly such as Pathogenesis
antiepileptics and antituberculosis agents, was
Undesirable cutaneous or mucocutaneous
approximately one week or more, suggesting a
reactions to systemically absorbed drugs occur
first exposure. Antibiotics were responsible for
through three mechanisms (Table 1)1, .
cutaneous eruptions in 27 patients, followed by
antiepileptics in 17, analgin in 4, and 1. Non-immune mechanisms: They include
metronidazole and albendazole in 1 each. drug induced hemolysis (G6PD deficiency),
Cotrimoxazole, a combination of sulfamethoxa- mast cell degranulation (codeine,
zole and trimethoprim, was the most common radiocontrast media), exacerbation of disease
antibacterial responsible for eruptions (11 (psoriasis by lithium or beta blocker), drug
patients), followed by penicillin and its deposition in skin, alopecia etc.
semisynthetic derivatives (8 patients),
sulfonamide alone (3 patients), and other 2. Immune mechanisms: All the four
antibiotics (4 patients). Antiepileptics were the hypersensitivity mechanisms may be
most frequently incriminated drugs in EM, TEN, involved.
and SJS.
Type I IgE dependent reactions cause
Multiple medical problems increase the urticaria, pruritus, bronchospasm and
chance of developing adverse drug eruptions8. laryngeal oedema within minutes, hours or
Adverse drug reactions amongst pediatric patients days.
are influenced by several factors like prolonged
Type II Cytotoxic reactions may cause
hospital stay, the classes of drugs used and
thrombocytopenia.
polypharmacy.
Type III Immune complex dependent
Characteristics of drug eruptions
reactions result in serum sickness, urticarial
These eruptions may closely mimic other or leukocytoclastic vasculitis within a week
skin disorders10. Following features characterize or so.
drug eruptions:
Type IV Cell mediated immune response
1. There is a history of drug intake preceding
may lead to eczematous and other types of
the eruption. The history of drug intake must
eruptions in 3 to 4 weeks time.
include all systemic drugs, nonprescription
drugs, home remedies and topical 3. Miscellaneous mechanisms: Under this
medications. comes, Jarisch-Herxheimer reaction and
2. Drug eruption is sudden in onset. infectious mononucleosis like reaction.
19
Indian Journal of Practical Pediatrics 2005; 7(2) : 96
21
Indian Journal of Practical Pediatrics 2005; 7(2) : 98
and epidermal necrosis. This is a form of SJS, and clinical findings of epidermolysis10. It is a
which is usually not seen in adults. Internal organ potentially life threatening, severe
involvement may come as late as 1-2 weeks. The mucocutaneous reaction pattern characterized by
most common inflammatory reaction is hepatitis fever, systemic toxicity, erythema and tenderness
followed by renal involvement. Other less of skin followed by flaccid bullae formation
common, but important internal reactions resembling a burn case. Nikolskys sign is
includes that of central nervous system positive. Mortality from TEN is 11 to 33%.
(encephalitis, aseptic meningitis), lungs
Diagnosis
(interstitial pneumonitis, respiratory distress
syndrome), myocarditis, and pancreatitis, etc.6 Diagnosis is basically based on suspicion
Fixed drug eruption: It differs from other and history of drug intake. A general rule of
eruptions in that it occurs and then recurs at fixed thumb is that drugs started within one week of
sites 10. Single or multiple circular or oval the onset of the eruption are the most suspects10.
erythematous macule(s) or plaque(s) develop The proper diagnosis of drug eruptions
with burning or stinging sensation. These lesions requires a stepwise approach12. These are making
sometime develop into bullous lesions and when the best diagnosis of eruption, determining the
heal leave behind slate gray coloured differential diagnosis of the event and the causes,
pigmentation. Mucocutaneous junctions are finding every drug that patient was exposed to
commonly affected. and estimating the probability that the drug was
Erythroderma: It is a generalized erythema, responsible for the reaction6, 12.
infiltration and scaling of the skin (involving Making a diagnosis of skin eruption:
more than 90% of the surface area of the body)10.
It may be a manifestation of drug eruption but The first step in managing an ACDR is to
usually occurs due to dermatological disorders make the proper diagnosis. Reactions in the skin
like psoriasis, contact dermatitis, pityriasis rubra can be diagnosed at three levels. These are based
pilaris, etc. on the determination of a specific morphology
Erythema multiforme: Erythema multiforme is of skin disease or syndrome.
characterized by many types of lesions including Morphology: The morphology of an ACDR is
urticaria, target lesions (iris lesions or bulls-eye usually exanthematous, urticarial or blistering.
lesions) and vesicles and bullae, bilaterally Sometimes, it is not possible to be more specific.
symmetrically over acral areas of the body10. Synonyms used for exanthematous reactions are
They may also involve mucous membranes. morbiliform, scarlatiniform or toxic erythema.
Steven Johnson syndrome: It is severe form of These reactions can progress to erythroderma or
erythema multiforme associated with exfoliative dermatitis. Urticarial reactions may
constitutional symptoms (fever) and visceral represent simple urticaria or be in association with
organ involvement e.g. kidneys10. Both the skin other symptoms or pathological changes, or they
as well as mucous membranes are involved. may represent urticarial vasculitis or serum
Toxic epidermal necrolysis (TEN): The term sickness like reaction. Until further diagnostic
toxic referred to a presumed toxin responsible steps are taken, the urticarial morphology is often
for the prodrome and the eruption, epidermal to the only clue to the diagnosis.
the presence of significant epidermal damage and Skin disease: Specific diseases would include
necrolysis for the pathologic findings of necrosis eruptions as diverse as fixed drug eruptions
22
2005; 7(2) : 99
(FDE), acute generalized exanthematous Some authorities maintain that high dose steroid
pustulosis (AGEP) or urticaria. These are based therapy promotes or masks signs of infection,
on cutaneous findings and the specific diagnosis delays healing, prolong hospital stay. Some
relates to a purely cutaneous manifestation of a favour its use on the basis that it reduces
drug eruption without internal organ inflammation and keratinocyte necrosis if used
involvement. early in the disease. The other modalities of
treatment are intravenous immunoglobulin
Syndromes: There are many syndromes that fall
therapy, plasmapheresis, cyclosporine and
into the hypersensitivity reaction category and
cyclophosphamide. Supportive care such as
these are associated with cutaneous
maintenance of fluid and electrolyte balance,
manifestations as well as internal organ
body temperature, nutrition, and wound care are
involvement. Serum sickness like reaction
utmost important. In case of HSR, the role of
(SSLR) and hypersensitivity syndrome reaction
corticosteroids is still debatable, but has a definite
(HSR) are two examples6, 12.
role if kidneys are involved1,6, 13.
Differential diagnosis
Rechallenge test may be done, once rash has
The second step in diagnosing a drug settled10. However, in patients who have had
reaction requires an evaluation of differential urticarial, bullous or erythema multiforme-like
diagnosis of the rash or syndrome6. Etiologies eruptions, it can be dangerous.
that may enter into discussion include viral
Points to remember
exanthems (infectious mononucleosis, human
parvovirus infection, etc), bacterial infections, 1. There is a history of drug intake preceding
Kawasakis disease and collagen vascular the eruption. The history of drug intake
diseases. For erythema multiforme, the common must include all systemic drugs,
alternative causes include herpes virus and nonprescription drugs, home remedies and
mycoplasma infection. topical medications.
2. Drug eruption is sudden in
Treatment
onset.Generalized eruption is often pruritic.
Clearly, prevention is better than cure1, 6, 13. 3. Eruption is bilateral and symmetrical;
Drugs implicated in a previous reaction should exception to this is fixed drug eruption.
be avoided. In case of suspected penicillin 4. Regression of eruption occurs on
allergy, an alternative antibiotic, such as withdrawal of drug.
erythromycin should be substituted. The 5. Similar type of rash recurs on re-exposure
approach to treatment of an established presumed to the same or similar drug.
drug eruption obviously depends on the severity
References
of the reaction. For minor conditions, withdrawal
of the suspected drug, and symptomatic therapy 1. Breathnach SM. Drug reactions. In: Champion
with emollients, topical corticosteroids and RH, Burton JL, Burns DA, Breathnach SM, eds.
systemic antihistamines is all that is necessary. Rook/Wilkinson/Ebling Textbook of
The management of TEN is perhaps best carried Dermatology, 6th edn., Oxford: Blackwell
out in an intensive care or burns care unit. The Science Ltd, 1998: pp 3349-3517.
mortality of TEN is around 20-30% despite 2. Shapiro S, Slone D, Siskind V, et al. Drug rash
intensive care therapy. There are both merits and with ampicillins and other penicillins. Lancet
demerits of using corticosteroid therapy for TEN. 1969; 2: 969-972.
23
Indian Journal of Practical Pediatrics 2005; 7(2) : 100
3. Baer RL, Witten VM. Year Book of agents in a tertiary care center in South India.
Dermatology 1960-61 series (Drug eruptions). Indian J Dermatol Venerol Leprol 2004; 70:
Chicago: Yearbook Medical Publishers, 1961; 20-24.
pp 9-37.
9. Sharma VK, Dhar S. Clinical pattern of
4. Scott HD, Thacher-Renshaw A, Rosenbaum cutaneous drug eruption among children and
SE, et al. Physician reporting of drug reactions. adolescents in north India. Pediatr Dermatol.
Results of Rhode Island Adverse Drug Reaction 1995;12(2): 178-183.
Reporting Project. JAMA 1990; 263: 1785-
1788. 10. Thappa DM. Urticania, Pruritus and Drug
Eryptions. In: Textbook of Dermatology,
5. Menniti-Ippolito F, Raschetti R, Da Cas R, et
urticaria, Prunitus and Drug Eruptions,
al. Active monitoring of adverse drug reactions
Venereology and Leprology, 2nd edn., New
in children. Lancet 2000; 355:1613-1614.
Delhi: Elsevier, 2005: pp 193-198.
6. Shear NH, Landau M, Shapiro LE.
Hypersensitivity reactions to drugs. In: Harper 11. Khopkar U. Reporting of drug eruptions: The
J, Oranje A, Prose N, eds. Textbook of National Pharmacovigilance Program. Indian
Paediatric Dermatology. 1st edn., Oxford: J Dermatol Venereol Leprol 2005; 71:1-2.
Blackwell Science. 2000; pp 1743-1752. 12. Shear NH. Diagnosing cutaneous adverse
7. Kramer MS, Hutchinson TA, Flegel KM, et al. reaction to drugs. Arch Dermatol 1990; 126:
Adverse drug reactions in general paediatric out 94-97.
patients. J Pediatr 1985; 106:305-310. 13. Renfro L, Grant-Kels JM, Daman LA. Drug
8. Pudukadan D, Thappa DM. Adverse cutaneous induced toxic epidermal necrosis treated with
drug reactions: Clinical pattern and causative cyclosporine. Int J Dermatol 1989; 28:441-444.
Venue: Bharati Vidyapeeth Deemed University Medical College, Pune 411 043.
Address for Correspondence: Dr.Sanjay Lalwani, 63/2B, Kamia Heritage, Opp.Ashwamegh Auto,
Pune Satara Road, Pune 411 009. Mobile: 9373314322,Email: lalwani@necpccpune.com,
medvents@nepccpune.com
24
2005; 7(2) : 101
DERMATOLOGY
Impetigo contagiosum (Tilbury Fox): This is of crusts using potassium permanganate 1:10000
the crusted variety and may be caused by either soaks is of help. Nasal carriage of Staphylococci
staphylococci or streptococci, or even both causing recurrent impetigo is managed with daily
together. The infection may follow minor application of mupirocin or sodium fusidate
scratches or insect bites. The anterior nares may ointment in the anterior nares for a fortnight.
be the reservoir for the infection leading to
recurrent episodes. The lesion is initially a small Ecthyma
red macule, which develops into a vesicopustule. Ecthyma is a deeper infection caused mainly
This ruptures rapidly to leave behind a crusted by Group A streptococci, but also may be due to
seropurulent oozing area of a typical yellowish Staphylococcus aureus, or both together4. The
honey colour (Fig. 1). Multiple lesions develop typical feature of this infection is the formation
and may coalesce on areas such as the face, of a thick crust following small pustules on an
especially around the nose and mouth. Buttocks erythematous base. It is difficult to detach this
and limbs may also be involved. Local crust, and underlying it is an irregular ulcer with
lymphadenopathy may develop, more commonly purulent discharge. Lesions are seen mainly on
with streptococcal rather than staphylococcal the lower limbs and buttocks. At any given time
impetigo. there may be few lesions, however, new ones
Bullous impetigo: This is caused by keep developing through auto-inoculation.
Staphyloccocus aureus. It is distributed similarly Healing may take a few weeks and leave behind
as in impetigo contagiosum and may also occur scarring. Ecthyma is treated with topical and oral
in neonates. The initial red macules develop in antibiotics similar to impetigo. General measures
to larger vesicles or bullae, which are fragile and to improve hygiene and nutrition are always
rupture leaving annular or circinate erythematous helpful.
scaly areas.
Folliculitis/Furuncle
Lesions of impetigo heal rapidly leaving
behind no sequelae, except mild transient post This term refers to pyogenic infection of the
inflammatory pigmentation. Impetigo can be follicles. It maybe superficial or deep. Superficial
widespread in the setting of atopic dermatitis or folliculitis1 is seen more commonly in children
scabies with secondarily impetiginized lesions. on the scalp and face (Bockharts impetigo) as
Patients with multiple or recurrent infections are yellow pustules on an erythematous base, and
more likely to be contagious to other children. may be recurrent and chronic. Folliculitis of the
Streptococcal impetigo may be followed by post- beard area (Sycosis barbae) may be seen in
streptococcal acute glomerulonephritis, urticaria, postpubertal males following shaving. Chronic
erythema multiforme or scarlet fever, but not and recurrent folliculitis of the legs (Dermatitis
rheumatic fever1. cruris pustulosa et atrophicans) has been observed
in young males in India1,3. The pustules are seen
In mild and localized infection, topical symmetrically on the thighs and shins, grow
antibiotics such as mupirocin, sodium fusidate Staphylococcus aureus and heal with atrophy and
or even neomycin and bactitracin may be scarring. Treatment is with topical and oral
sufficient. Resistance to topical therapy may be antibiotics.
minimized by judicious short term use. Oral
antibiotics such as erythromycin and cloxacillin Furuncles (boils) are acute staphylococcal
may be used for more severe infection. Removal infections leading to abscesses of the hair follicle.
26
2005; 7(2) : 103
They are not as common in childhood, however irritation of the genital area with severe erythema
mechanical trauma and malnutrition may be and purulent discharge 6. Dysuria may be a
predisposing factors. A furuncle first appears as feature. Perianal infection with Strep. pyogenes
a small reddish inflammatory nodule, then presents similarly with redness, inflammation,
becomes pustular and necrotic, and heals after irritation and pain on passing stools7. It may
discharge of necrotic and purulent material accompany vulvovaginitis in girls. Oral and
leaving behind a scar. The lesion is extremely topical antibiotic therapy is recommended.
tender. Few or multiple lesions may be seen, and
Secondary bacterial infection
may be accompanied by fever or constitutional
symptoms. Recurrent episodes may be due to Pruritic conditions in children such as
nasal or perineal carriage of staphylococci. scabies and eczemas are often complicated by
Furuncles need to be treated with oral antibiotics the development of secondary pyogenic infection
and may require in addition anti-inflammatory and impetiginization mainly due to Staph. aureus.
drugs. Management of the infection with topical and oral
Periporitis antibiotics helps to hasten the healing of the
original condition.
This is an infection of the sweat glands,
commonly seen on the forehead, face and scalp Toxin-mediated conditions: Staphylococcal
in young children in the hot summer months. Scalded Skin Syndrome
Lesions are erythematous, not very tender or This is a condition resulting from
pustular, and are usually found in a bed of miliaria epidermolytic toxins released by the
rubra (prickly heat). staphylococci. Typically seen in young children,
Cellulitis/Erysipelas fever and irritability are followed by a diffuse
Both these terms refer to deeper infection erythematous rash8. The skin is tender to touch,
of the skin, subcutaneous tissue and often the and the child cries on handling. Superficial flaccid
lymphatics. Cellulitis and erysipelas are caused blisters develop and rupture leaving painful raw
by Strep. pyogenes, but may be rarely due to areas. The condition heals within two weeks of
Staph aureus 5. Lesions are characterised by intravenous antibiotic therapy with scaling,
redness, swelling, pain and tenderness. The leaving behind no sequelae. Swabs from the
margins are sharply defined and elevated. Lesions blister fluid do not grow staphylococci. Most
tend to heal with appropriate therapy leaving children will give a preceding history of
behind post-inflammatory pigmentation and staphylococcal infection either cutaneous or
scaling. Erysipelas is known to follow a respiratory.
streptococcal sore throat and typically presents Toxic shock syndrome
on the face in children. Cellulitis may follow a
history of trauma or insect bite, and may be seen This is a severe condition characterised by
anywhere on the body, but commonly the limbs. the acute onset of fever, vomiting, a widespread
Oral antibiotics and anti-inflammatory drugs are erythematous macular rash, mucosal erythema
required. and edema, multisystem involvement with
circulatory shock. It was earlier thought to be
Streptococcal vulvovaginitis and perianal exclusively associated with the use of tampons
infection in menstruating women leading to staphylococcal
Vulvovaginitis in prepubertal girls may be infection9. IV antibiotics and supportive ICU
due to Strep. pyogenes. There is soreness and management are required.
27
Indian Journal of Practical Pediatrics 2005; 7(2) : 104
Fig. 1 Honey coloured crusts of impetigo Fig. 2 Deeper crusted lesions of ecthyma
contagiosum with eroded areas on the legs
29
Indian Journal of Practical Pediatrics 2005; 7(2) : 106
DERMATOLOGY
PEDICULOSIS AND SCABIES IN such as typhus, trench fever, and relapsing fever,
CHILDREN whereas pubic louse infestation often is acquired
as a sexually transmitted disease. The head louse
Shahbaz A.Janjua infestation, which crosses all economic and social
Abstract: Scabies, followed by pediculosis, is the boundaries, commonly affects young children,
commonest cause for itchy skin disorders in the occurring in affluent, rural and urban schools
tropics. Apart from the climatic conditions, the alike. The lice that infest human beings are
poor living conditions seem to contribute towards almost always sucking lice that live in close
this malady. One has to remember that these association with the host and lay their eggs on
diseases have protean manifestations in infants hair shafts or in the seams of clothing. The
and children, hence they are difficult to diagnose. importance of environmental measures to prevent
infestation is still a matter of controversy.
Key words: Ectoparasitosis, Sarcoptes scabiei,
Scabies is a highly pruritic condition caused
pediculus capitis
by the mite Sarcoptes scabiei var. hominis. It is
Pediculosis and scabies are the most transmitted mainly by direct personal or sexual
prevalent parasitic infestations of humans contact and, less often, by contact with infested
worldwide. Both the conditions are caused by bedding or clothing. It is characterized by severe
ectoparasites sharing a common characteristic pruritus that is often worse at night and
feature of causing intense pruritus. Both are recognized by the presence of burrows on the
treated by the topically administered chemical skin and a papular eruption with excoriations.
agents, preferably, 1 % permethrin, but growing Scabies presents differently in neonates and
resistance to the topical agents remains a infants causing a generalized papulovesicular
challenge for the treating physicians and eruption.
dermatologists. Only pediculosis capitis and scabies in
young children will be discussed further in this
The lice are obligate human ectoparasites.
review.
The three lice species that infest humans are;
Pediculus humanus capitis, Phthirus pubis, and Pediculosis capitis (Head louse)
Pediculus humanus corpus. They are known as Pediculosis capitis or head louse is caused
as head louse, pubic louse and body louse by infestation of scalp with the highly host-
respectively. All three types are transmitted by specific insect, Pediculus humanus capitis. It
close person to person contact. The body louse remains a major health problem worldwide. No
infestation preferentially affects the homeless and age or economic stratum is immune to the head
displaced, and remains a major vector of diseases louse infestation and generally a higher
prevalence is associated with crowded conditions.
* Dermatologist,
Ayza Skin and Research Center, Lalamusa, The highest incidence occurs in school-aged
1
Pakistan children, primarily girls, aged 3-12 years .
30
2005; 7(2) : 107
Transmission is thought to occur through head- neck and behind the ears. An average host carries
to-head close contact, or contact with the infested a population of less than 20 adult lice but the
fomites such as shared headgears, hats, brushes, diagnosis is confirmed by the presence of a single
combs, earphones, bedding, upholstered furniture live louse. Other associated findings may include
2
and rugs . It has been observed that transfer is excoriations and pyoderma and possible cervical
optimal to hairs that are parallel and slow- lymphadenopathy. If only nits are found, they
moving. Hence, the most important mode of should be examined microscopically for viable
transmission remains direct head-to-head contact embryos.
for a prolonged period. Infestation may be more
common during warmer months .
3 Because adult lice prefer to avoid light, they
can move quickly along hairs and cannot readily
Life cycle: The life cycle of the head louse begins be seen on clinical examination. A bright light, a
as an egg, laid near the scalp and attached firmly magnifying lens, and separating the hair may help
to a hair shaft in an egg case, also referred to as inspection. However, combing through the hair
nit. The nits move distally with hair growth, and with a louse comb and examining the teeth of
prefer an environment that is at least 82 F and the comb for living lice usually detects more cases
5
70% humidity. They are readily identified by the than direct visualization alone .
naked eye on clinical inspection and can be
differentiated from hair casts, dandruff, and dried Treatment and prevention: The treatment of
hair spray that can be easily removed from the choice for the pediculosis capitis remains
hair shaft (Fig 1). The embryos central nervous topically applied 1% permethrin6. Permethrin is
system is fully developed within three to four a synthetic compound derived from pyrethrin that
days and it hatches as a nymph in seven to 10 acts on the nerve cell membranes of the parasites
days. Nine to 12 days after hatching, the nymph causing paralysis of the exoskeletal muscles and
develops into a sexually mature male or female. subsequent suffocation of the lice. Permethrin is
also an ovicidal. Permethrin is applied to the
Within 24 hours of mating on the hosts scalp as cream rinse after the hair is shampooed
surface, the mature female louse begins laying and dried. The product is rinsed out with water
seven to 10 eggs a day and repeated fertilization after 10 minutes. Surviving nits can cause
is not required. The head lice of both sexes have reinfestation if not removed. Higher cure rates
a life span of as much as 30 days and they survive would be obtained by a second application one
4
only 15 to 20 hours off the host . Nymphs and week after the initial usage7. The resistance can
adult head lice take frequent blood meals, be treated with 5% permethrin and left on
contributing to the symptoms of itching. overnight under a shower cap6.
Clinical presentation and diagnosis: The head
Pyrethrins have the same mechanism of
louse is almost always confined to the scalp hair
action as permethrin. Piperonyl butoxide is added
and the presenting feature in young children is
to potentiate the effect of the pyrethrin and may
pruritus of variable severity. Sensitization or an
decrease the development of resistance.
allergic reaction to louse saliva, feces, or body
parts may cause pruritus. It may take more than Malathion is highly pediculicidal. It is a
two weeks for the infestation to establish and relatively weak organophosphate cholinesterase
cause symptoms. The infestation is diagnosed inhibitor that causes respiratory paralysis in
by direct visualization of the lice or viable nits, arthropods. It does require an 8- to 12-hour
found most often on the back of the head and treatment period and has an unappealing odor.
31
Indian Journal of Practical Pediatrics 2005; 7(2) : 108
Lindane 1% shampoo had been a popular head shaving and wet combing. Wet combing
treatment but is no longer the preferred topical involves combing wet hair with a specially
remedy 6 . There also appears to be some designed comb every 3-4 days. The hair is wetted
resistance of the louse to lindane. because, when exposed to water, lice are
temporarily immobile and therefore easier to
Cotrimoxazole twice daily for three days has
comb out. The duration of this treatment is 2
been reported as an effective treatment for head
weeks or more. This treatment is time-consuming
lice. The putative mechanism of action is on
for parents.
symbiotic gram-negative bacteria in the gut of
the louse that are required for digestion of Contact with untreated classmates and
ingested blood products. Unfortunately, it is only playmates can result in apparent treatment failure
effective against adult and nymphal stages but in the absence of drug resistance. There is no
not the eggs and so prolonged courses are recent evidence that exclusion from school is
required 8 . According to one study, the effective in controlling head lice in school
combination of permethrin and trimethoprim- children. There may be benefit to separating hats,
sulfamethoxazole was more effective than either scarves, and jackets in the classroom. It is a
agent alone9. simple step for each child to store them under his
Ivermectin is an anti helminthic agent or her desk. Louse repellents may have potential
structurally similar to the macrolide antibiotics to prevent reinfestation. Piperonal has been used
but without antibacterial activity. A single, oral as a pediculicide, but it also exhibits a repellent
dose of ivermectin (Stromectal) 200 mcg/kg action against lice. A low-fragrance pump spray
repeated in 10 days has been shown to be formulation of 2% piperonal was tested against
6,10
effective in eradicating head lice . In humans, body lice, and exhibited high repellency for 24
13
ivermectin has been proved effective in the hours
treatment of onchocerciasis, loiasis,
For the community control of pediculosis
strongyloidiasis, bancroftian filariasis, and
capitis, an approach should be outlined that will
cutaneous larva migrans. The use and safety of
screen and identify cases, educate the physicians,
oral ivermectin to treat pediculosis capitis in
parents, and patients on optimal treatments,
young children below 5 years has not been well
fomite control, and environmental clean-up.
studied.
Development of head lice resistance to Scabies
current therapies, including lindane, permethrin, Scabies is known to mankind since middle
and malathion, has become a worldwide ages and its descriptions can be found in ancient
11
problem . According to one study 0.5% writings from the Greeks, Egyptians, Romans,
malathion lotion was the fastest-killing and medieval Europeans. It is caused by a highly
pediculicide and the most effective ovicide. One contagious mite, Sarcoptes scabiei which is an
percent lindane shampoo was the slowest-acting obligate human ectoparasite. It is characterized
11
pediculicide and least effective ovicide . by intense pruritus, papular eruption, superficial
Some home remedies that are still used burrows, excoriations and secondary infection.
include kerosene oil, alcohol, and insecticides; No sex, age or racial predilection has been noted,
but some of these can be hazardous
12 but scabies commonly affects infants, young
children, sexually active adults, and
Mechanical methods of treatment include stitutionalized elderly.
32
2005; 7(2) : 109
Life cycle of the scabies mite: The tortoise Diagnosis: The diagnosis of scabies is often
shaped female mite is approximately 0.3 mm long difficult but a combination of history of pruritus
and has eight legs. The male which is about half especially at night, the presence of burrows on
of the size of the female, mates with the female areas of predilection, and pruritus in the close
on the skin surface. After fertilization, the adult family contacts are adequate for the diagnosis.
female burrows into the stratum corneum. The The diagnosis of scabies can be rapidly confirmed
mite lays 2 to 3 eggs a day and dies after 5 weeks by establishing the presence of mites, eggs,
at the end of the burrow14. Larvae from these or scybala in the microscopic examination
eggs hatch after approximately 2 weeks and of scrapings of suspicious lesions 17 .
emerge to the skin surface. These mites then Videodermatoscopy can be utilized for primary
reinfest the skin. diagnosis to detect signs of infestation (mites,
eggs, and faeces), especially in children, who may
Modes of transmission: Transmission occurs by refuse skin scraping.
close skin-to-skin contact, especially in
overcrowded living conditions. In adults Presentation in neonates and infants: Scabies
transmission is common during sexual contact, presents differently in neonates and infants than
and infestation from fomites, icluding infested in adults. The pathognomonic threadlike,
bedding and clothing, is also possible. sinuous burrows of scabies are rarely seen in
neonates and infants. A history of a pruritic
Clinical features: Most patients complain of an eruption in hospital personnel or close family
intense pruritus especially at night and following members is often present18. In neonates, scabies
a hot shower. The pruritus has been associated is characterized by a large number of
with a hypersensitivity reaction to the excreta papulovesicular and nodular lesions,
deposited by the mite within the burrow15. The eczematization, and secondary infection, often
lesions are generally symmetrically distributed with widespread distribution of lesions on the
and usually spare the face and neck. These head, neck, scalp, palms, and soles. The affected
include small papules and vesicles, often neonates can appear irritable, feed poorly and fail
accompanied by plaques, pustules, or nodules. to thrive. The lesions of scabies in infants
The pathognomonic sign of scabies is the constitute a variety of morphologies that produce
presence of multiple burrows on the skin typically a flea-bitten look. Such lesions include
located in the interdigital web spaces, flexural erythematous papules, vesicles, pustules, bullae,
aspects of the wrist and elbows, belt line and and crusts19.
genitals. The burrow is a fine, wavy and slightly
scaly line a few millimeters to one centimeter Indiscriminate use of topical corticosteroids
long. A tiny mite is often visible at one end of due to misdiagnosis of atopic dermatitis may
the burrow. Although the patient may have blunt the inflammatory appearance of scabies in
hundreds of itching papules, often there are less infants, but it does not prevent spread of the
than 10 burrows. Secondary lesions include infestation. More importantly, it can also lead
papular excoriations, scaly eczematoid patches, to the heavily crusted, hyperkeratotic lesions of
and red-brown nodules and vesiculopustules. Norwegian scabies that are usually seen only in
The burrow is often found surrounded by immunocompromised patients19. Also, in infants
infiltrates of eosinophils, lymphocytes, and there is a generalized distribution of lesions to
histiocytes on histopathology16 all body areas, including the face, neck, palms,
33
Indian Journal of Practical Pediatrics 2005; 7(2) : 110
and soles, which are not affected in adults. Again, Lindane 1 % cream was the treatment of
the associated clinical symptoms include poor choice before the introduction of permethrin, but
feeding, irritability, and failure to thrive. The due to concerns about its systemic and CNS
possibility of scabies should be entertained for toxicity (up to 10 % is absorbed), it is no longer
any infant who has these findings20. Scabies in the treatment of choice, especially in infants and
an infant usually means that a close adult contact young children. Moreover lindane resistant cases
22
is the source of the infection. The differential have been reported . The role of oral ivermectin
diagnosis for the scabies in neonates and infants, in the treatment of scabies remains to be
includes infantile acropustulosis, atopic determined, but it has been reported to be
dermatitis, eosinophilic pustular folliculitis, effective for the treatment of the severe crusted
miliaria rubra, impetigo and insect bites. form of scabies even in severely immuno-
23
suppressed patients in one study . It is
Treatment and prevention: Treatment of mandatory to treat all the family members and
scabies involves the control of symptoms and close contacts even if they are not having
secondary infections, and eradication of the mites symptoms. Bed linen and clothing should be
themselves. The treatment of choice for neonates, washed in water that is at least 120F. Dry
infants and young children remains topical cleaning or storage for 1 week also may be
application of 5 % permethrin lotion due to effective.
relative high safety profile and minimal
absorption of the drug21. This is applied for 8-14 Antihistamines has to be used for a
hours followed by a reapplication in one week. minimum period of 2 weeks. Mild-to-
The entire body surface including the scalp and intermediate strength topical corticosteroids may
face should be covered for infants and young be also used to ameliorate pruritus.
children, avoiding the areas around the eyes and
mouth. The lotion should be applied from the Complications, including impetigo and
neck down in older children and adults and should pustulosis due to secondary bacterial infections
include intertrigenous and genital areas, the of excoriated scabies, should be treated with
intergluteal cleft, and under trimmed nails. A topical and/or systemic antibiotics. It is also
single application is associated with an overall necessary to inform the parents that the pruritus
cure rate of 89% to 92% and could be safely used may persist for several weeks despite treatment.
above 24 months of age safely used above 2 However, once the treatment is complete, young
months of age. Less than 2% of the lotion is children can return to childcare or school.
absorbed into the skin. Side effects include mild Treatment failure is quite common and
transient burning, stinging and erythema. usually attributed to failure to treat all the family
Sulfur 5-10 % in petrolatum and crotamiton members and close contacts simultaneously.
10% cream are the alternative therapies. Sulfur, Points to remember:
which is the oldest known treatment of scabies,
is the choice for infants and for pregnant or 1. Scabies is by far the commonest cause of
lactating women . It should be applied at night itching in children in the tropics.
for 3 consecutive nights and washed off 2. Scabies and pediculosis are communicable
thoroughly 24 hours after the last application. diseases.
Crotamiton cream is regarded less effective and 3. Treatment is always aimed at a family/
is usually applied for five days. community level.
34
1
2005; 7(2) : 111
35
Indian Journal of Practical Pediatrics 2005; 7(2) : 112
DERMATOLOGY
37
Indian Journal of Practical Pediatrics 2005; 7(2) : 114
of ecchymosis, rare. Vesicles and bullae may orally is effective for mild infections, and
develop and rupture, occasionally with necrosis parenteral gentamicin 5 mg/kg/day for severe
of the involved skin. infections. Although S. aureus rarely causes
typical cellulitis, many clinicians prefer using
Systemic manifestations: Fever, chills,
antibiotics also active against this organism:
tachycardia, headache, hypotension, delirium
cloxacillin 25-50 mg/kg/day orally for mild
may precede the cutaneous findings by several
infections, or cefotaxime 50-100 mg/kg/day IV
hours, but many patients do not appear ill.
for severe infections. For penicillin-allergic
Leukocytosis is common but not constant.
patients or those with suspected methicillin-
Diagnosis: The diagnosis usually depends on the resistant S. aureus infection, vancomycin 40 mg/
clinical findings. Unless pus has formed or an kg/day in four divided doses as IV is the drug of
open wound is present, the responsible organism choice. When pus or an open wound is present,
often is difficult to isolate, even on aspiration or results of a Gram stain should dictate antibiotic
skin biopsy. Blood cultures are occasionally choice. Immobilization and elevation of the
positive. Serologic tests, especially measurement affected area help to reduce edema, and cool, wet
of rising titers of anti-DNase B, confirm a dressings relieve local discomfort.
streptococcal cause but are usually unnecessary.
Cellulitis in a neutropenic patient requires
Although cellulitis and deep vein thrombosis antibiotics effective against aerobic gram-
usually are easily differentiated clinically, many negative bacilli until culture results are available.
physicians confuse these entities when edema Penicillin is the drug of choice for P. multocida,
occurs in the lower extremities. an aminoglycoside (e.g., gentamicin) is effective
Local abscesses form occasionally, against A. hydrophila, and tetracycline is the
requiring incision and drainage. Serious but rare preferred antibiotic for V. vulnificus.
complications include severe necrotizing Treating concomitant tinea pedis, which
subcutaneous infection and bacteremia with often eliminates the source of bacteria residing
metastatic foci of infection. Even without in the inflamed, macerated tissue prevents
antibiotics, most cases of superficial cellulitis recurrent leg cellulitis. If such therapy is
resolve spontaneously; however, recurrences in unsuccessful or not indicated, recurrent cellulitis
the same area are common, sometimes causing sometimes can be prevented by benzathine
serious damage to the lymphatics, chronic penicillin 1.2 million U IM monthly, or penicillin
lymphatic obstruction, marked edema, and, V or erythromycin 250 mg orally qid for 1 week
rarely, elephantiasis. With antibiotics, such every month.
complications are uncommon. Symptoms and
signs of superficial cellulitis usually resolve after Staphylococcal Scalded Skin Syndrome 3
a few days of antibiotic therapy. (Ritter-Lyell Syndrome)
Treatment: For streptococcal cellulitis, Staphylococcal scalded skin syndrome
penicillin is the drug of choice: For mild (SSSS) almost always occurs in infants and in
outpatient cases, penicillinV 250 to 500 mg orally children below 6 years. Epidemics may occur in
qid is adequate. For severe infections, which nurseries, presumably transmitted by the hands
require hospitalization, aqueous penicillin G of personnel in contact with an infected infant.
400,000 U IV q 6 h is indicated. In penicillin- However, nursery personnel may be nasal carriers
allergic patients, erythromycin 20-40 mg/kg/day of S. aureus. Sporadic cases also occur.
38
2005; 7(2) : 115
Aetiology: Group II coagulase-positive scarlet fever, but none of these causes a painful
staphylococci, usually phage type 71 and often rash. Bullae, erosions, and an easily loosened
resistant to penicillin, elaborate exfoliatin (also epidermis occur in thermal burns, genetic bullous
called epidermolysin), an epidermolytic toxin that diseases (e.g., some types of epidermolysis
splits off the upper part of the epidermis just bullosa), and acquired bullous diseases (e.g.,
beneath the granular cell layer. The inciting pemphigus vulgaris, bullous pemphigoid).
infection may be on the skin but usually is in the
Treatment: With prompt diagnosis and therapy,
eye or nasopharynx. The toxin enters the
death rarely occurs. Systemic penicillinase-
circulation and affects the skin systemically, as
resistant antistaphylococcal antibiotics (e.g.,
in scarlet fever.
cloxacillin) must be started as soon as the clinical
Clinical features: In infants, illness often begins diagnosis is made, without waiting for culture
during the first few days of life with a localized results. In early-stage disease, oral cloxacillin
crusted infection (often impetigo-like), most often 12.5 mg/kg q 6 h (for infants and children
at the umbilical stump or in the diaper area. weighing <= 20 kg) and 250 to 500 mg q 6 h (for
Sporadic cases often start with a superficial older children) may be given; in severe disease,
crusted lesion, frequently around the nose or ear. gentamicin IV in 2 divided doses should be
Within 24 hours, tender scarlet areas appear additionally given until improvement is noted,
around the crusted area and may become painful followed by oral cloxacillin 25 mg/kg/day up to
and generalized. Large, flaccid blisters arise on 100 mg/kg/day for more than 10 days.
the erythematous skin and quickly break to Corticosteroids are contraindicated, and topical
produce erosions. The epidermis peels off easily, therapy and patient handling must be minimized.
often in large sheets, when the red areas are If the disease is widespread and the lesions are
rubbed (Nikolskys sign). Widespread weeping, the skin should be treated as if it were
desquamation of the skin occurs within 36 to 72 burned. Hydrolyzed polymer gel dressings may
hours, and patients may become very ill with be very useful, and the number of dressing
systemic manifestations (e.g., malaise, chills, changes should be minimized. Because the split
fever). Loss of the protective skin barrier can lead is high in the epidermis, the stratum corneum is
to sepsis and to fluid and electrolyte imbalance. quickly replaced and healing is usually within 5
to 7 days after the start of treatment. Steps to
Symptoms and signs are indistinguishable
detect carriers and prevent or treat nursery
clinically from toxic epidermal necrolysis; yet
epidemics are to be taken.
SSSS must be distinguished rapidly from TEN
because therapy is different. Neonatal herpes simplex virus infection 4
Diagnosis: Cultures should be obtained from the Epidemiology: Infection with herpes simplex
skin and nasopharynx. Diagnosis is confirmed virus by transmission during parturition, typically
by skin biopsy and examination of frozen tissue causing vesicular eruption and subsequent
sections or exfoliative cytology, showing disseminated disease. Neonatal herpes simplex
epithelial cells. Although final biopsy results may virus (HSV) infection has high mortality and
not be available until well after treatment has been significant morbidity. Incidence estimates range
started, frozen tissue sections and cytology can from 1/3,000 to 1/20,000 live births. HSV type 2
provide rapid confirmation. occurs in about 80% of cases; 20% are caused
Differential diagnosis: Drug hypersensitivity by HSV type 1. HSV type 2 is usually transmitted
(most notably, TEN), viral exanthemas, and to the newborn during delivery by passage
39
Indian Journal of Practical Pediatrics 2005; 7(2) : 116
through an infected maternal genital tract. skin vesicle; the mouth, eye, and CSF are also
Transplacental transmission of virus and high-yield sites. In some newborns presenting
nosocomial spread from one newborn to another with encephalitis, virus is found only in the brain;
by hospital personnel or family has also been however, accurate testing (such as HSV
implicated in about 15% of cases. Mothers of polymerase chain reaction) is available in only a
newborns with HSV infection tend to have no few research and specialized laboratories.
history or symptoms of genital infection at the Cytopathologic effects usually can be
time of delivery. demonstrated in tissue culture within 24 to 48
hours after inoculation. The diagnosis can also
Clinical features: Manifestations generally
be confirmed by neutralization with appropriate
occur between the first and second week of life;
high-titer antiserum; immunofluorescence of
however, symptoms may not appear until as late
lesion scrapings, particularly with use of
as the fourth week. The hallmark of infection is
monoclonal antibodies; and electron microscopy.
skin vesicles, which, if untreated, frequently leads
If no diagnostic virology facilities are available,
to progressive or more serious forms of disease
a Leishman smear of the lesion base may show
within 7 to 10 days. However, up to 45% of
characteristic histopathologic evidence
infected newborns initially have no skin vesicles;
(multinucleated giant cells and intranuclear
usually these newborns have localized CNS
inclusions), but this is less sensitive than culture,
disease. Other signs of infection, which can occur
and false-positive results occur.
singly or in combination, include temperature
instability, lethargy, hypotonia, respiratory In newborns with untreated disseminated
difficulty (apnea or pneumonia), convulsions, disease, mortality rate is 50%, while in untreated
hepatitis, and disseminated intravascular local disease and encephalitis it is 50%. At least
coagulation (DIC). 95% of the survivors have severe neurologic
sequelae. Death is uncommon in those with local
Newborns with disseminated disease and
(skin, eyes, mouth) disease but without CNS or
visceral organ involvement have hepatitis,
organ disease, except as the result of concomitant
pneumonitis, and/or DIC with or without
medical problems. About 30% develop
encephalitis or skin disease.
neurologic impairment, which may not manifest
Newborns with localized disease can be until 2 to 3 years of age. Morbidity in each group
subdivided into two groups. The first group has parallels mortality and is directly proportional to
encephalitis manifested by neurologic findings, disease extent. About 90% of infants with
CSF pleocytosis, and elevated protein viscerally disseminated neonatal HSV infection
concentration, with or without concomitant have subsequent sequelae. Only 5% of those with
involvement of the skin, eyes, and mouth. The CNS infection return to normal. Therapy with
second group has only skin, eye, and mouth acyclovir not only decreases the mortality rate
involvement and no evidence of CNS or organ by 50% but also increases the percentage who
disease. recovers completely from 10 to 50%.
Diagnosis: Rapid and specific diagnosis of Treatment: Acyclovir 30 mg/kg/day as infusion
neonatal HSV infection is essential. Infection can with normal saline is given in 3 divided doses
be confirmed by isolating virus in tissue culture, for 10 to 14 days. Vigorous supportive therapy
using various cell lines of human or nonhuman is required, including appropriate IV fluids,
origin. The most common site of retrieval is a alimentation, respiratory support, correction of
40
2005; 7(2) : 117
41
Indian Journal of Practical Pediatrics 2005; 7(2) : 118
hydrocortisone 100 mg IV, which may be over the trunk, often with accentuation in the
followed by an oral corticosteroid for a short perineal region. The rash may be urticarial,
period. morbilliform, or scarlatiniform and is
accompanied by injected pharynx; reddened, dry,
Kawasaki syndrome 7 fissured lips; and a red strawberry tongue. During
A syndrome occurring usually in infants and the first week, pallor of the proximal portion of
children less than 5 years, characterized by the fingernails or toenails (leukonychia partialis)
prolonged fever, exanthem, conjunctivitis, may occur. Erythema or a purple-red
mucous membrane inflammation, cervical discoloration and variable edema of the palms
lymphadenopathy, and polyarteritis of variable and soles usually appear on about the third to
severity. Though its etiology is unknown, the fifth day. Although edema may be slight, it is
epidemiology and clinical presentation suggest often tense, hard, and nonpitting. Periungual,
an infection or an abnormal immunologic palmar, and plantar desquamation begins on
response to an infection. about the tenth day after onset. The superficial
layer of the skin sometimes comes off in large
Since the syndrome was first described in casts, revealing new normal skin. Tender,
Japan in the late 1960s, thousands of cases have nonsuppurative cervical lymphadenopathy (>=
been reported worldwide in diverse racial and 1 node >= 1.5 cm in size) is present throughout
ethnic groups, although children of Japanese the course in about 50% of patients; the other
descent have a higher incidence. The male: findings each are present in about 90% of
female ratio is about 1.5:1. Eighty percent of patients. The illness may last from 2 to 12 weeks
patients are less than 5 years (median, 2 years); or longer. Other less specific findings indicate
true cases in teenagers or adults are rare. Cases involvement of many systems. Arthritis or
occur year-round, but most often in spring or arthralgias (mainly involving large joints) occur
winter. Clusters have been reported in in about 1/3 of patients. Other clinical features
communities without clear evidence of person- may include urethritis, aseptic meningitis,
to-person spread. Recurrences occur in about 1% diarrhea, hydrops of the gallbladder, and anterior
of patients. uveitis.
The pathology is nearly identical to infantile The most important complications are those
polyarteritis nodosa, with vasculitis primarily of cardiac inflammation, most notably coronary
affecting the coronary arteries but also other arteritis. Cardiac manifestations usually begin on
medium-sized and large arteries. about the tenth day, as the rash, fever, and other
early acute clinical symptoms begin to subside;
The illness tends to progress in stages,
i.e., in a subacute phase of the syndrome.
beginning with fever, usually remittent and
Inflammation of the coronary arteries with
>39 C (> 102.2 F), which is associated with
dilation and aneurysm formation occurs in 5 to
irritability, often extreme, and occasional lethargy
20% of all cases, sometimes associated with acute
or intermittent colicky abdominal pain. Fever
myocarditis with heart failure, arrhythmias, and
lasts 1 to 2 weeks or more in untreated patients.
pericarditis, and rarely with cardiac tamponade,
Usually within a day or two of fever onset,
thrombosis, or infarction.
bilateral bulbar conjunctival injection without
exudate appears. Within 5 days, a polymorphous, Diagnosis is based on the clinical findings
erythematous macular rash appears, primarily and on exclusion of other diseases. Results of
42
2005; 7(2) : 119
cultures for bacteria and viruses, as well as drug (e.g., penicillin, sulfonamides, isoniazid,
serologic tests for evidence of infection, are phenytoin, barbiturates) or a topical agent.
negative but may be useful for diagnosing other Exfoliative dermatitis may also be associated with
illnesses with similar presentations. mycosis fungoides or lymphoma.
Differential diagnosis includes bacterial The onset may be insidious or rapid. The
diseases (especially scarlet fever, staphylococcal entire skin surface becomes red, scaly, thickened,
exfoliative syndromes, and leptospirosis), viral and occasionally crusted. Pruritus may be severe
exanthems (e.g., measles, viral hemorrhagic or absent. The characteristic appearance of any
fever), toxoplasmosis, acrodynia (caused by primary dermatitis is usually lost. Localized areas
mercury poisoning), Stevens-Johnson syndrome, of normal skin may be seen when the exfoliative
and juvenile RA. dermatitis is caused by such conditions as
psoriasis, mycosis fungoides, or pityriasis rubra
Children with Kawasaki syndrome should pilaris. Generalized superficial lymphadenopathy
be treated by or in close consultation with an is frequent, but biopsy usually shows benign
experienced pediatric cardiologist or pediatric lymphadenitis.
infectious disease specialist. Therapy is started
as soon as possible, optimally within the first 10 The child may feel cold and have an elevated
days of illness, with a combination of high-dose temperature caused by excessive heat loss from
intravenous immunoglobulin (IVIGa single increased blood flow to the skin. Generalized
dose of 2 g/kg given over 10 to 12 h) and oral exfoliative dermatitis may also cause weight loss,
high-dose aspirin (80 to 100 mg/kg/day in 4 hypoproteinemia, hypocalcaemia, iron
divided doses). The aspirin dose is reduced to 3 deficiency, or (in patients with borderline cardiac
to 5 mg/kg/day as a single dose when the child compensation) high-output heart failure.
becomes afebrile. Every attempt must be made to determine
A small risk of Reyes syndrome exists in the cause. A history or signs of a primary
children receiving long-term aspirin during dermatitis may be helpful. Biopsy is usually not
outbreaks of influenza or varicella. Parents of helpful, but pemphigus foliaceus or mycosis
children receiving aspirin should be instructed fungoides may be diagnosed by skin biopsy, or
to contact the physician promptly if the child is lymphoma by a lymph node biopsy. Szary
exposed to or develops symptoms of influenza syndrome may be diagnosed by a blood smear.
or varicella. Temporary interruption of aspirin The disease may be life-threatening, and
may be considered (with substitution of hospitalization is often necessary. Because drug
dipyridamole for children with documented eruptions and contact dermatitis cannot be ruled
aneurysms). Annual influenza vaccination is out by history alone, all drugs should be stopped,
indicated for children receiving long-term aspirin if possible, or essential systemic drugs should be
therapy. changed to chemically dissimilar ones.
Generalized exfoliative dermatitis 8 Petrolatum applied after tap-water baths gives
temporary relief. Oral corticosteroids should be
Usually no cause is found. Some cases are used only when other measures fail. Prednisolone
secondary to certain dermatitides (e.g., atopic, 40 to 60 mg/day is given; after about 10 days,
psoriatic, pityriasis rubra pilaris, contact the drug is given on alternate days. Usually the
dermatitis); others may be induced by a systemic dose can be further decreased, but if an
43
Indian Journal of Practical Pediatrics 2005; 7(2) : 120
underlying cause is not eliminated, long-term the mouth. The eyes may become very painful;
prednisolone will be required. purulent conjunctivitis may make it impossible
for the patient to open them. Symblepharon
Erythema multiforme 9
production, keratitis with corneal ulceration, iritis,
An inflammatory eruption characterized by and uveitis may occur. The conjunctival lesions
symmetric erythematous, edematous, or bullous may leave resistant corneal opacity and synechia.
lesions of the skin or mucous membranes. The condition is occasionally fatal.
No cause of erythema multiforme can be The skin lesions of erythema multiforme
found in over 50% of cases. Most other cases are must be distinguished from bullous pemphigoid,
due to infectious diseases (e.g., herpes simplex urticaria, and dermatitis herpetiformis; the oral
[probably most common], coxsackie and echo lesions, from aphthous stomatitis, pemphigus,
viruses, Mycoplasma pneumoniae, psittacosis, and herpetic stomatitis. Hand, foot, and mouth
histoplasmosis) or drug therapy. Almost any drug disease produced by coxsackieviruses A5, A10,
can cause erythema multiforme; penicillin, and A16 must also be considered. Pneumonia
sulfonamides, and barbiturates are the most should be treated with tetracycline. Local
likely. Vaccinia, Bacille Calmette-Gurin (BCG), treatment depends on the type of lesion. Vesicles
and poliomyelitis vaccines have also induced and bullous or erosive lesions can be treated with
erythema multiforme. intermittent Burrows solution, saline, or tap-
water compresses. Cheilitis and stomatitis of
The mechanism by which infectious agents, erythema multiforme require special care. Use
drugs, or vaccines cause erythema multiforme is of systemic corticosteroids is controversial; some
unknown, but it is generally considered a patients, especially those with severe mouth and
hypersensitivity reaction. throat lesions, seem to succumb more readily to
Onset is usually sudden, with erythematous fatal respiratory complications. The cause, if
macules, papules, wheals, vesicles, and found, should be treated, eliminated, or avoided.
sometimes bullae appearing mainly on the distal Simple erythema often needs no treatment.
portion of the extremities (palms, soles) and on Systemic antibiotics (as indicated by culture and
the face; hemorrhagic lesions of the lips and oral sensitivity) and fluid and electrolyte replacement
mucosa can also occur. The skin lesions (target may be lifesaving in children with extensive
or iris lesions) are symmetric in distribution and mucous membrane lesions. If frequent or severe
often annular, with concentric rings, central erythema multiforme is preceded by herpes
purpura, and greyish discoloration of the simplex, acyclovir 200 mg orally five times daily
epidermis or vesicle. Itching is variable. Systemic may prevent attacks.
symptoms vary; malaise, arthralgia, and fever are Toxic epidermal necrolysis 10
frequent. Attacks sometimes last 2 to 4 weeks
and recur in the fall and spring for several years. Toxic epidermal necrolysis (TEN) more
often occurs in adults. Sulfonamides,
Stevens-Johnson syndrome is a severe form barbiturates, NSAIDs, phenytoin, allopurinol,
of erythema multiforme (erythema multiforme and penicillin are most frequently associated, but
major) characterized by bullae on the oral numerous other drugs have been less commonly
mucosa, pharynx, anogenital region, and implicated. Intake of drugs is denied by about
conjunctiva; target-like lesions; and fever. The 1/5 of patients. In about 1/3 of cases, the cause is
patient may be unable to eat or properly close unclear because of concomitant serious disease
44
2005; 7(2) : 121
and drug treatment. TEN is one of the few true TEN closely resembles staphylococcal scalded
dermatologic emergencies and mortality rate is skin syndrome, these disorders can be
61%. differentiated by the patients age, the clinical
setting, and the level of the epidermal split seen
TEN typically begins with painful localized on biopsy (Table 3).
erythema that disseminates rapidly. At the sites
of erythema, flaccid blisters occur or the Patients should be hospitalized; excellent
epidermis peels off in large sheets with gentle nursing care and close observation are essential.
touching or pulling (Nikolskys sign). Malaise, Suspected drugs should be stopped immediately.
chills, myalgias, and fever accompany the Patients should be isolated to minimize
denudation. Widespread areas of erosion, exogenous infection and treated as are those with
including all mucous membranes (eyes, mouth, severe burns by protecting the skin and denuded
genitalia), occur within 24 to 72 hours, and the areas from trauma and infection and by replacing
patient may become gravely ill. Affected areas fluid and electrolyte losses.
of skin often resemble second-degree burns. Although controversial, systemic
Death is caused by fluid and electrolyte corticosteroid use has been successful when
imbalance and multiorgan sequelae (e.g., initiated early in the course of disease. The idea
pneumonia, GI bleeding, glomerulonephritis, is to stop further immunologic injury to the skin,
hepatitis, infection). Rapid diagnosis is important but systemic corticosteroids will not breathe life
so that a possibly offending drug can be stopped. into dead keratinocytes or reverse programmed
Before widespread erythema and epidermal death of skin. Some severe cases require high-
denudation occur, it may be difficult to dose parenteral corticosteroids for several days.
distinguish TEN from morbilliform drug This type of corticosteroid therapy has been
eruptions or erythema multiforme minor and the associated with many adverse effects and should
Stevens-Johnson syndrome (erythema be given under well-controlled conditions.
multiforme major). TEN is often thought to be a Corticosteroids often seem to enhance the
continuum of the latter two diseases. Although propensity to gram-negative or other sepsis and
increase the mortality rate; thus, if these drugs Children 6 months to 4 years until about
are used, a short course is safer. Septicemia, the 6 months immunity from the mother is
most common cause of death, often occurs with present. Beyond 4 years many children have
pulmonary infections and must be recognized and developed immunity to many strains of
treated promptly. Ophthalmologic consultation Neisseria meningitidis.
is often required because there may be
Individuals with complement deficiencies.
considerable crusting of the conjunctiva. To
Complement is a part of the immune system
prevent phimosis, urologic consultation may be
required for the breakdown of
necessary.
meningococcal bacteria.
Collodion baby 11 Individuals without spleen (asplenic).
Autosomal recessive lamellar ichthyosis Individuals taking immunosuppressive drugs
manifest as collodion babies. These babies are such as prednisolone or cyclosporin.
born with a thick armour-like collodion
membrane around them that is replaced much Individuals with a current viral infection.
later by essentially normal skin. Such babies are The most common signs and symptoms of
at a high risk of dehydration, sepsis, and meningococcal disease are listed in the Table 2.
temperature lability. Emollients such as liquid
paraffin are the best topical agents helpful along If an individual has both meningococcal
with control of infection. Topical salicylic acid meningitis and meningococcemia, they may
should never be used because of the danger of present with a mixture of symptoms and signs
salicylism and likewise topical steroids are to be characteristic to each of the diseases.
avoided to prevent rapidly developing adrenal Meningococcal meningitis and
suppression. meningococcemia is often suspected from the
Meningococcal disease 12 history and physical examination. Blood culture
and/or lumbar puncture are used to confirm
Meningococcal disease is an illness caused diagnosis. An increased number of white cells
by the bacteria Neisseria meningitidis. The two are seen under the microscope
common presentations of meningococcal
infection are meningococcal meningitis and Early recognition of meningococcal
meningo-coccemia. An infected individual may infection is critical as meningococcemia spreads
suffer one or both of these diseases. so quickly that within hours of symptoms of
appearance, a patient may rapidly deteriorant and
Meningococcal disease is a medical die. Patients may initially just have a rash and
emergency and patients showing signs and not be particularly unwell. Meningococcemia can
symptoms suspicious of meningococcal infection kill more rapidly than any other infectious
need to seek medical advice from their doctor or disease. Patients with either meningococcemia
a hospital immediately. A delay of even hours or meningococcal meningitis must be
can be fatal. hospitalized and treatment with antibiotics and
Most patients with meningococcal disease supportive care instituted immediately. Many
are otherwise healthy individuals. However, there patients are admitted to an intensive care unit.
are some patient groups who are at an increased Penicillin is the drug of choice. Some strains
risk for developing meningococcal infection. of Neisseria meningitidis are resistant to penicillin
46
2005; 7(2) : 123
have been isolated; in these cases, third- Complications from meningococcal disease
generation cephalosporins are a suitable may occur at the time of the acute disease or
alternative. Very sick patients are often treated during the recovery period. Some complications
with both penicillin and cephalosporins prior to are so severe that they may reduce the chances
obtaining the laboratory results. of survival.
Other treatments may include: Massive hemorrhage of the adrenal glands
intravenous fluids to treat shock and prevent Disseminated intravascular coagulopathy
organ damage (DIC), which prevents blood clotting
medications such as noradrenaline for Arthritis
patients with very low blood pressure Heart problems, e.g. pericarditis
blood products such as platelets and fresh (inflammation of the sack surrounding the
frozen plasma heart)
oxygen and mechanical ventilation as needed Neurological problems, e.g. deafness or
Patients who survive very severe cases of peripheral neuropathy (damage to the nerves
meningococcemia may have suffered severe in feet and hands)
necrosis of skin and underlying tissue. Skin grafts Permanent musculoskeletal problems
and amputation may be necessary. Amputation
47
Indian Journal of Practical Pediatrics 2005; 7(2) : 124
48
2005; 7(2) : 125
49
Indian Journal of Practical Pediatrics 2005; 7(2) : 126
50
2005; 7(2) : 127
since the disease has been recognized, TPN has prognosis. Sclerema does not show necrosis but
included zinc supplementation. shows cleft-filled fat cells that contain triglyceride
crystals. The presence of erythema, bluish
Clinical features include
discolouration of the skin, focal distribution, and
Red and inflamed patches of dry and scaly the histologic presence of inflammatory cells,
skin, particularly around body openings such giant cells, and calcium crystals may differentiate
as the mouth, anus, and eyes, and the skin subcutaneous fat necrosis. Children with
on elbows, knees, hands, and feet. It may sclerema may respond to corticosteroids with
look like atopic dermatitis. packed cells transfusion.
Patches evolve into crusted, blistered, pus-
Leiners disease 21
filled and eroded lesions.
There is usually a sharp demarcation Leiners disease occurs in infants and is
between the affected area and normal skin. characterized by severe generalized seborrhoeic
dermatitis, recurrent diarrhea, recurrent skin and
Skin around nails becomes inflamed and
internal infections, and failure to thrive. It may
there may be abnormal nail growth.
be present at birth but more commonly develops
Hair loss on the scalp, eyebrows and, within the first few months of life. It appears to
eyelashes. be more common in females than males and in
Conjunctivitis. breast-fed infants.
Sensitivity to light. The precise cause of Leiners disease
Loss of appetite. remains unknown but it is known that a defect in
Diarrhea, mild or severe. the bodys complement system has a major role
Irritability and withdrawal. to play in its development. The complement
system is a vital part of the bodys immune
Blood zinc level is abnormally low.
system, and in Leiners disease an inherited
Acrodermatitis enteropathica is easily and dysfunction or deficiency in the C5 component
effectively treated with zinc supplementation. of complement alongside other factors have been
Daily oral zinc supplementation will need to be implicated. Other immune deficiencies may
continued for life. Secondary bacterial and/or present in an identical fashion in infancy.
fungal infection of lesions require appropriate
The condition usually starts off as a scaly
antibiotic therapy. If acrodermatitis enteropathica
rash on the scalp, face or napkin area. Very
is left untreated, symptoms of zinc deficiency
rapidly it spreads to other parts of the body. The
progress further and may even result in death.
affected area is bright red and may look swollen.
Sclerema neonatorum 20 Infants appear uncomfortable but do not itch.
Other symptoms include recurrent diarrhea,
It is seen in a preterm, ill neonate. Almost
infant not thriving or gaining weight, and local
always associated with metabolic acidosis,
skin infections. There is also a risk of developing
hypothermia, and infection, the mortality rate of
more severe infections that may lead to
this condition is around 60%. The disease
pneumonia, meningitis and septicemia.
presents as woody induration of the skin and
subcutis over the buttocks, cheeks, thighs, and Initially affected babies may need to be
lower legs. Histopathology helps to differentiate hospitalized to manage fluid and heat loss. Bland
from subcutaneous fat necrosis that has a good emollients may be used to treat the rash.
53
Indian Journal of Practical Pediatrics 2005; 7(2) : 130
skin failure occurs secondary to several changes 2. Feingold DS. Gangrenous and crepitant
such as fluid loss, electrolyte imbalance, cellulitis. J Amer Acad Dermatol 1982; 6: 289-
infections, etc. in fact cardiac or renal failure may 299.
be the terminal eventuality of acute skin failure. 3. Snyder RA and Eliaz PM. Toxic epidermal
Diseases such as toxic epidermal necrolysis have necrolysis and staphylococcal scalded skin
to be managed just as a case of extensive burns. syndrome. Dermatologic Clin 1988; 235-248.
Precise watching of haemodynamic and 4. Whitley RJ, Namiaz AJ, Soong SJ, et al.
cutaneous bacteriological data does assessment Therapy of Neonatal Herpes simplex virus
of prognosis. The guidelines of treatment include infection. Paediatrics 1980; 66: 495-501.
careful attention to electrolyte equilibrium, 5. Jacobs MI, Magid MS, Jarowski CT.
nutrition, aseptic precautions, energy Disseminated Candidiasis. Arch Dermatol
expenditure, and environmental temperature. All 1980; 116: 1277-1299.
these therapeutic measures should best be given
6. Kramer MS, Leventhal JM, Hutchinson TA, et
in specialized wards that will get to be known as
al. Adverse drug reactions. JAMA 1979; 242:
intensive skin care units in future. 623-628.
Points to remember: 7. Kawasaki T, Kosaki F. A new infantile acute
1. There are a wide range of dermatological febrile mucocutaneous lymph node syndrome
emergencies (MLNS) in Japan. Paediatrics 1974; 54: 271.
2. Intensive care is absolutely necessary in 8. Ramsay DL, Hurley HJ. Papulosqamous
these disorders eruptions and exfoliative dermatitis. In
Dermatology. Eds, by Moschella SL and
3. Acute skin failure occurs secondary to Hurley HJ, WB Saunders, Philadelphia yr; pp
several changes such as fluid loss,
electrolyte imbalance, infections, etc. in fact 9. Tonnesen MG. Soter NA. Erythema
multiforme. J Am Acad Dermatol 1978; 1: 357-
cardiac or renal failure may be the terminal
364.
eventuality of acute skin failure.
10. Heinbeck DM, Hengrave LH, Marvin JA, et
4. Toxic epidermal necrolysis have to be
al. Toxic epidermal necrolysis. A step forward
managed just as a case of extensive burns. in the treatment. JAMA 1985; 257: 2171-2175.
5. Management includes careful attention to 11. Lentz CL, Altman J. Lamellar ichthyosis. The
electrolyte equilibrium, nutrition, aseptic natural history of collodion babies. Arch
precautions, energy expenditure, and Dermatol 1968; 97: 3-5.
environmental temperature. All these
12. Ognibene AJ, Dito WR. Chronic
therapeutic measures should best be given
meningococcemia: further comments on the
in specialized wards that will get to be pathogenesis of associated skin lesions. Arch
known as intensive skin care units in Intern Med 1964; 114: 29.
future.
13. Grogen TM, Odom RB, Bargeta JH. Graft
References versus host reaction. Arch Dermatol 1977; 113:
806-812.
1 Roujeau JC, Revuz J. Intensive care in
dermatology In: Recent advances in 14. Briggaman RA. Hereditary epidermolysis
dermatology. No.8. Eds by Champion RH and bullosa with special emphasis on newly
Pye RJ, Churcill Livingstone, London, 1990; recognized syndromes and complications.
pp 85-99 Dermatologic Clin 1983; 1: 263-280.
55
Indian Journal of Practical Pediatrics 2005; 7(2) : 132
15. Chorzelski TP, Jablonska S. IgA linear 19. Moynahan EL. Acrodermatitis enteropathica:
dermatosis of childhood. Br J Dermatol 1979; A lethal inherited human zinc-deficiency
101: 535-542. disorder. Lancet 1974; 2: 399-400.
16. Lang PG, Dubin HV. Hemangioma- 20. Kellum RE, Ray TL, Brown GR. Sclerema
thrombocytopenia syndrome: A disseminated neonatorum. Arch Dermatol 1968; 97: 372-375.
intravascular coagulopathy. Arch Dermatol 21. Miller ME, Koblenzer PJ. Leiners diease and
1975; 111: 105-107s C5 dysfunction. J Paediatr 1972; 80: 879-88.1
17. Vogel JM, Vogel P. Idiopathic histiocytosis: A 22. Shuster S. Systemic effects of skin disease.
discussion of eosinophilic granuloma, the Lancet 1967; 1: 907-912.
Hand-Schuller Christian disease, and Letterer- 23. LeGall JR, Loirat P, Alperovitch A, et al. A
Siwe syndrome. Semin Hematol 1972; 9: 3-19. simplified acute physiological score for
18. Demis DJ. The mastocytosis syndrome. Ann intensive care unit patients. Critical Care
Intern Med 1963; 59: 194-206. Medicine 1984; 12: 975-977.
BOOK REVIEW
Name Pediatric Nephrology
4th Edition, 2005
Editors Dr. R.N. Srivastava
Dr. Aravind Bagga
Review Two senior pediatric nephrologists of India have come out with 4th Edition of their book
Pediatric Nephrology, which is already popular among postgraduates and practicing
pediatricians for its simple but elegant presentation of various intrinsic aspects of pediatric
nephrological care. On going through the book, one can appreciate the inclusion of recent
advances in every chapter compared to its third edition, which is correctly reflected in an
increase of about 100 pages over its previous edition. Every aspect of Pediatric Nephrology
is well dealt by experienced authors. Color photographs are new additions to this book.
Topics on anatomy, physiology, evaluation of renal function and imaging and diagnostic
modalities are well dealt with in a simple and understandable way. All essential aspects of
clinical nephrology including developmental anatomy to malignant disorders are discussed
in a classical way by the authors. A special content on neonatal nephrology justify the book
to be included as a full and complete reference on pediatric nephrology. Algorithmic
approaches throughout the book are a welcome step for easy understanding. Including key
points separately in every topic has made this book a special one. We recommend this book
on Pediatric Nephrology for every medical personnel interested in learning finer aspects of
pediatric renal medicine.
56
2005; 7(2) : 133
MANAGEMENT UPDATE
BACTERIAL MENINGITIS IN THE meningitis are caused by viruses and present with
POST NEONATAL PERIOD symptoms that are typically milder and resemble
the flu. Bacterial meningitis is a medical
* Potharaju Nagabhushana Rao emergency. Other infectious causes of meningitis
** Potharaju Anil Kumar include
Abstract: Despite advances in antibacterial a. Viruses: Enteroviruses (Echo, Polio,
therapy, bacterial meningitis is associated with Coxsackie), Arboviruses (Japanese
high morbidity and mortality rates even in Encephalitis), Herpes simplex type 2,
developed countries because consequences are Lymphocytic choriomeningitis, Varicella
potentially devastating and isolates with reduced zoster, Mumps
susceptibility to penicillin are found in increasing b. Fungi: Coccidioidomycosis, paracoccidioi-
numbers. Causative bacteria depends on age, domycosis, Cryptococcus, Candida,
route of infection and risk factors. Clinical Aspergillus, Zygomycetes
presentation depends on age. The laboratory gold
c. Protozoa: Amebic
standard is the isolation of the causative bacteria
(Naegleria, Acanthameba),
from the cerebrospinal fluid. Repeat LP is not
Trypanosomiasis
usually indicated if the patient makes uneventful
recovery. In complicated meningitis d. Helminthes: Angiostrongylus
neuroradiological examination plays a Causative organisms and route
fundamental diagnostic role. Management of
H. influenzae, Streptococcus pneumoniae
drug resistant meningitis and recurrent
and Neisseria meningitidis are the common
meningitis require special care.
bacteria causing meningitis in under five year old
Key words: Bacterial meningitis, pyogenic children1. Currently, Streptococcus pneumoniae
meningitis, postneonatal. (pneumococcus) and Neisseria meningitidis
(meningococcus) are the leading causes of
Meningitis is an inflammation of the bacterial meningitis, which can occur as isolated
meninges, the membranes that cover the brain cases or epidemics. Streptococcus pneumoniae
and spinal cord. Pathologically, acute bacterial is associated with highest mortality.
meningitis (ABM) results in congestion and Meningococcus infects humans only, it colonizes
hyperemia of the pia-arachnoid and distention of the nasopharynx and is the most common cause
the subarachnoid space by an exudate containing of bacterial meningitis between the ages of 2 and
polymorphonuclear neutrophils. Most cases of 18 years. Serogroups B and C each account for
* Prof. & Head of Department of Neurology, nearly half of cases. Haemophilus influenzae type
Osmania Medical College and b (Hib) persists as a major cause of pediatric
Chief Pediatric Neurologist, Niloufer meningitis and pneumonia in developing
Hospital, Hyderabad countries where Hib conjugate vaccines are not
** Secunderabad Brain Clinic, Hyderabad used2.
57
Indian Journal of Practical Pediatrics 2005; 7(2) : 134
58
2005; 7(2) : 135
fever (~ 50% in infants, ~ 45% in older children), triad of high BP, high respiratory rate and low
neck stiffness (60 80%, more useful in children heart rate usually occurs in later stages and should
beyond 3 years of age) and back pain, Kernigs always raise a suspicion of raised ICT.
sign and Brudzinkis sign are due to reflex muscle Meningococcal meningitis may occur with
spasm to reduce pain on stretching the inflamed or without other manifestations of invasive
spinal nerves and roots and may be present in meningococcal infection or meningococcemia.
older children. Their absence does not exclude Characteristic skin rash of meningococcemia is
meningitis. Inflammation of cranial nerves causes usually seen on trunk and legs and includes
dysfunction of III, VI, VII and VIII cranial palpable purpura or ecchymoses with irregular
nerves. margin due to associated vasculitis. Hypotension
or fatal shock may occur (Waterhouse
Focal neurological signs indicate vascular
Friderichsen syndrome) due to hemorrhagic
occlusion (arteritis, cerebral venous thrombosis),
infarction of the adrenals in the setting of
subdural collection, cerebritis, abscess formation
overwhelming clinical sepsis and usually
or raised ICT with herniation.
indicates meningococcal infection but rarely
Papilledema in uncomplicated early Streptococcus pneumoniae6 or any other severe
bacterial meningitis is rare. The presence of sepsis.
papilledema within a day or two of presentation Seizures: Seizures are seen in less than 40%.
suggests ruptured abscess causing pyogenic Generalized seizures during initial 4 days have
meningitis or hitherto undetected chronic no prognostic significance. The younger the
meningitis like tuberculous meningitis and if it brain, the more likely a seizure is provoked by
appears after a few days of pyogenic meningitis, infection and pyrexia and so the more common
it suggests complications like venous sinus the seizures are. Multifocal seizures may occur
thrombosis or subdural empyema. A swollen due to electrolyte imbalance (Syndrome of
optic disc associated with marked reduction of Inappropriate Secretion of Anti-Diuretic
visual acuity may indicate septic optic neuritis. Hormone-SIADH) or major organ dysfunction
due to sepsis. Early recognition and treatment of
Raised ICT is very frequent. Rise is maximal generalized seizures in a metabolically
within initial 48 hours with endangering cerebral compromised child is important due to the risk
ischemia due to decreasing cerebral perfusion. of serious sequelae. Persistent focal seizures or
Fulminant presentation is seen with Neisseria Todds palsy indicate subdural effusion/
meningitides. Features of Raised Intracranial empyema /abscess/vascular lesions (infectious
Tension (ICT) include bulging fontanelle, vasculitis) such as arterial infarct, cortical vein
decreasing level of consciousness (due to thrombosis with venous infarcts/dural sinus
brainstem compression), an abnormal pupillary thrombosis/bacterial encephalitis. No child
reaction to light asymmetrical reaction, or develops late seizures unless there were acute
unreactive pupils, abnormal oculocephalic (dolls seizures. Factors associated with seizures during
eye) reflex, abnormal respiratory pattern, viz. acute bacterial meningitis include disturbed
neurogenic hyperventilation, shallow, ataxic or consciousness on admission (may signify an
apneic breathing, decorticate posturing, and underlying encephalitis), abnormal neuroimaging
decerebrate posturing, which may be findings, and low glucose and high concentration
spontaneous, or a response to pain and rising of total proteins in cerebrospinal fluid7. Bacterial
blood pressure with falling heart rate. Cushings meningitis may also present as acute torticollis8.
60
2005; 7(2) : 137
Minimising delay in diagnosis: To avoid a delay prior to the LP, a CT scan obtained and LP
in the diagnosis of meningitis, a high index of performed 8-24 hours after both antibiotics and
suspicion should be maintained, Meningitis must antiedema treatment are started. With this
be considered in any child with unexplained procedure, the risk of LP is lessened, and the CSF
fever, seizures in association with fever, may still be purulent. However, if the correct
particularly if under 12 months, prolonged in antibiotic is chosen, cultures of CSF will be sterile
nature or refractory to management. The presence within 48 hours.
of an apparent explanation for fever, e.g.
Diffusely elevated ICT occurs in almost all
pharyngitis or otitis media does not rule out the
cases of bacterial meningitis and is not in itself a
possibility of meningitis. Apparent improvement
contraindication to LP. The decision to perform
with paracetamol is not helpful in excluding the
cranial computed tomography (CT) before the
diagnosis.
LP delays the diagnosis. Although concerns about
Diagnostic tests herniation following an LP exist, herniation is
The laboratory gold standard for establishing unlikely in children unless they have focal
the diagnosis of bacterial meningitis is the neurological findings or are comatose. A CT scan
isolation of the causative bacteria from the cannot rule out raised intracranial pressure and a
cerebrospinal fluid (CSF). However, laboratory normal CT does not absolutely exclude
diagnosis is often made using the combination subsequent risk of herniation.
of blood and/or CSF cultures along with Gram Interpreting the CSF : White cells in CSF:
stain and chemical analysis of the CSF. Examination of any CSF samples taken is
URGENT. Any delay will not give correct cell
Lumbar puncture (LP) : CSF analysis should
count. The presence of polymorphonuclear
be performed once the diagnosis of meningitis is
(PMN) cells is always abnormal and if present,
suspected and after the patient is stabilized. Blood
suggests bacterial meningitis or rarely, early
for glucose must be drawn and a secure IV line
stages of tuberculous meningitis and viral
started before starting the LP. Simple aseptic
meningitis although lymphocytosis is more
precautions under- taken before the procedure
commonly seen in the latter two conditions. In
prevent iatrogenic meningitis9.
partially treated bacterial meningitis, the
Child must be assessed every 15 minutes relationship between PMNs and lymphocytes
for the next 4 hours and hyperosmolar agents may be reversed. In tuberculous (TB) meningitis,
administered if there is neurologic deterioration. the total WBC is usually < 500 x 10 6/L and
lymphocytes predominate.
If there are reasons to delay LP (like clinical
diagnosis of febrile seizure, infection / anatomical CSF glucose concentration: Changes in the CSF
abnormality at LP site, unstable cardiorespiratory glucose level follow changes in the blood glucose
status, status epilepticus, raised ICT signs by about 30 minutes. So, the best way is to draw
especially decerebrate or decorticate posturing, blood glucose and then draw CSF 15-30 minutes
abnormal reaction of pupils, focal seizure, later so that the ratio can be accurately calculated
marked neck stiffness or neuroimaging showing for interpretation. Hypoglycorrhachia is due to
shift of midline structures, obliteration of CSF decreased glucose transport by the cerebral tissue,
pathways, herniation) and bacterial meningitis is utilization of glucose by inflammatory cells and
clinically suspected, blood must be drawn for the pathogen. CSF glucose < 2.2 mmol /L is found
culture (useful in 66% of cases), antibiotics given in about 2/3 of patients with bacterial meningitis.
61
Indian Journal of Practical Pediatrics 2005; 7(2) : 138
CSF: blood glucose ratio <0.3 is found in 70%. 0.015 g/L increase in protein levels for every
Very low levels of CSF glucose are found in 1000 X 10 6/L RBCs in uncentrifuged CSF
overwhelming infection, fungal and malignant samples). For every 500 RBC in the CSF, one
meningitis. However, a normal glucose does not WBC is acceptable. However this depends on the
exclude meningitis. While the CSF glucose rarely peripheral white and red cell counts. A more
influences treatment decisions, the CSF glucose precise formula to estimate the WBC in CSF has
level was found useful in the following been described12. But it is more practical to rely
situations10: patients pre-treated with antibiotics, on the bacteriologic result rather than to attempt
CSF pleocytosis (suggests the most likely class to interpret the CSF leukocyte and protein results
of organism), patients > 8 weeks of age and of a traumatic LP.
patients at risk of unusual organisms. In bacterial
meningitis other than that caused by Neisseria Gram stain: This is the best single test for rapidly
meningitidis and independent of the duration of diagnosing bacterial meningitis and initiating
symptoms prior to diagnosis, CSF glucose levels appropriate therapy (Table 3). In untreated
are significantly lower in patients developing a bacterial meningitis, CSF Gram stains reveal
sensorineural hearing loss compared to controls11. bacteria in about 50% to 80% of cases and
cultures are positive in at least 85% of cases.
CSF protein concentration: Raised CSF protein Occasionally, the Gram stain will be positive
is due in part to increased vascular permeability despite the absence of pleocytosis. However,
(disruption of blood brain barrier) resulting in sensitivity of both gram stain and cultures
leakage of albumin rich fluid from the capillaries decreases to less than 50% in patients already
and veins traversing the subdural space. taking antibiotics, but other CSF indices may still
Continued transudations result in subdural indicate a likely bacterial infection. In patients
effusions. 90% of patients with bacterial suspected of having meningitis, blood cultures
meningitis will have elevated protein levels. should always be done because the organism can
be cultured in 66% cases and occasionally they
Traumatic tap: Traumatic LP complicates the may uncover a pathogen that was not found on
interpretation of CSF changes. The protein levels CSF cultures.
may be elevated in a traumatic tap. Methods for
correction for the presence of RBC and protein CSF changes after starting antibiotics:
elevation are proposed (approximately 0.01 Antibiotics may sterilize the CSF within 1 hour
62
2005; 7(2) : 139
in meningococcal meningitis and within 4 hours organism is relatively difficult to treat (e.g.,
in pneumococcal meningitis and the cell response enteric gram-negative rods, Listeria, Staphyloco-
changes to lymphocytes within 24 hours. ccus aureus, -lactam resistant Streptococcus
However, instituting antibiotics 1-2 hours prior pneumoniae), an LP should be done 72 hours
to LP does not decrease the diagnostic sensitivity after starting antibiotics to confirm sterilization
if the CSF culture is done in conjunction with of CSF. Rare indications include lack of clinical
blood cultures. But, CSF protein may continue response, persistent fever, unusual etiologic
to be high and CSF glucose may be low for 2 organism or suspicion of antibiotic resistance.
weeks or longer despite curative therapy. Persistence of the organism in the CSF beyond
the expected interval implies a need to change
Repeat LP: is not usually indicated if the patient the antibiotic or presence of an occult
makes uneventful recovery. A repeat LP at 24 para-meningeal focus of infection seeding the
48 hours may be indicated when clinical CSF. An LP at the conclusion of therapy has not
indicators of meningitis are present but initial proved useful in predicting those patients who
CSF examination is normal. When the causative will relapse.
Table 4. Possible additional tests based on clinical presentation
a. Platelet count, coagulation profile including fibrin degradation products - if there is shock, rash,
or bleeding diathesis. DIC must be suspected.
b. Erythrocyte sedimentation rate and C-reactive protein as inflammatory markers add useful
information on clinical progress13.
c. Blood glucose, urea, electrolytes and serum calcium, if seizures are refractory.
d. Serum and urine sodium must be monitored every 8-12 hours during the first 2 days if SIADH
is suspected. If patient has hyponatraemia, SIADH or cerebral salt wasting syndrome (CSWS)
is possible.
e. Plasma osmolality and Urinary osmolality.
f. CT scan of Head - Indicated if space occupying lesion is suspected (Patient should be clinically
stable.)
g. Mycobacterium tuberculosis (MTB) stain - if Tuberculous Meningitis is suspected. Adequate
volumes should be obtained for mycobacterial culture aim for 5 10 ml minimum. Concentration
methods / repeat LP may be necessary.
h. Scrapings of skin lesions In meningococcal purpura. Gently deroof the skin lesion with a
needle. Roll the sterile swab over the base of the lesion and then onto a glass slide and examine
by Gram stain. Collect another swab and place into Stuarts Transport media for culture.
i. Cryptococcal stain - Immunocompromised patients including HIV patients. (Gram stain is a
good screening test as cryptococcus appears as large gram positive cocci. India ink can then be
used to identify Cryptococcal capsule followed by latex agglutination for identifying cryptococcal
antigen).
j. Renal Function Tests and Liver Function Tests Sepsis causes renal and hepatic dysfunction.
63
Indian Journal of Practical Pediatrics 2005; 7(2) : 140
Investigations for all patients with suspected occupying lesions result from abscess or
bacterial meningitis (Table 4, 5) infarction due to arteritis or phlebitis. Subdural
a. Basic investigations include complete blood collections may be seen. Paranasal sinusitis or
count (A normal WBC count does not fracture may be detected.
exclude meningitis). MRI is the examination of choice in the
b. S.electrolytes, blood glucose, renal function assessment of parenchymal lesions due to its
tests (monitor serum sodium to detect superior sensitivity. Meningeal enhancement is
SIADH). associated with a slight signal increase of both
c. Chest X-ray (for focus of infection) T1- and T2-weighted images (due to the high
d. Cultures from throat, blood and urine proteinaceous content of the exudate).
Parenchymal foci of involvement are visible as
Neuroradiology T2 hyperintensities and they may represent
In complicated meningitis neuroradiological arterial or venous infarcts or cerebritis. The
examinations play a fundamental diagnostic role. presence or absence of conformity to a distinct
Neuroimaging is indicated if there are focal signs/ vascular distribution, and the presence of venous
seizures, if seriously raised ICT is suspected, if T1 hyperintensities representing thrombosis (to
there is papilledema, lack of significant response be searched for in particular in the veins near the
to medical treatment, fever or coma persist, head sagittal sinus) are features that assist in the
circumference increases or when complications differentiation of these entities. Sometimes
are suspected. Cranial sonography is most differentiation of cerebritis from infarction may
economical and easily available for young infants only become apparent with time as cerebritis
but use is limited. CT is usually preferred because typically evolves into a well formed abscess.
it is cheaper than MRI, faster and can be done in
Hydrocephalus and its sequela,
ill patients with an airway. Additionally, there is
transependymal migration, are equally well
a positive correlation between CT scan results
demonstrated on CT and MRI but identification
and neurological signs20. Ventricular imaging
of an eventual site of obstruction benefits from
findings may be unremarkable or show
the multiplanarity of MRI. Early/minimal
ependymal enhancement on contrast if there is
transependymal migration is better demonstrated
ventriculitis. Meningeal enhancement with
on MRI. Postcontrast imaging enables differential
contrast injection may be absent in viral
diagnosis between ependymitis (enhancement of
meningitis and bacterial meningitis of children.
the ependymal lining) and simple transependymal
In severe bacterial meningitis it is nevertheless
migration (no enhancement).
usually present and is associated with distention
of the subarachnoid space with widening of the Subdural effusions and empyemas are also
interhemispheric fissure by the inflammatory well documented on both CT and MR imaging
exudate. On CT this distention is seen as an studies. Differentiation between the two entities
obliteration of CSF space due to the increased is possible on MRI on the basis of signal
density of the exudate. Small ventricles and intensities (subdural effusion presents a CSF-like
effacement of sulci imply brain swelling and signal, whereas empyema shows hyperintensities
raised ICT. Hydrocephalus results from on both T1 and T2 weighted images).
malabsorption due to basal meningeal adhesions. Additionally empyema shows an enhancing
Sediment in the posterior horns of the lateral membrane and it is usually associated with foci
ventricles indicates pus collection. Focal space of parenchymal involvement.
65
Indian Journal of Practical Pediatrics 2005; 7(2) : 142
66
2005; 7(2) : 143
The clinical presentations and CSF findings culture. On the other hand, tuberculous
in children who have received previous meningitis, especially in infants, may present with
antibiotics may be modified. The relationship a polymorphonuclear reaction in the CSF and
between polymorphonuclear cells and blood and low CSF sugar. Rarely later stages of
lymphocytes in CSF may be reversed. Positive TBM may also present with neutrophilia.
cultures can be obtained up to 4 hours after the Usually, in about 30% of all cases of meningitis,
first dose of antibiotic and bacterial antigens can there is diagnostic confusion between tuberculous
be detected in CSF up to several days after meningitis and pyogenic meningitis. Yet both are
initiation of therapy. The diagnosis of acute serious life threatening infections requiring early
bacterial meningitis is delayed in children pre- aggressive treatment to prevent death and
treated with antibiotics but the complication rate disability. Pyogenic meningitis is diagnosed if:
is not necessarily increased23. (1) CSF is positive for C-Reactive Protein13 (2)
CSF is positive for Gram stain / bacterial culture
Pyogenic or Tuberculous Meningitis? Patients or (3) No basal enhancement on contrast CT scan,
with pyogenic meningitis, even if treated with oral (4) there is a sustained response without
or intramuscular antibiotics, usually have a antituberculous treatment. In case of doubt, child
polymorphonuclear CSF response. Some patients could be treated both for TBM and pyogenic
with pyogenic meningitis, immediately after meningitis. Later, treatment for TBM should be
intravenous antibiotics, have a predominant continued depending upon the response and other
lymphocytic response in CSF and a sterile evidence of extracranial TB.
67
Indian Journal of Practical Pediatrics 2005; 7(2) : 144
68
2005; 7(2) : 145
Leptospira interrogans) that induce a while other tests and imaging are being carried
lymphocytic response rather than out since abnormalities of CSF and visible
neutrophilic response. organisms in CSF will persist for more than 24
hours. Antibiotics must always be given
CSF becomes turbid when the leukocyte
intravenously.
count exceeds about 300/mm 3. 20% of
patients of pyogenic meningitis have <250 Empiric antimicrobial therapy for bacterial
leukocytes/mm3. meningitis: Current recommendations for
Pleocytosis is absent when severe sepsis is empiric therapy are third generation
associated with meningitis and is a bad cephalosporins, cefotaxime or ceftriaxone being
prognostic sign. the preferred antibiotics26 before investigation
results are available due to their efficacy against
Gram stain and culture results are affected penicillin resistant H. influenzae type b and
in partially treated pyogenic meningitis but Streptococcus pneumoniae. Where affordability
not glucose and protein results. is a problem, Ampicillin plus Chloramphenicol
Gram stain and cultures are not affected by is an economical substitute if there is no
traumatic LP and are presented in Table XIII. significant penicillin resistance27. Table 9 and
Table 10 summarize the important drugs details.
Presence of RBC in CSF may imply Herpes
Simplex meningoencephaltis provided a Penicillin allergic patients: In patients with a
traumatic tap has been ruled out (by the 3 history of serious allergic reactions to penicillin
tube test). (i.e., bronchospasm, angioedema, or hives within
48 hours), useful alternative agents are
A combination of the following CSF values
chloramphenicol in known H influenzae type b
predicts bacterial meningitis with 99% accuracy:
or meningococcal meningitis, vancomycin in
WBC count >2,000/mm 3, Neutrophil count
pneumococcal meningitis, and trimethoprim-
>1,180/mm3, Protein level >220 mg/dL, CSF-
sulfamethoxazole in suspected or proven Listeria
serum glucose ratio <0.23, Glucose level <34 mg/
monocytogenes infection. Panipenem-
dL. Wet smear for microscopy is useful for fungi
betamipron appears to be effective for the
and amoebae.
treatment of listerial meningitis29.
Treatment
Drug Resistance: It is increasing and requires
Specific measures special care (Table 10).
*
Penicillin resistance should only be tested by using oxacillin discs and not ampicillin discs. For
P.aeruginosa meningitis, the combination of intrathecal and intravenous amikacin should be used37
lysis of bacteria in the CSF after administration of vancomycin into the CSF with steroid use as
of antibiotic. Adjuvant dexamethasone is vancomycin does not penetrate the non-inflamed
unequivocally recommended in children with meninges.
Haemophilus meningitis or pneumococcal Limitations: A practical problem is how often
meningitis 38 . The benefit of adjunctive can we diagnose H. influenzae and Streptococcus
dexamethasone is likely to be greatest in patients pneumoniae meningitis before giving the first
who are otherwise healthy and present early with dose of antibiotic? Secondly, it cannot be
acute bacterial meningitis. Dexamethasone, assumed that if dexamethasone is beneficial for
before or with the first dose of antibiotic, is likely H. influenzae and Streptococcus pneumoniae
to be one of the most significant practice changes meningitis, it should be efficacious for other
that has been of proven value in the developed pathogens. The role of steroids in cephalosporin
world. Dexamethasone has no effect on Neisseria (cefotaxime or ceftriaxone) treated bacterial
meningitidis meningitis 39 . Children with meningitis in developing countries should be
Haemophilus influenza type B meningitis who further studied. Steroid use as adjunctive therapy
were given dexamethasone had less fever, lower in childhood meningitis remains controversial in
CSF protein and lactate levels, lower incidence the post-Hib vaccination era where Streptococcus
of neurologic sequelae, including hearing loss. pneumoniae (penicillin resistant) and Neisseria
There is no basis for restricting the use of meningitidis have become the pathogens of
dexamethasone to more severe cases. A concern in infants and children. Steroids must
speculative concern is the reduced penetration not be used in newborns (bacterial spectrum is
71
Indian Journal of Practical Pediatrics 2005; 7(2) : 148
different, role of inflammatory mediators is not meningitis. Patients with evidence of shock
documented), suspected cerebral malaria should be treated with a rapid infusion
(increases the severity), gram-negative bacillary intravenous/introsseous crystalloid (Normal
meningitis, nonbacterial meningitis, aseptic saline) 20ml/kg. Septic shock must be treated
meningitis or viral encephalitis (not useful), with fluid resuscitation and vasoactive drugs like
partially treated meningitis and undiagnosed dopamine, epinephrine and sodium nitroprusside.
meningitis or in areas with high penicillin- Considerations for fluid restriction (for SIADH)
resistant pneumococcal invasive disease. Major should only be undertaken after controlling
concern is a potential decrease of antibiotics shock.
concentration in cerebrospinal fluid that may be
detrimental in patients with meningitis caused by Disability (level of consciousness): must be
Streptococcus pneumoniae strains that are highly assessed. Multisystem monitoring in an intensive
resistant to penicillin or cephalosporins. care unit till the patient is stable is necessary40.
Adjunctive corticosteroid therapy is not Life threatening complications (septic shock,
recommended for bacterial meningitis in children brain herniation) occur during initial 4 days and
vaccinated against H influenzae type b. There is so admission to PICU and monitoring of
insufficient evidence to support recommen- cardiorespiratory status, fluid and electrolytes,
dations for the routine use of steroids for all frequent urine specific gravity, daily weights and
children with bacterial meningitis treated with frequent neurologic assessment is essential. Oral
penicillin and chloramphenicol in developing feeding should be withheld till patient is stable.
countries. When cerebral edema/raised ICT and shock
The dose of dexamethasone is 0.15 mg/kg/ (tachycardia, reduced skin perfusion, poor skin
dose every six hours intravenously in a single turgor) coexist, shock takes priority and
push 20 30 minutes before or at the time of hypotension and hypovolemia are immediately
first antibiotherapy and continued for 2 to 4 days. treated with normal saline and inotropic support
Complications like Gastrointestinal bleeding, along standard lines. Solutions that contain more
hypertension, hyperglycemia could result from than 50% free water (e.g., 5% Dextrose in
steroids. Rebound fever on stopping steroids may water) should not be administered, except in small
occur. volumes when they are used to dissolve
antibiotics.
Supportive measures: Assessing the Airway,
Breathing, Circulation and Disability (level of I. ICP elevation is maximal in the initial 48
consciousness) is the first main concern. hours. It must be reduced to maintain cerebral
perfusion and prevent cerebral infarction.In an
Resuscitation: Airway and breathing: An open emergency situation, elevate the head end by 30
airway and adequate ventilation must be to improve venous drainage from the brain and
established. Supplemental oxygen should always reduce the ICP. In raised ICP head end should
be administered. If ventilation or oxygenation is be elevated but when herniation is suspected,
inadequate, then respiratory support should be head end should be lowered.
commenced by endotracheal intubation and
ventilatory support. (a) Prevent flexion of neck and any possible
obstruction to jugular venous outflow
Circulation: Fluid restriction is not an issue in
(caused by turning of the head to a side).
the initial stabilization of children with
72
2005; 7(2) : 149
(b) Mannitol is an osmotic diuretic, Osmotic may be used if the child can take orally or
diuretics must be used in minimum necessary through Ryles tube.
doses for the minimum necessary period (d) The loop diuretic frusemide alone causes a
only. Mannitol infusion loading dose is 5 ml/ slow reduction in ICP but when combined
kg (1g/kg) of 20 % Mannitol, to be given IV with Mannitol, the fall in ICP is rapid and
rapidly over less than 20 minutes, followed remains low for a considerably longer period
by 1.25 ml/kg (0.25 g/kg) every 6-12 hours than when either agent is used alone.
to treat persistent ICP elevation. Response Frusemide 1 mg/kg/dose every 12 hours
to mannitol depends upon intracranial
(e) Urine output must be carefully monitored
pressure, dose given over the previous 3
and replaced to avoid hypovolemia and
hours (better effect with lesser doses), and
hypotension.
rate of administration. Rapid administration
is more effective in reducing intracranial (f) Normalize temperature. The increased
pressure (ICP) for a shorter duration, where metabolic demand from hyperthermia
as a slower infusion rate reduces the ICP to increases cerebral blood flow (CBF),
a lesser degree, but for a longer duration. cerebral blood volume (CBV) and
Mannitol and glycerol slowly cross the blood intracranial pressure (ICP). Increased CBV
brain barrier and on reaching a significant and ICP result in increased cerebral edema,
concentration after a few days result in water reduced CBF and deterioration of the supply
entering the brain from the vascular to demand ratio. Shivering (can occur during
compartment due to osmotic pressure sponging) increases ICP by increasing
gradient. This is called rebound pleural (intrathoracic pressure). This can be
phenomenon. To delay this mannitol must prevented by promethazine 1 mg/kg in 3
be used at a dose of only 0.25 g/kg and not divided doses in a day.
higher doses. It must not be used if serum (g) Hyperventilation can be used to reduce the
Osmolality exceeds 300 mOsm/l since renal intracranial pressure immediately. Over
tubular damage with consequent renal failure enthusiastic hyperventilation causes
results at a serum osmolality of 330 mOsm/ reduction of cerebral blood flow and must
l. Chronic continuous therapy must be be avoided. Long-term hyperventilation
avoided as the brain adapts to the sustained worsens the outcome by inducing oligemia
hyperosmolality of plasma with an increase in marginally perfused brain tissue.
in intracellular free amino acids, which (h) Sedation: Restlessness and agitation require
contribute to the idiogenic osmoles that diazepam.
appear in the brain in its adaptation to
(i) Control Seizures.
hyperosmolality. Mannitol is contraindicated
in congestive cardiac failure, renal failure (j) If ICP is uncontrolled short acting barbiturate
and pulmonary edema. narcosis may be useful.
(c) Give Mannitol for the first three days (k) If facilities are available, ICP monitoring
followed by oral glycerol (either orally or should be instituted and maintained below
through nasogastric tube) for a few days and 15 mm Hg.
then taper it off over the next few days. (l) CSF pressure can be presumed to have
Glycerol 0.5 ml/Kg diluted in twice the returned to normal if the patient is afebrile,
volume of water or fruit juice 3 times daily awake and alert, without focal signs.
73
Indian Journal of Practical Pediatrics 2005; 7(2) : 150
II. Seizures: Seizures occur in about one third Then, flush the line with a few ml of normal
cases and must be treated aggressively. saline since phenytoin irritates the veins due
For the treatment of uncontrolled seizures give to its high pH (pH is 12). Give maintenance
drug (if only diazepam was enough to stop
Diazepam IV or PR or Lorazepam
Status Epilepticus), Phenytoin 5 - 10 mg/Kg
may be given through a nasogastric tube.
Repeat Diazepam IV or PR or Lorazepam
(f) Suspension of Sodium Valproate (up to 60
Phenytoin IV or Phenobarbitone IV mg/Kg) may be diluted 1:1 with water and
administered as retention enema. It may be
continued 30-60 mg/kg/day in 3 divided
Paralyze and Ventilate
doses by either oral or rectal route.
Midazolam or propofol infusion Intravenous valproate also may be infused
(a) IV Diazepam 0.1 - 0.3 mg/Kg in 1-5 minutes. in a dose of 20 mg/kg at 20 mg/min after
The dose may be repeated in 5 - 20 minutes. failure of lorazepam and phenytoin regimen.
(b) Rectal Diazepam: Diazepam: Dose in The drug may be repeated whenever
general, is 0.5 mg/kg. Not recommended for required.
children under 10 kg for technical reasons.
(g) Anticonvulsants may be tapered off after a
For children of 10-15 kg body weight a dose
few days unless there is evidence of
of 5 mg should be used. For children of over
persistent seizure activity.
15 kg, 10 mg should be used. Diazepam
rectal solution is available. Otherwise, oral III. The basis of fluid restriction and current
syrup may be diluted 1:1 with ordinary water views: Animal studies of experimental meningitis
and used rectally. and a human study from India suggests that fluid
(c) Lorazepam (0.05 mg/kg IV) is preferable to restriction may be harmful but the evidence is
diazepam because of its longer half life. inconclusive41. In normovolemic patients fluids
are empirically restricted to 2/3 of maintenance
(d) Midazolam: Midazolam, 0.15mg/kg, IV or
or 800-1000 ml/m2 /24 hours initially only till
IM.
raised ICP and SIADH are excluded. Fluids may
(e) Considerations to a loading dose of be given normally (1500-1700 ml/m2/24 hours)
phenytoin (20 mg/kg over 20 minutes) when serum sodium levels are normal.
should be given if seizures continue.
Phenytoin is preferable to phenobarbitone Serum Sodium level alterations: Hyponatremia
since the latter sedates the child and so is the most common and important electrolyte
interferes with the assessment of depth of disorder encountered in the neurologic intensive
coma. Phenobarbitone may be used if care unit. Hyponatremia can cause several types
sedation also is desired along with seizure of CNS and circulatory disorders such as cerebral
control. Phenytoin 10 - 20 mg /Kg over 10 - edema and increased intracranial pressure.
20 minutes at a rate of less than 1 mg/Kg/ SIADH, CSWS, and hyponatremia caused by the
Minute. Repeat dose of 5 - 10 mg /Kg IV inappropriate use of hypotonic solutions, causing
may be given after 1 hour, up to a maximum life threatening central nervous system (CNS)
of 1000 mg. Never give IM, mix only in pathophysiology 42 . Iatrogenic causes, most
normal saline (never in dextrose) to a conspicuously inadequate tonicity of intravenous
maximum concentration of 1mg in 1ml. fluids, should be promptly identified and removed
74
2005; 7(2) : 151
when possible. Bacterial meningitis is associated correction must be done slowly as mentioned
with increased total body water, low serum above as by this time the brain generates free
sodium and high ADH levels in more severe osmoles.
cases, SIADH. Current opinion is that the high
IV. Fever: Paracetamol, salicylates or tepid water
ADH levels probably represent compensatory
bath may be used.
mechanisms to maintain cerebral perfusion in the
presence of cerebral edema. V.Treatment of predisposing factors:
Parameningeal infection, systemic foci of
Cerebral salt wasting (CSW) syndrome is
infection or CSF leak etc require specific
far less well-known than SIADH and also
management.
different from SIADH in diagnosis and treatment.
Fig. 1 summarizes the current understanding of VI.Waterhouse-Friderichsen syndrome:
SIADH and CSWS. Emergency treatment with replacement doses of
Treatment of hyponatremia depends on the corticosteroids is warranted.
clinical manifestations. If it is acute in onset and VII. Nursing Care: The nursing care is as
is causing neurological dysfunction (serum important as medical care and is to prioritize
sodium <120 mEq/L with CNS symptoms) then Airway, Breathing and Circulation, accompanied
hypertonic saline is justified to correct it43. Central by a rapid assessment of conscious level using
pontine myelinolysis (clinically presents as the AVPU scale (Is the patient Awake,
locked-in syndrome) may occur from osmotically responding to Voice, responding to Pain or
induced demyelination due to overly rapid Unresponsive) and management of the
correction of serum sodium and hypoxic-anoxic unconscious child. Urinary catheterization in all
episodes during hyponatremia may contribute to unconscious children is a must. If not done,
the demyelination. In long standing hyponatremia bladder distension makes the child restless. This
(Low Sodium without any CNS abnormalities), restlessness will not respond to sedatives.
Hypotonic Hyponatremia
Volume Status
Hypovolemic Euvolemic
CSWS SIADH
Due to Increased secretion of Brain Natriuretic Low urine output due to water retention by ADH
Peptide (BNP) with suppression of aldosterone Low Blood Urea Nitrogen BUN < 10 mg/dL
secretion (High BUN excludes SIADH)
High urine output Inappropriately increased urine osmolality (>150
mosm/Kg)
UNa+ >20 meq/L UNa+ >20 mq/L
Treat by replacing lost volume with isotonic No cardiac or renal or liver or thyroid or adrenal
or half-normal (0.45%) saline or lactated disease
Ringers solution. Treat by water restriction
Fig. 1 SIADH and CSWS
75
Indian Journal of Practical Pediatrics 2005; 7(2) : 152
Epidural hemorrhage and spinal abscess should compromised cranial nerves. Early identification
be considered in the differential diagnosis46. of major risk groups is important to adopt
measures to improve prognosis49.
Sequelae: Though significant improvement
occurs due to neuronal plasticity, proper medical Conclusion
management, developmental and occupational Despite advances in antibacterial therapy,
therapy, excessive cytokine-induced bacterial meningitis in childhood is associated
inflammation continues after the CSF has been with morbidity rates of about 20% and mortality
sterilized and is partly responsible for the rates of about 5% even in developed countries50.
sequelae. Sequelae reflect complications and are The disease is of special concern because
seen in 10-20% of survivors. Axonal pathology consequences are potentially devastating and
contributes significantly to neurologic sequelae because isolates with reduced susceptibility to
after bacterial meningitis47. penicillin are found in increasing and alarming
Sensorineural hearing loss occurs in about numbers. Hib is the most predominant cause of
10-47% of survivors48. Because of compliance meningitis in young Bangladeshi children.
problems with outpatient audiological assessment Resistance to ampicillin and chloramphenicol and
and because early identification and expedient the high cost of third-generation cephalosporin
amplification lead to better academic and highlight the importance of disease prevention
language outcomes, routine inpatient audiological through vaccination against Hib51. An effective
screening of postmeningitic children is vaccination program against Streptococcus
advocated. All recovered cases must be screened pneumoniae and H. influenzae type b should
for this. reduce the prevalence of sensorineural hearing
loss due to bacterial meningitis in India52.
Hydrocephalus occurs in <5% and can
present years later as CSF absorption and Points to remember
circulation are disrupted as meningeal adhesions 1. High index of suspicion of Pyogenic
mature. Other sequelae are epilepsy (4.2%), meningitis and educated guess in initial
mental retardation (4.2%), visual impairment, selection of antibiotics before culture
behavioral problems, motor deficits 3.5%, results are available is useful in reducing
learning disabilities, syringomyelia and focal the morbidity and mortality.
neurologic problems (e.g., spasticity, paresis, 2. Presence of papilledema has important
ataxia, cortical blindness). implications.
The mortality rate for pyogenic meningitis 3. Nursing care is as important as medical
varies according to organism (high with care.
pneumococcus 10-30%), age (high in infants),
References
underlying predisposing factor (Listeria, 9% with
no immune defect to about 60% with immune 1. Sahai S, Mahadevan S, Srinivasan S, Kanungo
suppression) and clinical status when treatment R. Childhood Bacterial Meningitis in
Pondicherry, South India. Indian J Pediatr 2001;
is started (the later the initiation of therapy, the
68:839-841.
worse the mortality rate).
2. Martin M, Casellas JM, Madhi SA, et al. Impact
Factors associated most frequently with poor of Haemophilus influenzae Type b Conjugate
outcome include absence of respiratory infection, Vaccine in South Africa and Argentina. Pediatr
high cerebrospinal fluid protein, and Infect Dis J 2004 ; 23(9):842-847.
77
Indian Journal of Practical Pediatrics 2005; 7(2) : 154
3. Cheng BC, Chang WN, Lu CH, et al. Bacterial 15. Nigrovic LE, Kuppermann N, McAdam AJ,
meningitis in hemodialyzed patients. J Nephrol. Malley R. Cerebrospinal latex agglutination
2004 ;17(2):236-241. fails to contribute to the microbiologic
4. Callanan V, Poje C. Cochlear implantation and diagnosis of pretreated children with
meningitis. Int J Pediatr Otorhinolaryngol. meningitis. Pediatr Infect Dis J 2004;23(8):786-
2004;68(5):545-550. 788.
5. Ginsberg L. Difficult and recurrent meningitis. 16. Kanungo R, Bhaskar M, Kumar A, Badrinath
J Neurol Neurosurg Psychiatry. 2004;75 Suppl S, Rajalakshmi B. Detection of pneumolysin
1:i16-21. in cerebrospinal fluid for rapid diagnosis of
Pneumococcal meningitis. Indian J Med Res
6. Hamilton D, Harris MD, Foweraker J, Gresham
2004;119(2):75-78.
GA. Waterhouse-Friderichsen syndrome as a
result of non-meningococcal infection. J Clin 17. Smith K, Diggle MA, Clarke SC. Automation
Pathol 2004;57(2):208-209 of a fluorescence-based multiplex PCR for the
laboratory confirmation of common bacterial
7. Chang CJ, Chang HW, Chang WN, et al.
pathogens. J Med Microbiol. 2004;53
Seizures complicating infantile and childhood
(Pt 2):115-117.
bacterial meningitis. Pediatr Neurol. 2004;
31(3):165-171. 18. Schuurman T, de Boer RF, Kooistra-Smid AM,
van Zwet AA. Prospective study of use of PCR
8. Mukherjee S, Sharief N. Bacterial meningitis amplification and sequencing of 16S ribosomal
presenting as acute torticollis. Acta Paediatr. DNA from cerebrospinal fluid for diagnosis of
2004; 93(7):1005-1006. bacterial meningitis in a clinical setting. J Clin
9. Pandian JD, Sarada C, Radhakrishnan VV, Microbiol 2004; 42(2):734-740.
Kishore A. Iatrogenic meningitis after lumbar 19. Parmar RC, Warke S, Sira P, Kamat JR. Rapid
puncture-a preventable health hazard. J Hosp diagnosis of meningitis using reagent strips.
Infect 2004; 56(2):119-124. Indian J Med Sci. 2004;58(2):62-66.
10. Givens TG, Paul RI, Bothner JP, Hardwick WE, 20. Tuncer O, Caksen H, Arslan S, et al. Cranial
Jr., Walsh-Kelly CM. Cerebrospinal fluid computed tomography in purulent meningitis
glucose and protein in disposition and treatment of childhood. Int J Neurosci 2004;114(2):167-
decisions. Acad Emerg Med 2000; 7(3):298- 174.
302.
21. Polk DB, Steele RW. Bacterial meningitis
11. Eisenhut M, Meehan T, Batchelor L. presenting with normal cerebrospinal fluid.
Cerebrospinal fluid glucose levels and Pediatr Infect Dis J 1987; 6(11):1040-1042.
sensorineural hearing loss in bacterial 22. Wong M, Schlaggar BL, Landt M. Postictal
meningitis. Infection 2003; 31(4):247-250. cerebrospinal fluid abnormalities in children.
12. Lipton JD, Schafermeyer RW. Evolving J Pediatr 2001;138(3):373-377.
concepts in pediatric bacterial meningitisPart 23. Bonsu BK, Harper MB. Fever interval before
I: Pathophysiology and diagnosis. Ann Emerg diagnosis, prior antibiotic treatment, and
Med 1993; 22(10):1602-1615. clinical outcome for young children with
13. Pemde HK, Harish K, Thawrani YP, bacterial meningitis. Clin Infect Dis
Shrivastava S, Belapurkar KM. C-reactive 2001;32(4):566-572.
protein in childhood meningitides. Indian J 24. Sinner SW, Tunkel AR. Antimicrobial agents
Pediatr 1996; 63(1):73-77. in the treatment of bacterial meningitis. Infect
14. Beratis NG, Eliopoulou MI, Syrogiannopoulos Dis Clin North Am 2004 Sep;18(3):581-602.
GA. Beta-glucuronidase in the diagnosis of 25. Stahl JP. [Antibiotic treatment of bacterial
bacterial meningitis and response to treatment. meningitis] [Article in French]. Rev Prat 2004;
Acta Paediatr 2003; 92(11):1272-1276. 54(9):963-967
78
2005; 7(2) : 155
26. Prasad K, Singhal T, Jain N, Gupta PK. Third meningitis due to methicillin-resistant
generation cephalosporins versus conventional Staphylococcus epidermidis with linezolid. J
antibiotics for treating acute bacterial Clin Microbiol 2004; 42(2):929-932.
meningitis. Cochrane Database Syst Rev 2004; 36. Lalueza Broto MP, Lopez Martinez R,
(2): CD001832. Dominguez Cenzano L, Garnacho de Vega A.
27. Fuller DG, Duke T, Shann F, Curtis N. [Treatment of multiresistant Staphylococcus
Antibiotic treatment for bacterial meningitis in epidermidis meningitis with linezolid] [Article
children in developing countries. Ann Trop in Spanish]. Med Clin (Barc) 2004;
Paediatr. 2003; 23(4):233-253. 21;122(6):238-239.
28. Balbi HJ. Chloramphenicol: a review. Pediatr 37. Corpus KA, Weber KB, Zimmerman CR.
Rev 2004; 25(8):284-288. Intrathecal amikacin for the treatment of
29. Hitomi S, Ohto T, Okamoto M, Nishimura Y, pseudomonal meningitis. Ann Pharmacother
Iwasaki N, Matsui A. A case of listerial 2004;38(6):992-995.
meningitis treated with a regimen containing 38. Chaudhuri A. Adjunctive dexamethasone
panipenem-betamipron. J Infect Chemother treatment in acute bacterial meningitis. Lancet
2004 ; 10(4):242-544. Neurol 2004; 3(1):54-62.
30. Lee NY, Song JH, Kim S, Peck KR, Ahn KM, 39. Gupta S, Tuladhar AB. Does early
Lee, et al. Carriage of antibiotic resistant administration of dexamethasone improve
pneumococci among Asian children A neurological outcome in children with
multinational surveillance by the Asian network meningococcal meningitis? Arch Dis Child
for surveillance of resistant pathogens 2004; 89(1):82-83.
(ANSORP). Clin Infect Dis 2001;32:1463- 40. Singhi SC, Khetarpal R, Baranwal AK, Singhi
1469. PD. Intensive care needs of children with acute
31. Cottagnoud PH, Tauber MG. New therapies for bacterial meningitis: a developing country
pneumococcal meningitis. Expert Opin Investig perspective. Ann Trop Paediatr. 2004
Drugs. 2004 ; 13(4):393-401. ;24(2):133-140.
32. Hasegawa K, Chiba N, Kobayashi R, et al. 41. Singhi SC, Singhi B, Srinivas B, Narakesri HP,
Rapidly increasing prevalence of beta- Ganguli NK, Sialy Rea. Fluid restriction does
lactamase-nonproducing, ampicillin-resistant not improve the outcome of acute meningitis.
Haemophilus influenzae type b in patients with Pediatr Infect Dis J 1995; 14:495-503.
meningitis. Antimicrob Agents Chemother 42. Miyasaka K, Shimizu N, Kojima J. Recent
2004; 48(5):1509-1514. trends in pediatric fluid therapy. Exp Clin
33. Sudo F, Nakamura A, Hoshino T, Ishiwada N, Pharmacol 2004; 26(4):287-294.
Kohno Y. [Successful treatment of beta- 43. Rabinstein AA, Wijdicks EF. Hyponatremia in
lactamase-negative ampicillin-resistant critically ill neurological patients. Neurologist.
Haemophilus influenzae type b meningitis with 2003; 9(6):290-300.
high-dose ceftriaxone administration]
Kansenshogaku Zasshi 2004;78(7):604-608. 44. Ranjini EK, Agarwal I, Kirubakaran C.
Pneumococcal subdural empyema in young
34. Pistella E, Campanile F, Bongiorno D, et al.
infants. Indian Pediatr. 2004; 41(5):505-508.
Successful treatment of disseminated cerebritis
complicating methicillin-resistant 45. Lin PC, Chiu NC, Li WC, et al. Characteristics
Staphylococcus aureus Endocarditis unres- of nosocomial bacterial meningitis in children.
ponsive to vancomycin therapy with linezolid. J Microbiol Immunol Infect. 2004; 37(1):35-
Scand J Infect Dis 2004;36(3):222-225. 38.
35. Krueger WA, Kottler B, Will BE, Heininger 46. Van Egeraat SC, Van Munster ET, Bodewes
A, Guggenberger H, Unertl KE. Treatment of HW, Van Der Hoeven JG. Spinal cord
79
Indian Journal of Practical Pediatrics 2005; 7(2) : 156
80
2005; 7(2) : 157
Fig. 5 MR cholangiography showing the The final confirmative and diagnostic test
normal GB, CBD and the right and left (L) is the operative cholangiogram. This test as its
hepatic ducts. name suggests is invasive. The gall bladder is
82
2005; 7(2) : 159
Those who are interested in joining the study group should contact Dr.BC Mehta at
(labmed@ghrc-bk.org). It is necessary that those who wish to join the group have easy access to internet.
All communications of the study group will be through e-mail and web. Members will have access to
the data/information on web.
83
Indian Journal of Practical Pediatrics 2005; 7(2) : 160
CASE STUDY
84
2005; 7(2) : 161
Discussion
Esophageal stenosis in children can be either
congenital (5%) or acquired (95%). Congenital
esophageal stenosis is of 3 types membranous
diaphragm, fibromuscular stenosis and stricture
due to ectopic tracheo-bronchial tissue containing
cartilage1. Frey and Duschel reported the latter
in 19362. CES commonly affects the middle and
distal third of esophagus. They are usually
asymptomatic in the neonatal period. Later the
children may present with vomiting of undigested
food, regurgitation, food impaction, dysphagia
and failure to thrive. CES involving the upper
Fig 1. Upper GI scopy shows a whole green
third of esophagus is very rare and presents with
grape in the mid esophagus
stridor and recurrent respiratory infections1. CES
may be associated with esophageal atresia,
tracheo-esophageal fistula or other cricothyroid junction and rarely at other sites. It
developmental anomalies of the gastrointestinal is a dictum that all FB in the esophagus should
tract1,3. be removed as an emergency. After its removal
unlike bronchial foreign body it is essential to
Barium swallow and upper GI scopy
exclude underlying strictures. This report
confirms the diagnosis. The membranous type
highlights the importance of excluding
can be distinguished easily. The other two types
underlying anatomical abnormalities in children
appear similar but response to endoscopic
presenting with esophageal foreign body.
dilatation is excellent in the fibromuscular type
compared to the ectopic tracheobronchial type References
that is usually seen in the lower end of the
1. Congenital esophageal stenosis. Pediatric
oesophagus. The management of CES prior to surgery update Vol 17 (4); 2001. Available
the endoscopic era was surgical resection and from: URL: http://home.coqui.net/titolugo/
anastomosis, the advantage of this procedure PSU17.htm#1741 Accessed on July 5,2004.
being the possibility of good histopathological
2. Shorter NA, Mooney DP, Vaccaro TJ, Sargent
examination. Nowadays endoscopic dilatation
SK. balloon dilation of congenital esophageal
over the guide wire using tapered polyvinyl stenoses associated with esophageal atresia. J
bougies or balloons is an accepted method of Pediatr Surg 2000; 35(12):1742-1745.
management1,2,4. If the CES is due to ectopic
3. Ibrahim NB, Sandry RJ. oesophageal stenosis
tissue with cartilage as a component, the
caused by tracheobronchial structures in the
therapeutic response is not satisfactory and
oesophageal wall. Thorax 1981; 36(6): 465-
surgery is advocated. Since these two children 468.
responded to endoscopic dilatation fibromuscular
type is a possibility. 4. Ramesh JC, Ramanujam TM, Jayaram G.
Congenital esophageal stenosis: report of three
Foreign body in the aero digestive tract is a cases, literature review, and a proposed
common problem in children. In the normal classification. Pediatr Surg Int 2001;
oesophagus the common site of impaction is the 17(2):188-192.
85
Indian Journal of Practical Pediatrics 2005; 7(2) : 162
CASE STUDY
86
2005; 7(2) : 163
thumbs. Awareness of the association clinches encouraging results7. Etidronate has inhibitory
the diagnosis. The most common sites of effect on bone mineralization and has a potential
heterotopic calcification are the neck, spine and to impair rapid ossification. Isotretinion also
shoulder girdle. The pattern of progress is from inhibits differentiation of mesenchymal tissue
axial to appendicular, cranial to caudal and into cartilage and bone. Despite therapy all the
proximal to distal5. Lesions follow different patients develop new ossifications.
stages on its progress; they are, stage of
References
inflammation (pain, erythema, swelling, warmth
and tenderness), intermediate lesion and a late 1. Lutwak L. Myositis ossificans progressiva
irreversible ossified lesion6. Radiography shows mineral, metabolic and radioactive calcium
studies of the effect of hormones. Am J Med
ectopic calcifications. Trauma to deep muscles
1964; 37:269-293.
is a stimulus for ossification (e.g.immunization).
Lesions must not be biopsied as it aggravates the 2. Smith DM, Russel RGG, Woods CG. Myositis
ossificans progressiva clinical features of eight
process of calcification and the child must be
patients and their response to treatment. J Bone
protected from even most trivial trauma. Surg 1976; 58:48-57.
Debilitating joint immobility due to ossification
3. Mahoboubi S, Glauser DL, Shore EM, Kaplan
of almost all joints is the ultimate outcome on FS. Fibrodysplasia ossificans progressiva.
account of the progressive nature. Most of the Pediatr Radiol 2001; 31:307-314.
patients are confined to wheel chair by third
4. Gannon FH, Kaplan FS, Olmsted E. Bone
decade of life and often succumb to pulmonary morphogenetic protein 2/4 in early fibromatous
complications in the fifth or sixth decade of life3. lesions of fibrodysplasia ossificans progressiva.
Extraocular, diaphragm, cardiac and smooth Hum Pathol 1997; 28:339.
muscles are characteristically spared. Premature 5. Herring JA. Orthopedic related syndromes. In:
death can occur from respiratory failure due to Ed Herring JA. Tachdjians Pediatric
thoracic cage involvement5. Till date there is no Orthopedics, .3rd ed, Ed Herrang JA,
definite therapy to impede the progression of Philadelphia, WB Saunders company, 2002;
disease. Oral steroids and etidronate have some pp.1632-1639.
87
Indian Journal of Practical Pediatrics 2005; 7(2) : 164
6. Kaplan FS, Tabas JA, Gannon FH. The 7. Bridges AJ, Hsu KC, Singh A: Fibrodysplasia
histotopathology of fibrodysplasia ossificans (myositis) ossificans progressiva. Semin
progressiva: an endochondral process. J Bone Arthritis Rheum 1994; 24: 155.
Joint Surg 1993; 75-A: 220.
OBITUARY
Dr. Ramesh K. Puri hailed from Hoshiarpur in Punjab. He was a graduate of the Patiala Medical College
and a postgraduate in Pediatrics from JIPMER, Pondicherry. Prof. Puri began his teaching carrier as a faculty
in the Department of Pediatrics at JIPMER, Pondicherry and later rose to the post of Professor and Head in the
same institution. He joined the Department of Pediatrics at Maulana Azad Medical College (MAMC), New
Delhi as its Head in February 1989 and retired from there as the Director Professor and Head in January 1995.
The Department of Pediatrics at MAMC was modernized during his tenure. Prof. Puri also efficiently discharged
additional important institutional responsibilities.
During an illustrious career that spanned four decades, Prof. Puri held many responsible positions and
was respected as an academician and an astute clinician. He was the Editor-in-Chief of Indian Pediatrics from
1990-1994. During his tenure the publication scaled new heights and was adjudged as the best medical journal
from India. He was the Organizing Secretary of the VIII Asian Congress of Pediatrics (ACP) held at New
Delhi in February 1994. Under his dynamic stewardship the VIII ACP established a global precedent by not
accepting any financial support from the Infant Milk Substitute industry, which received international acclaim.
The conference was not only an academic success but also a financial accomplishment, with huge savings for
the Indian Academy of Pediatrics. During his tenure at MAMC, he was the principal investigator of large
community projects funded by the World Health Organization and the World Bank. He had several indexed
research publications to his credit and also edited popular books. Dr. Puri was an eminent teacher who was
dearly loved by his students. Other noteworthy virtues were his compassionate attitude, easy accessibility to
all, and the ability to encourage junior colleagues to perform better. He could easily lower the anxiety level by
taking of problems others on his shoulders and stating do not worry, I am there! (main hun na!).
Consequent to his retirement from MAMC, he joined the Apollo Hospitals at Delhi as a Senior Consultant.
At the time of his untimely death on January 21, 2005, at the age of 68 years, he was also the Academic
Advisor to the Apollo Centre for Advanced Pediatrics and Editor-in-Chief of Apollos Medical Journal. He is
survived by his wife and son. His death has left a void in the pediatric fraternity that would be hard to fill.
88
2005; 7(2) : 165
BOOK REVIEW
Name Immunization in Clinical Practice
Editors Naveen Thacker, Nitin K Shah
Review: Immunization is one of the important child health survival strategies. The pediatrician who was
administering 3 or 4 vaccines and following a fairly straightforward immunization schedule two de
cades ago, is currently confronted with a multitude of vaccines and the problem of devising an appro
priate immunization schedule for the children under his care. He has to know the epidemiology of
vaccine preventable diseases where he practices, the efficacy of the vaccines and the affordability of
parents before he decides on a set of vaccines for the individual child in consultation with parents.
Immunization along with growth monitoring and counseling forms a major part of pediatric practice
especially in urban and semi urban areas. It is said, A future physician is a vaccinator. Hence a
pediatrician has to be well informed about the indications and limitations of all the conventional and
newer vaccines and should be prepared to respond to the queries of well-informed parents. This
book on immunization titled Immunization in clinical practice is an authentic source of such infor-
mation.
The book has been divided into four parts: basics, widely used vaccines, immunization in special
circumstances and future vaccinology. Various authors from India and abroad have comprehensively
and extensively discussed the topics. The extent of the disease burden in our country based on
available information is provided in each chapter. Some historical background on each vaccine
makes it interesting to read. The common as well as unusual side effects of various vaccines and
their management are discussed well. The schedule adopted by Government of India and Indian
Academy of Pediatrics (IAP) and the rationale behind the differences if any are described. For the
newer vaccines, guidelines based on IAP recommendations are given to the practitioners so that they
may make a rational choice. Almost all the chapters are provided with excellent references to stimulate
the readers to learn more about immunization. The note worthy features in the book are chapters on
safe injection practices, immunization guidelines for all diseases prevalent in our community including
rabies and Japanese encephalitis, adolescent and adult immunization and new technologies and future
vaccines. The chapter on combination vaccines backed up by good evidence will help the pediatrician
in decision-making. Literature on immunization available in internet is a good valuable addition.
The book is written in simple English and the print and lettering are reader friendly.
A few points need clarification. It has been mentioned under Immunization against Diphtheria,
Tetanus and Pertussis (Chapter 8) that these vaccines may be kept in cool and dark place in case of
electrical failure. It should be remembered that cold chain should be maintained between +20C to
+80C under all circumstances by appropriate method (vaccine carrier, back- up generator etc). Some
simple errors like DTP at birth in IAP schedule (Chapter 3) and the ambiguity about one syringe and
two needles for each vaccination (Chapter 5 and 6) and passive immunity for pertusis from mother to
infant (partial - chapter 3; absent chapter 8) could have been avoided. Clearcut guidelines could
have been provided for BCG vaccination in preterm / low birth weight infants on similar lines as
given for hepatitis B vaccine and the need / otherwise for repeat BCG vaccination when there is no
scar following immunization. Under the chapter Immunization against poliomyelitis a brief note
on acute flaccid paralysis (AFP) surveillance would have been useful.
As the editors have pointed it out in the preface, the topic of immunization evokes tremendous
interest and many queries in the minds of pediatricians. The book through, insipite of its few
ambiguities is a comprehensive evidence based review on immunization, which will be of great use
to pediatricians, postgraduates and general practitioners and is worth possessing for ready reference
for immunization practice.
Publishers M/s. Jaypee Brothers Medical Publishers (P) Ltd.,EMCA House, 23/23 B Ansari Road, Daryaganj,
New Delhi 110 002. India.
Price Rs.250/-
89
Indian Journal of Practical Pediatrics 2005; 7(2) : 166
The Dakshin
SOUTH PEDICON 2005
19th South Zone Confernce &
34th Annual Conference of IAP Keral State Branch
on 30th September, 1st & wnd OCtober, 2005 at Thiruvananthapuram, Kerala
Theme : Healthy Child; A National treasure Venue : Co-Bank Towers & Mascot Hotel
Pre-conference CME : 30th September, Conference : 1st & 2nd October.
Till Till Till After 15th Spe. 2005
15.05.2005 1.07.2005 15.09.2005 & spot
IAP Member 1200 1500 2000 2500
Non IAP Member 1500 1750 2250 3000
PG Students 750 1000 1250 1500
Paytments by DD in favour of South Pedicon 2005 payable at Thiruvananthapuram. Outstation cheques to
add Rs.50/-
M.K.C. Nair, Princial Advisor Lalitha Kailas, Org. Chairperson
Correspondence to : M.Zulfikar Ahmed, Organizing Secretary South Pedicon 2005 Dept. of Pediatrics,
SAT Hospital Medical College, P.O. Thiruvananthapuram - 695 011, Phone : 0471-2528437
2005; 7(2) : 167
Name ..................................................................................................................................
Address ................................................................................................................................
...............................................................................................................................................
Signature
Subscription rate
Individual Annual Rs.300/- Send your subscription, only by crossed demand draft,
Ten Years Rs.3000/- drawn in favour of INDIAN JOURNAL OF PRACTICAL
PEDIATRICS, payable at Chennai and mail to
Institution Annual Rs.400/-
Dr.A.BALACHANDRAN, Editor-in-Chief, F Block,
Ten Years Rs.4000/-
No.177, Plot No.235, 4th Street, Anna Nagar East, Chennai
Foreign Annual US $ 50/- - 600 102, Tamilnadu, India.
90
Indian Journal of Practical Pediatrics 2005; 7(2) : 168
Signature
Kinldy send your payment by crossed demand draft only drawn in favour of
Indian Journal of Practical Pediatrics and art work / matter to
MANAGING EDITOR
Indian Journal of Practical Pediatrics
IAP-TNSC Flat, Ground Floor,
F Block, Halls Towers,
56 (Old No.33), Halls Road,
Egmore, Chennai - 600 008. India
Phone : 2819 0032
Email : ijpp_iap@rediffmail.com
91
2005; 7(2) : 169
Indian Journal of
Practical Pediatrics IJPP
Subscription Journal of the
Indian Academy of Pediatrics
Indian Academy
of Pediatrics
IAP Team - 2005 Kailash Darshan,
Kennedy Bridge,
Mumbai - 400 007.
President Karnataka
Dr.Raju C Shah Dr.M.Govindaraj
President-2006 Dr.Santosh T Soans
Dr.Nitin K Shah Kerala
President-2004 Dr.T.M.Ananda Kesavan
Dr..M.K.C.Nair Dr.M.A.Mathew
Dr.T.U.Sukumaran
Vice President
Madhya Pradesh
Dr.Anoop Kumar Verma
Dr.M.L.Agnihotri
Secretary General Dr.Chandra Has Sharma
Dr.Bharat R. Agarwal Maharashtra
Treasurer Dr.Pramod Jog
Dr.Deepak Ugra Dr.Rajendra V Kulkarni
Editor-in-Chief, IP Dr.Sandeep Bapu Kadam
Dr.Panna Choudhury Dr.Yashwant Patil
Manipur
Editor-in-Chief, IJPP Dr.K.S.H.Chourjit Singh
Dr.A.Balachandran Orissa
Joint Secretary Dr.Gadadhar Sarangi
Dr.A.K.Dutta Punjab
Dr.Harmesh Singh
Members of the Executive Board
Rajasthan
Andhra Pradesh Dr.B.D.Gupta
Dr.V.Ram Narsimha Reddy Tamilnadu
Dr.P.Venkateshwara Rao Dr.D.Gunasingh
Assam Dr.K.Meer Mustafa Hussain
Dr.Garima Saikia Dr.P.Velusamy
Bihar
Uttar Pradesh
Dr.Radha Krishna Sinha
Dr.Ashok Kumar Rai
Chandigarh
Dr.V.N.Tripathi
Dr.R.K.Marwaha
Dr.Vineet K Saxena
Delhi
West Bengal
Dr.Ajay Gambhir
Dr.Debasis Biswas
Dr.Anupam Sachdeva
Dr.Sukanta Chatterjee
Gujarat
Dr.Baldev S Prajapati Services
Dr.Satish V Pandya Col.M.K.Behera
Haryana Presidents Spl. Representative
Dr.Dinesh Khosla Dr.Rajesh Mehta
Jharkhand A.A.A.
Dr.Brij Bhushan Sahni Dr.Tanmay Amladi