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St. John’s Medical College
BECAUSE OF ME
Journal of Medicine
August 2004
Editorial
Erectile Dysfunction (ED): Treatment options
A. Mohan
1
Surgery in HIV positive patients - An appraisal
Angamuthu Natarajan
7
The newer antidepressants
Iby Neerakal
13
The elderly India - A health challenge
Arvind Kasthuri
19
Laser therapy
Sujatha Raj Harshad
22
Management of epilepsy
Sarma G.R.K.
25
The IMCI - An important initiative for the sick child
Reynold G. Washington
35
Neonatal Resuscitation
Fulton D’Souza
42
INFORMATION FOR CONTRIBUTORS
SUBMITTING THE MANUSCRIPTS
The St. John’s Medical College Journal of Medicine accepts scientific contributions from all fields of
medicine from all institutions and health care professionals. The journal will be published twice a year.
Articles and editorial communications should be addressed to the Editor, Alumni Office, St. John’s
Medical College, Bangalore 560 034.
PREPARING THE MANUSCRIPTS
All manuscripts should be submitted in 2 copies (including the glossy prints). They should be neatly
typewritten on bond paper, one side of the paper only, with double spacing and margins of at least
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ILLUSTRATIONS AND TABLES
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REFERENCES
Reference should be compiled at the end of the articles. They should be typewritten and double
spaced under the heading REFERENCES. Abbreviations for titles of medical periodicals should
conform to those used in the latest edition of Index Medicus. Give inclusive page numbers.
EXAMPLES OF REFERENCES
Journal articles upto six authors, list all names:
Kurpad AV, Shetty PS. Dietary fibre and the colon, St. John’s J Med. 1988; 1:5-12.
Journal articles more than six authors, list three authors followed by et al.
Complete Book
Gallagher JR. Medical Care of the Adolescent (ed 2). New York, Appleton, 1966:pp 208-215.
EDITOR
DR, SUNITA SIMON KURPAD
EDITORIAL COMMITTEE
DR. JENNIFER GEORGE
DR. ARVIND KASTHURI
DR. KANISHKA DAS
The St. Johns Medical College Journal of Medicine is a publication of the Alumni Association of St.
John’s.
For private circulation- bhly. Not for sale.
EDITORIAL
Well, this is the final curtain for me and hopefully not for the St John’s Journal. After six years, the
Editorship now passes on to the able hands of Dr. Kanishka Das. When I look back on to what we
have achieved, I am happy that we have been able to bring out all the issues, even though this one
has been delayed.
Getting good quality articles has always been a challenge. Our Editorial policy has been very clear
that the Journal publishes good quality peer reviewed articles or none at all. We have therefore had to
reject some articles based on the comments of our reviewers. In the interest of fairness to the
authors, I have sometimes had to tell authors of original research that it might be better to try and get
their articles published in an indexed Journal before trying our Journal. Another strategy we used to
get quality articles was to directly approach some authors to write on issues which we thought would
be of benefit not just to our alumni in rural areas but to our other readers as well. Funds were also a
problem, but luckily the Alumni Association has been very supportive about the money needed to
finance the issues. Our future strategy to get the Journal out on the internet would probably save us
some money. And I hope that it will be pursued enthusiastically.
Another future strategy is to continue to get our articles peer reviewed and get the Journal out
regularly so that we could aim to get our Journal into Index Medicus. That should not be an
impossible goal for us at St. John's.
All the best Kanishka! I must also take this opportunity to thank Dr. Jennifer and Dr. Arvind for their
support and enthusiasm over the years.
Dr. Sunita Simon Kurpad
St. John's Medical College Journal of Medicine
ERECTILE DYSFUNCTION (ED): Treatment Options
A. MOHAN
Introduction
One of the commonest problems faced by
married couples is the inability to initiate, or
continue, marital relations due to the inability of
the male partner to complete the act of
intercourse to satisfaction. While this complaint
is not forthcoming in the usual doctor-patient
encounter, it constitutes a major obstacle to a
satisfactory family life. In India, this 'diffidence
*
is
perpetuated by prevalent cultural practices,
increasing
urbanization
and
access
to
information through mass media has brought
this problem out into the open and more and
more couples are seeking medical help for this.
Erectile dysfunction (ED) is defined as "the
inability to have or sustain an erection adequate
for satisfactory sexual activity".1 According to
recent estimates, as many as 30 million men in
the United States may experience some form or
degree of ED.2 Generally believed by many to
be an inevitable consequence of ageing, it is not
necessarily confined to the ageing population. It
does however correlate with advancing age. In
the United States, The Massachusetts Male
Ageing Study3 found some evidence of ED in
39% of men between the ages of 40 and 50
years, in 46% of men between the ages of 50
and 60 and in almost 70% of men over the age
of 70. Severity of ED is also correlated with age,
moderate-to-severe ED becomes more common
as men get older. As age advances, conditions
like vascular diseases, degenerative neurologic
disorders and hormonal changes, affect the
physiology of erections, leading to ED. The
prevalence in different countries differ as erectile
dysfunction is linked to cultural and sexual
practices — in some societies it is accepted as
an inevitable occurrence with advancing age
and no medical help is sought.
A. MOHAN M.S. M.Ch.
Professor & Head
Department of Urology
St. John’s Medical College Hospital
Bangalore
Far from being an “inevitable consequence of
age", we are dealing with a large number of
patients with ED today. Changing social mores
and the plethora of information available on this
subject seem to have both contributed to the
increasing number of men seeking medical
assistance for ED in India, too. There are also
many younger persons coming with ED today in these the aetiology is somewhat different
Stress plays a very important role. While this
form
of
ED
used
to
be
considered
“psychogenic”, it is obvious that the problem is
mediated through the same neuro-vascular
pathways as in the ageing. This has a direct
bearing on the treatment strategy for younger
patients too.
ED: The medical history
A detailed medical and sexual history is the first
step in assessing a patient with ED, particularly
in the middle-aged or elderly individual. ED may
be the heralding sign of a serious underlying
disorder, for example, cardiovascular disease.2
Other potential risk factors for ED include
diabetes, hypertension, peripheral vascular
disease, prostate disease, hormonal and
metabolic disorders (primary or secondary
hypogonadism, hypothyroidism), chronic renal
failure, hepatic failure, psychiatric disorders
(mood and anxiety disorders), neurologic
disorders (multiple sclerosis, nerve-disrupting
pelvic injury) and inadequate lipid control. It is
necessary to carefully elicit history and findings
that point to one of the above before rushing to
prescribe treatment. Doing so might not drily
lead to treatment failure but also mean that
potentially life-threatening, underlying disease.
An adequate history for a patient with ED should
include
•
•
•
Onset, duration and frequency of ED
Whether obtaining an erection is difficult, or
maintaining an erection once sustained is
the problem.
Whether this inability prevents penetration
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St. John's Medical College Journal of Medicine
•
•
•
•
•
•
Whether it is situational (partner-specific or
present only under specific circumstances)
Occurrence and quality of spontaneous
morning,
nocturnal
or
self-stimulated
erections
History of perineal or back injury, or
operations on the prostate, urethra or
bladder neck
Presence of adequate desire/libido (absence
could indicate endocrine or psychiatric
disorders)
Use of prescription, non-prescription or
recreational drugs
Psychiatric symptoms or disorders
Physical examination should include
•
•
•
•
•
•
Measurement of blood pressure
Assessment of virilisation and male
secondary sex characteristics
Checking pulsations in the femoral,
popliteal, dorsalis paedis and posterior tibial
arteries
Focused neurological examination, including
evaluation of penile and perineal sensation
and anal sphincter tone
Digital rectal examination of the prostate for
texture, symmetry and tenderness
Physical examination of the penis to detect
any structural abnormalities - a plaque
indicating Peyronie’s disease, any scars,
deformities and penile sensation.
Laboratory investigations, which point to serious
underlying diseases, are recommended.5 These
include urinalysis, measurement of morning total
testosterone level and a test for prostate-specific
antigen (PSA), especially in men older than 50
years of age, lipid profile, complete blood cell
count and blood sugar assessment are
advisable if one or more years have elapsed
since previous testing. Points elicited in history
and physical examination findings will determine
what other investigations are necessary.
Specific investigations
With the evolution of a goal directed approach,
extensive investigations are not often necessary.
This is particularly so with the availability of oral
agents, such evaluation is now resorted to only if
the oral agent does not yield the desired results.
Dynamic duplex doppler,6 nocturnal penile
tumescence
(NPT)7
monitoring
and
cavernosography may reveal specific vascular
abnormalities or indicate
causes.
pure psychogenic
Pharmacologic penile duplex ultrasonography
can provide a dynamic vascular assessment.6 A
penile injection of alprostadil or papaverine to
produce smooth muscle relaxation allows for
evaluation of arterial and venous blood flow
patterns and can aid in the diagnosis of vascular
dysfunction.
If vascular insufficiency
is
diagnosed and the patient does not respond to
an adequate trial of sildenafil therapy,
intracavernosal injectable agents might be
considered. If however, ultrasonography reveals
normal vascular integrity, the next step might be
to perform a nocturnal penile tumescence and
rigidity test to assess nocturnal erectile activity.7
This test is perhaps the best way to discriminate
between organic and psychogenic ED and this
may aid in referral to a sex therapist, psychiatrist
or psychologist.
The Treatment Options
Once underlying conditions have been looked
for and treated or ruled out, the focus obviously
sifts to the treatment options available. ED can
often be associated with modifiable risk factors
such as smoking, overindulgence in alcohol,
obesity or stress. ED provides a good motivation
for change and a patient with ED should be
encouraged to make necessary changes in
lifestyle - the reward for doing so being normal
erectile function. In some cases, stopping
smoking,8 moderation of alcohol intake and
other lifestyle interventions may themselves lead
to considerable symptomatic improvement.
Reduction in stress through meditation or similar
“stress buster” techniques is of immense benefit
in appropriate cases. By inducing a feeling of
well being, these alterations will facilitate any
other intervention that may be necessary.
The options available for treating ED today are
many. These include
•
•
•
•
•
•
•
Hormone therapy
Oral pharmacotherapy
Vacuum constriction devices (VCDs)9
Intra-cavernosal pharmacotherapy
Intra-urethral pharmacotherapy
Oral vasoactive agents
Implantable penile prostheses
2
________________________________ - St. John's Medical College Journal of Medicine
With the advent of these multiple options, the
chances of success have grown accordingly in
recent years. Nearly all patients can be helped,
irrespective of the underlying aetiology.
Hormones
While the testosterone level declines with age, it
does not decline to a level that can cause ED by
itself. Therefore, testosterone administration has
no ’universal’ role in treatment. In the few men
who are found to have hypogonadism on
investigation and resultant low hormone levels,
testosterone therapy has a role. Such patients
are very few in number. Therefore, testosterone
replacement10 is an effective treatment only in a
small proportion of patients11 (about 1% to 5%).
Testosterone therapy may have serious side
effects (worsening symptoms of BPH, the risk of
activating occult prostate cancer and hepatic
dysfunction). Due to these potential risks and
low response rates, testosterone replacement is
best reserved for men whose baseline
testosterone levels are subnormal. Patients
receiving testosterone therapy must be
monitored with PSA tests and digital rectal
examinations every 6 months for the first 1 to 2
years, then annually thereafter. There is no
scientific basis for the empirical use of
testosterone in all cases of ED.
Oral non-hormonal agents
All kinds of oral agents used to be prescribed for
ED more in haste than in conviction. Yohimbine,
trazodone and L-arginine were the more
commonly prescribed drugs. Inspite of the
widespread use of these agents, there is no
scientific evidence about the efficacy of these
agents in the treatment of ED.12-14
Vacuum constriction devices
These devices draw blood into the cavernosal
spaces by creating a suction effect around the
penile shaft. The corpora cavernosa then
engorge with blood. This blood is trapped in the
cavernosal spaces by the application of a
constricting ring at the base of the penis,
resulting in an erect penis. Intromission and
intercourse is then possible as the required
rigidity is maintained as long as the constriction
ring is in place. Vacuum pumps9 and constriction
devices are inexpensive and may be effective
for men who prefer a non-pharmacologic, nonsurgical approach and have a comfortable, well-
established sexual relationship. Considerable
manual dexterity is necessary and there should
be no underlying impairment of penile
sensations (e.g., sensory neuropathy). Side
effects reported by some patients (or their
partners) include pain, blocked ejaculation and
penile "coldness and numbness". These devices
also have the advantage of being reusable.
These devices are definitely contraindicated
if the subject cannot be trusted to take all
due precautions - particularly with the
constricting ring, which should not be left in
place for longer than 30 minutes.
Intra-corporeal vasoactive agents
These agents are self-injected into the corpus
cavernosum. They produce relaxation of the
vascular smooth muscle and the smooth muscle
of the corpora. The blood flow into the corpora is
enhanced and the penis becomes turgid and
erect as it would in the normal course.
Intracavernosal injection of vasoactive agents is
highly effective with efficacy rates of 75% to
80%.15 The most commonly used agents are
alprostadil® (prostaglandin E0, papaverine
(alone and in combination with alprostadil), and
phentolamine (used in combination with the
other agents). Of these, only papaverine is freely
available in India. It is used in a dose of 15-90
mg, with the lowest effective dose being used.
The patient is taught the self-injection technique
under supervision. Once the technique is
mastered, the injections can be taken at home. It
is recommended that not more than one
injection per day is taken and not more than ten
injections per month.
The invasive nature of this treatment is a
disadvantage. Side effects.are pain following the
injection, fibrosis of the cavernosal tissue after
repeated injections and priapism. Priapism could
be the result of high dosage or independent of
the dosage. Counseling the patient about proper
administration is essential. The patient should
also be instructed that he should seek
immediate medical attention if the erection does
not subside within 45 minutes of intercourse.
Priapism is a medical emergency and will
require intervention for reversal. Prolonged
priapism can lead to gangrene of the penis. This
form of therapy therefore should not be chosen
for patients who cannot access specialist
medical services immediately, or those that
cannot be trusted to!
3
St. John’s Medical College Journal of Medicine
Another treatment option is the alprostadil
urethral suppository.16 It is a solid pellet about
the size of a grain of rice that is inserted with a
plunger-like device into the urethra. When the
pellet dissolves, the active agent is absorbed
and subsequent events are similar to that seen
with vasoactive injections. Side effects include
penile pain and “burning" rare cases of mild
bleeding from the urethra, hypotension and
syncope have also been reported. Called
MUSE®, this is not available in India. It is
obviously more acceptable than injections and
causes less direct damage to the cavernosal
smooth muscle. The danger of priapism is
present with this form of treatment too.
Penile Prostheses
Penile prostheses are modified cylinders of
synthetic bio-compatible material that are
surgically implanted into the cavernosal tunics in
order to provide the rigidity required for
intromission. These prostheses are available
now in the semi-rigid and inflatable forms. They
come in different sizes suitable for different
physical characteristics. The components and
actual design vary depending on manufacturer
and model, but the basic design and function is
the same. The devices are designed to improve
penile rigidity and not to affect urination,
ejaculation, or orgasm. Patient and partner
satisfaction rates are apparently high17, 18
reportedly ranging up to 98%.
Complications include a constant "erect" state
with the semi-rigid prostheses, prosthesis
extrusion, mechanical failure and infection. The
surgery is irreversible and that it tends to
diminish the normal functioning of the corpus
cavernosum. If the device is removed,
spontaneous and drug-induced erections should
not be expected to resume. It is therefore
reserved as the last option in the treatment of
ED. Prostheses is available in India and many
centres including ours are conversant with the
surgical procedure.
Psychotherapy
Referral to a psychiatrist, psychologist or sex
therapist might be considered for selected cases
in which the sexual dysfunction is suspected to
have a primary psychogenic cause.19 Most
cases of ED (upto 80%) are estimated to have
an organic pause. It is not unusual to have
persons with purely psychogenic ED in our
country. These may be brought on by
"performance anxiety”, venerophobia as a
reaction to a noxious experience, depression or
grief. Counseling and specifically directed
therapy in the case of psychiatric disorders is
necessary in these cases.
However, because of the emotional issues
involved in ED, secondary psychogenic
components are common. Often expectations
are unrealistic and the patient feels that he has
ED inspite of a normal sexual profile and
performance. Marital incompatibility sometimes
manifests with accusations of ED and is a
particularly important ground for seeking
dissolution of marriage. These are situations that
call for a meticulous evaluation of the cause and
a co-ordinated approach involving physician,
psychiatrist and psychologist will yield the
desired results.
Oral Agents
Sildenafil
Oral agents for the treatment of ED were
prescribed empirically until the advent of
sildenafil citrate, an original research molecule
of Pfizer. The pharmacological action of this
agent is interesting.
Sexual stimulation leads to the release of nitrous
oxide in the corpus cavernosum of the penis.
Nitrous oxide thus released causes an increase
in the cyclic GMP level in the cavernosum.
Cyclic GMP (cGMP) causes the cavernosal
smooth muscle to relax, facilitating the entry of
blood into the cavernosal spaces where it is
trapped, producing erection. Phosphodiestrase
type 5 (PDE 5), present in the smooth muscle,
breaks down cGMP at the termination of
erection, or on cessation of the stimulation and
the smooth muscle relaxation ceases, pushing
blood out and heralding the end of the erection.
Sildenafil inhibits PDE 5, thereby slowing the
breakdown of cGMP. By thus enhancing the
levels of cGMP, sildenafil sustains erections and
enhances them by promoting further smooth
muscle relaxation. In conjunction with sexual
stimulation, therefore, sildenafil improves and
prolongs erections.
Sildenafil is available in India as 25mg, 50mg
and 100mg tablets. It is recommended that the
dosing schedule begin with the lowest dose. It is
recommended that a single tablet is taken
4
St John's Medical College Journal of Medicine
approximately 1 hour before initiating sexual
activity. However, the drug can be taken up to 4
hours before sexual activity and may be
effective in as little as 30 minutes if taken on an
empty stomach. It is important to inform the
patient that sexual stimulation is necessary to
initiate the action of the drug and that it will not
produce erections in the absence of sexual
stimulation. The exact dose required will vary
and it may take a few days for the dose titration.
However not more than one tablet in a 24hour period is recommended.
Extensive safety data is available on sildenafil
and it is generally safe except for certain
documented side effects. It is reported by some
to produce a feeling of light-headedness.
Diarrhoea was another common side effect
reported. These were not serious and no
therapy was required. However, blurring of
vision and transient visual changes have been
reported. This is believed to be due to the
inhibition
of
another
phosphodiestrase
isoenzyme, PDE 6, that is present in the retina.
For this reason, the drug is contraindicated in
patients retinitis pigmentosa, a disorder where
PDE 6 is involved. Myalgia can also be a
distressing accompaniment of Sildenafil therapy.
It decreases over a period of time and needs no
specific treatment.
All side effects are higher at higher doses and a
dose higher than 100mg js not recommended.
The only absolute contraindication to the use of
sildenafil is concomitant use of an organic nitrate
such as nitro-glycerine, isosorbide nitrate or
dinitrate, pentaerythritol tetranitrate and erythrityl
tetranitrate.20
Sildenafil
potentiates
the
hypotensive effect of nitrates - its propensity to
produce smooth muscle relaxation can lead to
major haemodynamic compromise, which could
be refractory to treatment with vasopressors. Its
use in the elderly, hypertensive patients on
multiple drugs and those taking medications
interfering with the cytochrome pathways like
erythromycin
and
ketoconazole
is
contraindicated.20
Tadalafil (Eli Lily) and Vardenafil (Bayer) are two
new drugs in this category. They have a quicker
onset of action but act by the same mechanism.
The effects last longer.
Apomorphine
A new drug, apomorphine hydrochloride21 has
received a recommendation in the U.S.F.D.A. for
use in the treatment of ED. It is reported to act
more quickly than sildenafil, within 16-19
minutes. It is a centrally acting drug, acting on
the dopamine receptors in the brain. It is
believed that this drug can also enhance the
psychological factors necessary for initiating the
erectile response - something that sildenafil
cannot do. It is administered as a sub-lingual
tablet and nausea has been the commonest side
effect. Syncopal episodes have been reported
with the drug.
Conclusion
With particular reference to India, erectile
dysfunction is emerging as a major concern. The
unique cultural mores that are prevalent here,
keep patients away from doctors and rational
treatment. On the other hand, there are a
number of indigenous solutions that patients
resort to before seeking medical help.
There is an assortment of treatment modalities
now available - the particular choice in a given
case depends on the patient’s circumstances.
The advent of oral agents has simplified the
management of ED and the other modalities are
available
when
the
oral
agents
are
unsatisfactory.
References:
1.
NIH Consensus Conference. Impotence.
NIH Consensus Development Panel on
Impotence. JAMA 1993;270:83-90.
2.
Melman A, Gingel! JC. The epidemiology
and pathophysiology of erectile dysfunction.
J Urol. 1999, 161:5-11.
3.
Feldman HA, Goldstein I, Hatzichristou DG,
et al. Impotence and its medical and
psychosocial correlates: results of the
Massachusetts Male Ageing Study. J Urol.
1994;151:54-104.
4.
Miller TA. Diagnostic evaluation of erectile
dysfunction.
Am
Fam
Physician
2000;1;61:95-104.
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St. John's Medical College Journal of Medicine
5.
The process of care model for evaluation
and treatment of erectile dysfunction. The
Process of Care Consensus Panel. Int J
Impot Res. 1999;11:59-70; discussion 70-4.
6.
Wahl SI. Rubin MB. Bakal CW. Radiologic
evaluation of penile arterial anatomy in
arterogenic impotence. Int J Impot Res.
1997;9:93-97.
7.
Levine LA. Lenting EL. Use of nocturnal
penile tumescence and rigidity in the
evaluation of male erectile dysfunction. Urol
Clin North Am. 1995;22:775-788.
8
Jeremy JY. Mikhaildis DP. Cigarette
smoking and erectile dysfunction. J R Soc
Health. 1998;118:151-155.
9.
Derouet H, Caspari D, Rohde V, et al.
Treatment of erectile dysfunction with
external vacuum devices. Andrologic.
1999;31 (Suppl 1):89-94
10.
Winters SJ. Current status of testosterone
replacement therapy in men. Arch Fam Med
1999;8:257-263.
11.
Fahmy AK, Mitra S, Blacklock AR, Desai
KM. Is the measurement of serum
testosterone routinely indicated in men with
erectile dysfunction? BJU Int. 1999;84:482484.
12.
13.
Kunelius P. Hakkinen J, Lukkarinen O. Is
high-dose yohimbine hydrochloride effective
in the treatment of mixed-type impotence? A
prospective, randomized, controlled double
blind
crossover
study.
Urology.
1997;49:441-444.
14.
Klotz T, Mathers MJ, Braun M et al.
Effectiveness of oral L-arginine in first-line
treatment of erectile dysfunction in a
controlled crossover study. Urol Int.
1999;63:220-223.
15.
Linet Ol, Ogrinc FG. Efficacy and safety of
intracavernosal alprostadil in men with
erectile dysfunction. The Alprostadil Study
Group. N Engl J Med. 1996;334:873-877.
16.
Padma-Nathan H, Hellstrom WJ, Kaiser FE
et al. Treatment of men with erectile
dysfunction with transurethral alprostadil.
Medicated Urethral System for Erection
(MUSE) Study Group. N Engl J Med
1997;2;336:1-7.
17.
Porena M, Mearini L, Mearini E et al. Penile
prosthesis
implantation
and
couple’s
satisfaction. Urol Int. 2000,63:185-187.
18.
Sexton WJ, Benedict JF, Jarow JP.
Comparison of long-term outcomes of penile
prostheses and intracavernosal injection
therapy. J Urol. 1998;158:811-815.
19.
Beutel M. Psychosomatic aspects in the
diagnosis
and treatment of erectile
dysfunction
Andrologia.
1999;31 (Suppl
1):37-44.
20.
Langtry HD, Markham A. Sildenafil: A review
of its use in erectile dysfunction. Drugs.
1999;57:967-989.
21.
Heaton JP, Morales A, Adams MA, et al.
Recovery of erectile function by the oral
administration of apomorphine. Urology
1995;45:200-206.
Costabile RA, Spevak M. Oral tradozodone
is not effective therapy for erectile
dysfunction: a double blind, placebocontrolled trial. J. Urol. 1999;161:1819-1822.
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St. John's Medical College Journal of Medicine
SURGERY IN HIV POSITIVE PATIENTS
AN APPRAISAL
ANGAMUTHU NATARAJAN
Introduction
AIDS (Acquired Immuno Deficiency Syndrome),
first reported in 1981, has grown at an
alarmingly rapid rate to become one of the most
challenging major public health issues in both
developed and developing countries.1,2 It is a
modern day pandemic, which has spread across
190 countries in the world.3 The surgeon, though
not the primary care physician, plays an
important role in the surgical management of the
AIDS patient. Surgical management often
exposes the surgical team to body fluids and to
the potential risk of Human Immuno deficiency
virus (HIV) transmission. This risk is the basis
for major controversial issues like routine
preoperative serological testing, refusal to
administer surgical therapy, pursuing non
operative therapeutic modalities and the need
for and economics of universal precautions and
post-exposure chemoprophylaxis and treatment.
Definitions
HIV positive individual:
An individual who has tested seropositive for
HIV. The individual may or may not be
symptomatic.
The majority of HIV positive
individuals develop AIDS within 7- 9 years.4
AIDS: The occurrence of a complication of
immunosuppression including indicator diseases
like opportunistic infections with low virulence
pathogens or neoplasms (B-cell lymphomas,
Kaposi's sarcoma - KS) in a HIV positive
individual is defined as AIDS.4,5
ANGAMUTHU NATARAJAN
DNB, MNAMS, FRCS
Assistant Professor
Department of Surgery
St. John's Medical College Hospital
Bangalore-560034
The other current definition of AIDS is a HIV
positive individual with a CD4+ (helper T cell)
count of less than 200 cells per mm.3
ARC- AIDS Related Complex
A HIV positive individual with persistent
generalised
lymphadenopathy
(PGL),
unexplained continuous fever, significant weight
loss or oral candidiasis.
These definitions are periodically reviewed by
the CDC (Center for Disease Control) and are
used widely by health care professionals.
AIDS: The Global and Indian scenario
The estimated number of HIV cases globally
was 100,000 in 1980, nearly 20 million by 1993
and the projected number for the year 2000 was
40 million cases!2,3 An estimated 16,000 new
infections occur worldwide everyday with 90% of
them being reported from developing countries.6
The CDC estimates that for every patient with
AIDS there are 8 HIV positive individuals who
have not yet developed clinical AIDS.4
In Asia, the estimated number of HIV/AIDS
cases is 6 million of whom 90% are from India,
Thailand and Myanmar.3 In adults from South
and Southeast Asia, a prevalence of 0.6% has
been reported.6 An estimated 3-5 million adults
in India are infected with the Human
Immunodeficiency Virus.3 911 new cases were
reported in India (676 males, 235 females)
between January and April 2001 increasing the
number of cumulative AIDS cases in India to
21,215 (16,204 males, 5011 females).7 NACO
(National AIDS Control Organization, India) has
published data on HIV estimates in India based
on HIV sentinel surveillance. Their figures are
3.31- 3.97 million HIV infections in the year 2001
and 3.82-4.58 in 2002.8
Surgery in HIV Positive Patients
With the ever-increasing occurrence of HIV
infection and of awareness regarding its
7
St. John’s Medical College Journal of Medicine
consequences, the surgeon is frequently called
for a consultation or to perform a surgical
procedure.
The risk of transmission and subsequent
seroconversion is a crucial factor in the surgical
management of a HIV positive patient. It has a
profound impact on the personal, professional,
psychological and social aspects of the
surgeon's life, which are delicate issues, and the
subject of intense debate.
Indications 4,6,9
The indications for surgery in HIV patients can
be broadly grouped as follows:
1. Management of a surgical disease not
related to AIDS: These are the group of
diseases occurring both in HIV infected patients
and in the general population (e.g. - herniae,
common benign soft tissue tumours and trauma
management).
2. Management of a surgical disease related to
AIDS: These are the group of diseases
occurring more frequently in HIV patients as a
result of immunosuppression (e.g. - anorectal
diseases, KS).
3. Diagnosis of an AIDS associated infection or
neoplasm: This includes surgical procedures in
the diagnosis of a disorder (eg - excision biopsy
of a lymph node or soft tissue in the diagnosis of
tuberculosis, lymphoma or sarcoma).
4. Assist medical therapy of HIV associated
conditions: Minor surgical procedures to
facilitate therapy (e.g. - venous access line for
chemotherapy
of
Cytomegaloviral
(CMV)
retinitis, lymphoma).
5. Management of surgical complications of
AIDS and associated illnesses: This is often an
emergency surgical intervention for an acute
illness (e.g. - bowel obstruction or perforation
due to visceral lymphoma or KS).
High Risk Groups
It is important for the surgical team to be aware
of the high-risk groups who have a higher
seroprevalence rate than the general population
and hence a higher chance of transmission of
HIV to Health Care Workers (HCWs). The
important high risk population groups are. 4,10
•
•
Homosexual or bisexual individuals.
Patients with hemophilia or coagulation
disorders.
•
•
•
•
Intravenous drug abusers.
People residing in areas of high prevalence
(Central Africa).
Sexual partners of the above groups.
Children born to HIV positive mothers.
Spectrum of Surgical Diseases
Gastrointestinal Disease
Abdominal
pain
occurs with
increasing
frequency and the number of non-surgical
causes is also on the rise.5 Abdominal pain is
reported in about 10% of all AIDS patients and
only 5% of these cases need a surgical
intervention.9 Opportunistic infections of the
gastrointestinal tract are a common cause of
abdominal pain. This highlights the need for a
proper and systematic approach in a patient with
AIDS, presenting with abdominal pain.
Acute appendicitis is a common cause of acute
abdomen and right iliac fossa pain in surgical
practice. The total leucocyte count is normal in
the majority of patients with AIDS developing
acute appendicitis.5 Appendicitis in these
patients could be due to a visceral KS causing
obstructive appendicitis or due to an acute CMV
infection.5,6
Gastrointestinal obstruction or perforation could
be due to lymphoma or KS4. The terminal ileum
and colon is the commonest site of acute CMV
infection leading on to perforation, which
indicates advanced AIDS and an unfavourable
prognosis. AIDS enteropathy, an uncommon
entity resulting from primary infection of the gut
by HIV is diagnosed after excluding the other
common conditions.
Hepatobiliary Disease5,9
This system is commonly affected in AIDS
patients and persistent elevation of the liver
enzymes is a common occurrence. Acute
acalculus cholecystitis and AIDS cholangiopathy
are the important hepatobiliary disorders in
patients with HIV/AIDS. AIDS associated
cholangiopathy is a result of biliary infection with
CMV or cryptosporidium and can lead on to
cholecystitis or sclerosing cholangitis.
Ano-rectal disease1,9,10
Disorders of the anus and rectum are the
common indications for surgical intervention in
HIV positive patients.
8
St. John's Medical College Journal of Medicine
Anal warts are reported to be more aggressive,
dysplastic and difficult to treat. Excision by
electrocautery or laser is reported to be more
effective than podophyllin.
Ano-rectal suppuration and fistulae need
surgical intervention. Large perianal incisions
and division of internal sphincter in patients with
recurrent perianal sepsis and in homosexuals
could result in delayed healing, fistula formation
and incontinence. Setons are preferable in the
management of fistulae-in-ano.
Anal ulceration in HIV positive individuals could
be due to
herpes
simplex,
CMV or
cryptosporidium infections. Proper diagnosis and
adequate treatment of these infections followed
by surgical excision in patients with failed
medical therapy is reported to be beneficial.
Lymphoreticular disease1, 9
Splenomegaly is a common finding in AIDS but
the causes are multiple. Immunodeficiency
associated thrombocytopenic purpura has a
poor response to steroids and often necessitates
a splenectomy.
Lymphadenopathy is a common finding in
HIV/AIDS and the important causes are PGL,
tuberculosis, lymphoma or metastatic deposits
from a primary neoplasm or KS. Reactivation of
tuberculosis is more common than re-infection in
HIV infected patients and often tuberculosis
occurs early in HIV infection, even prior to the
diagnosis of AIDS.
Fine Needle Aspiration
Cytology (FNAC)
should
be the
initial
investigation prior to open biopsy in the
evaluation of lymphadenopathy. Increasing
awareness, familiarity and knowledge of AIDS
results in a decreased need for an open lymph
node biopsy. Lymph node biopsy is done either
to classify a lymphoma diagnosed by FNAC or in
patients with a negative FNAC of a clinically
suspicious node, which is persistent or
enlarging.
Vascular disease5
Infected pseudoaneurysms are common in HIV
individuals with intravenous drug abuse. An
interesting entity in AIDS is Salmonella arteritis
wherein salmonella has an increased affinity to
the atherosclerotic plaque. An invasive infection
could lead to pseudoaneurysm and potential
rupture.
Occupational risk of HIV transmission
The operating surgeon and the team should be
aware of the potential risk of HIV transmission
due to proven or unrecognized HIV infection in
their
patients.
Implementing
established
guidelines in these patients helps in avoiding or
minimizing the risk of transmission of HIV and
more importantly hepatitis B and C viruses. A
single ml of blood approximately contains 50
HIV particles in contrast to 109 hepatitis B
particles.10 Popejoy and Fry in their study of 684
operations reported that 28% of the operations
were associated with a blood contact and the
risk was higher in cardio-thoracic, trauma and
obstetric cesarean sections.11 Occupational risk .
of HIV transmission depends mainly on local
seroprevalence rates, route of exposure and
susceptibility of the HCW.12 Unrecognised HIV
infection is estimated to be 0.07% in low
prevalence areas and upto 10% in areas of high
prevalence.13 Based on current reports in
literature, the pooled net estimate of HIV
transmission following a percutaneous exposure
is 0.3% and following a mucus membrane
exposure is 0.09% - 0.11% 3'12,14. Needle stick
injury, a common event among HCWs, is
associated with a 0.2 to 0.3% risk of
seroconversion. •
Further ont the true
incidence of percutaneous exposure is underreported by 10-50 %.15 The .probability
(cumulative risk) of a surgeon being infected by
HIV during his surgical career (40 years) is
estimated at 1 % in low prevalence areas and
upto 10% in high prevalence areas.13. An
American or European surgeon in a high
prevalence area during his 30 year career has a
1 in 800 chance of acquiring HIV infection. In
contrast, in Africa, the risk is as high as 1 in 4.10
The important factors influencing the risk of
occupational HIV transmission are:3,14>15:
•
•
•
•
•
•
•
•
•
Patient HIV status and viral load.
Depth of injury
Visible blood on the injury device.
Vascular access related procedures.
Death of the source patient due to AIDS
within 2 months of the event.
Exposure to source material and its volume blood, body fluid or discharge.
Contact site - intact skin, breached skin or
mucus membrane.
Type and duration of surgery - cardiothoracic,
orthopaedic or general surgery.
Nature of surgery — emergency, elective or
9
St. John's Medical College Journal of Medicine
•
•
•
•
trauma surgery.
Infrastructure of the center.
Education and knowledge of HIV/AIDS
among the team.
Universal precautions - applicability and
compliance.
Exposure reporting and availability of
chemoprophylaxis.
Pre-operative HIV Testing
Routine pre-operative serological testing of all
patients is a controversial and hotly debated
issue and the CDC does not recommend it 4 6.
The CDC guidelines for serological testing are:
• Prior patient consent.
• Pre-test and Post- test counseling.
• Strict confidentiality.
• Ensure that care of a seropositive patient is
not compromised.
• Periodic evaluation of the efficacy of
Universal Precautions in the center.
Principles of Surgery in HIV/AIDS
A simple yet difficult to implement safety
measure- is to maintain an effective barrier
between the HCW (surgical team) and the
patient at all times. In 1987, the CDC laid down
Universal * Precautions, the basic guidelines
aimed
at
reducing
the
risk
of HIV
transmission.4,12 The basic tenet of “Universal
Precautions" is to assume that all patients
undergoing an invasive procedure are
potentially infectious and that applying
protective measures to all irrespective of
their
serological
status
avoids
HIV
transmission. This simple and attractive theory
in principle is difficult to practice with the
debatable issues being compliance, economic
and financial implications especially in low
seroprevalence areas.6 In 1994, the CDC issued
the modified infection control guidelines, which
incorporates the principles of Universal
Precautions and Body Substance Isolation
recommendations6,12,16. This is termed as
Standard Precautions, which are to be applied to
all patients receiving care in a hospital
regardless of their diagnosis or presumed
infection status. It applies to potential contact
with blood, all body fluids, secretions, excretions
etc. Some authors opine that applying and
maintaining universal precautions at a high level
is often not feasible at all times. HIV screening
increases the awareness of the surgical staff
and, for a seropositive patient, gives a better life
expectancy.
13
The Surgeon and HIV: Guidelines for Outpatient
Care and Surgical Wards1,4,6.
• Routine
use
of
appropriate
barrier
precautions to avoid skin or mucus
membrane exposure when contact with a
potential source is anticipated.
• Hands should be washed immediately and
thoroughly with soap and water after physical
examination and contact with a potential
source.
• Gloves should be used during contact with
open wounds and mask and eye protection
used during examination of a hollow viscus,
eg: proctoscopy, sigmoidoscopy, and during
vascular
puncture
for
diagnostic
or
therapeutic access.
• Proper disposal of sharps (eg: needles,
scalpel blades), infected dressings and body
fluids.
• Careful conduct of venepuncture, avoidance
of resheathing of needles.
• Samples and specimens collected for further
examination to be properly labeled as
infectious and adequately packed to prevent
spillage in the event of damage and to be
handled with care with use of gloves and
masks.
• HCWs with exduative lesions and weeping
dermatitis should refrain from all direct
contact with patients and instruments.
The Surgeon and HIV : Operating Room (OR)
guidelines in a HIV positive patient.1,6,10
• Surgeon
and
the
team
(assistants,
anesthetist, nurse and support theatre staff)
should have a basic knowledge of AIDS,
universal precautions, and potential risks of
HIV transmission and its implications.
• Surgery to be performed by a senior or fully
trained surgeon. Trainee surgeons are more
likely to have blood contact and injury.
• Pre-operative discussion of the steps of the
proposed surgery and anticipation of
bleeding.
• Proper scrubbing, use of impervious gowns,
caps, masks, goggles, shoes and covers.
• Double gloving and the use of colour
indicators to detect intra-operative glove
puncture.
• Use of appropriate eye protection to avoid
aerosol spray or high speed fragments (eg:
blood and bone during drilling or nailing in
orthopedic surgery).
10
St. John's Medical College Journal of Medicine
• No hand to hand passage of sharps.
• Avoid panic reaction and simultaneous use of
sharp instruments by surgeon and the
assistant.
• Orderly and systematic performance of the
surgical procedure.
• Avoid repetitive direct hand contact during
dissection, retraction and suturing.
• Avoid direct hand contact during removal of
shoe covers, gowns and masks.
• Proper disposal of blood, excised tissues, wet
mops, gauzes and drapes.
• Avoid patient transfer to the recovery room
and then to the ward. Allow patient to recover
on the table and then shift to the ward with
appropriate personnel for further post
operative care.
• Thorough hand wash and use of disinfectants
after performing the surgery.
The
Surgeon
Measures2,3,9,12,16
and
HIV:
Preventive
It is important to implement measures, which
limit occupational exposure and hence reduce
the risk of HIV transmission to the HCWs. It
includes minor modifications, innovative ideas,
techniques and technology that are classified as:
Engineering Controls.
• Magnetic trays for passage of sharps.
• Blunt tipped suture needles.
• Glove liners and cut-resistant gloves.
• Fingertip guards.
• Impervious gowns and drapes.
• The use of devices for intravenous access
which avoid venepuncture.
Work practice Controls.
• Step to step modification of the procedure to
reduce contact and use of sharps.
• Avoid use of hand to guide a needle, protect
a structure and pick up sharps.
• Hand ties only after removing the needle and
kept to a minimum.
• Use of instrument ties, stapling device for
anastomosis.
• Use of electrocautery or harmonic scalpel for
dissection.
• Use of staplers or tissue adhesive for skin
closure.
• Drains and open wounds to be minimized.
Administrative Controls.
• Formulation of an OR committee to enforce
and evaluate standard precautions.
•
Periodic rotation of HCWs to minimize the
risk to a particular HCW.
• Set up a programme for post-exposure
prophylaxis and follow-up.
• Ongoing education programmes for the
HCWs.
Exposure Event and the HCW4,8,10,14
An exposure to a potential infectious source is a
major issue of concern. The CDC issued
guidelines in 1998, which include:
• Event reporting and generation of a report.
• Management of the event.
- thorough wash with water and soap.
- irrigation with saline or a disinfectant.
• Contact patient — HIV testing with consent.
• The HCW - base line testing for HBV, HCV,
HIV.
• Counseling and risk assessment and post
exposure prophylaxis as indicated.
• Clinical and serological evaluation for HIV
infection.
• Repeat HIV testing at 6 weeks, 3 & 6 months.
• HCW to report any acute febrile illness within
12 weeks of exposure.
• HCW to have protected intercourse; refrain
from donation (organ, blood, semen).
• Health education.
Post exposure prophylaxis
Post exposure chemoprophylaxis is ideally
instituted 1-2 hours after the exposure event.
Following a percutaneous exposure, zidovudine
prophylaxis is reported to reduce the chances of
seroconversion by about 80%.2,15 Post exposure
prophylaxis depends on the exposure class and
contact patient. The drugs used are zidovudine,
lamivudine and or indinavir for a period of 4
weeks.
Surgery and its outcome
The morbidity and mortality’of surgery in AIDS is
influenced by a host of factors - degree of
immunosuppression, hypoalbuminaemia, pre
existing malnutrition and neoplastic process
(lymphoma, KS).1 Important factors considered
to determine survival are CD4+ counts, viral load
and the ability to receive antiretroviral therapy.10
However, there are reports that CD4+ counts
and HIV positive status as predictors of surgical
outcome are controversial but viral load assays
may be useful.8
11
St. John's Medical College Journal of Medicine
Conclusions
AIDS by itself is not a contraindication for
surgery. Surgical treatment should be offered to
a HIV positive patient when the intended
procedure is believed to have a positive impact
on the patient’s life. The surgeon’s role is not to
treat HIV/AIDS but to help in the diagnosis of
AIDS associated illnesses, recognize and
manage complications of AIDS and its
associated diseases. It is crucial for the surgeon
to understand AIDS; the routes of transmission,
the risk and implications of seroconversion and
finally to deliver surgical care in a safe and
acceptable
manner
based
on
existing
guidelines.
Acknowledgements
My sincere thanks to Dr Anthony Rozario, DNB,
FRCS
(Glasgow),
Associate
Professor,
Department of Surgery, for his guidance in the
preparation of this article.
References
1.
2.
3.
Miles AJG, Wastell C. AIDS and the General
Surgeon. In: Taylor I, Johnson CD (eds).
Recent Advances in Surgery - 14. Churchill
Livingstone. 1991: pp 85-98.
Al-Fallouji MAR. Postgraduate Surgery. The
Candidates’ Guide. Butterworth-Heinemann.
2nd edition. 1998.pp95-99.
Polsky BW, Clumeck N. HIV and AIDS. In:
Amstrong D, Cohen J (eds). Infectious
Diseases. Mosby-Harcourt Publishers Ltd.
1999: Sections: 1.1-28.6.
4.
Howard RJ. Surgical infections. In: Schwartz
SI (ed). Principles of Surgery. Me Graw Hill
Publications. 7th edition. 1999: pp138-142.
5.
Fry
DE.
Surgical
problems
in
the
immunosuppressed patient. In: Townsend
CM Jr (ed). Sabiston Textbook of Surgery.
Harcourt Asia Pte Ltd- W.B Saunders Co.
16th edition. 1999:pp190-192.
6.
Wastell C, Davis PA. The surgery associated
with HIV infection. In: Morris PJ, Wood WC
(eds). Oxford Textbook of Surgery. Oxford
University Press Ltd. 2nd edition. 2000: pp
99-108.
7.
AIDS update: 21. AIDS research and control
center (ARCON). Mumbai. vol:6, No:2. AprJun 2001.
8.
http:Zwww.naco.nic.in/indianscene/esthiv.him
(accessed April 2004)
9.
Schecter WP. Surgery in HIV infected
patients. In: Cohen PT, Sande MA,
Volberding PA. The AIDS Knowledge Base.
Lippincott Williams & Wilkins. Philiadelphia.
3rd edition. 1999: pp 363-368.
10.
Allen-Mersh TG. AIDS. In:. Russell RCG,
Williams NS, Bulstrode CJK (eds). Bailey &
Love’s Short Practice of Surgery. Arnold.
London. 23rd edition. 2000:pp 112-119.
11.
Popejoy SL, Fry DE. Blood contact and
exposure in the operating room. Surg
Gynaecol Obstet 1991;172:480-83.
12.
Rhodes RS, Bell DM. Prevention of
transmission of bloodborne pathogens. Surg
Clin North Am 1995;75:1047-1218.
13.
Evrard S, Meyer P, van Haaften K,
Christmann D, Marescaux J. Occupational
risk to Surgeons of Unrecognised HIV
infection in a low prevalence area. World J
Surg 1993; 17:232-36.
14.
Horowitz HW, Telzak EE, Sepkowitz KA,
Wormser GP. HIV infection. Part-ll. Dis Mon
1998;44:695-702.
15.
Cardo DM, Culver DH, Ciesielski CA,
Srivastava PU, Marcus R, Abiteboul D, et al.
A case control study of HIV seroconversion
in health care workers after percutaneous
exposure. N Eng J Med 1997;337:1485-90.
16.
De vita VT Jr, Hellman S, Rosenberg SA.
AIDS: Aetiology, diagnosis, treatment and
prevention. 4* ” edition. Lippincott-Raven.
Philadelphia. 1997: pp 645-718.
12
St. John's Medical College Journal of Medicine
THE NEWER ANTIDEPRESSANTS
IBY NEERAKAL
The last decade has seen a sea change in the
pharmacotherapy of depressive disorders with
the development of a wide array of newer
antidepressants. Till the late 1980’s tricyclic
antidepressants were the main stay of treatment
of depressive disorders. They were handicapped
by their troublesome anticholinergic side effects
like postural hypotension, constipation, blurring
of vision and dryness of mouth. The late 1980’s
saw the launch of a new group of
antidepressants called the”selective serotonin
reuptake inhibitors” (SSRIs). The first drug of
this group fluoxetine was launched in the United
States in 1987 and has been available in India
from the early 1990’s. The absence of
anticholinergic,
antihistaminergic,
anti-alpha
adrenergic, cardiotoxic effects, weight gain and
potential for lethality in overdose generated wide
patient and prescriber acceptance. The last few
years has seen the launch of several newer
antidepressants in India, which will be described
in some detail below.
Newer SSRIs
Sertraline
Sertraline was the second SSRI to be made
available in India. The antidepressant effect of
sertraline is believed to be due to sertotonin
reuptake inhibition at the presynaptic nerve
terminal. It is efficacious in a wide range of
psychiatric disorders like major depression,
panic disorder, OCD (obsessive compulsive
disorder), social phobia, dysthymia and atypical
depression. Sertraline is begun at 50 mg/day
with a target dosage of at least 100 mg/day in
healthy adults. The dosage range is 50 to 200
mg in single or divided doses. In patients with
hepatic impairment the mean half - life
of
IBY NEERAKAL M.D.
Assistant Professor
Department of Psychiatry
St. John’s Medical College Hospital
Bangalore
sertraline
increases
significantly.
This
necessitates dosage reduction in patients with
hepatic disease. The effect of renal impairment
on sertraline metabolism is not clear. Elderly
patients have a decreased clearance of
sertraline compared to younger patients. The
commonly reported side effects are nausea,
diarrhea, agitation and sexual dysfunction
(delayed ejaculation in males and anorgasmia in
males and females). Compared to fluoxetine,
certraline may have more gastrointestinal side
effects and less activating effects.1 Sertraline
being highly protein bound has the possibility of
interaction with other tightly protein bound drugs
like warfarin and digitoxin. But significant drug
interactions are much less compared to
fluoxetine. Because of its intermediate half-life
and favourable drug interaction profile it is a
preferred drug by many prescribers.
Fluvoxamine
Fluvoxamine maleate is a selective serotonin
reuptake inhibitor belonging to a new chemical
series, the 2-aminoethyl oxime ethers of
aralkylketones . Fluvoxamine has been mainly
used in OCD but can also be used in depressive
disorders. The recommended starting dose for a
fluvoxamine tablets in adult patients is 50 mg,
administered as a single dose at bedtime. The
dose should be increased in 50 mg increments
every 4 to 7 days, as tolerated until maximum
therapeutic benefit is achieved, not to exceed
300 mg per day. For pediatric population (age 817 years) the recommended starting dose is 25
mg with 25 mg increments every 4-7 days, not to
exceed 200 mg per day. In elderly patients and
those with hepatic impairment, the clearance of
fluvoxamine is decreased and hence will require
lower initiation and increment doses.
The most common side effects are nausea,
vomiting, headache and insomnia or sedation.
Fluvoxamine should not be used with
monoamine oxidase inhibitors (MAOI) or within
14 days of discontinuing treatment with a MAOI.
Fluvoxamine increases the level of drugs like
alprazolam,
terfenadine,
astemizole,
St. John's Medical College Journal of Medicine
theophylline, warfarin, carbamazepine, beta
blockers,
diltiazem,
sumatriptan,
tricyclic
antidepressants,
lithium,
clozapine
and
halperidol when used along with it. Fluvoxamine
should be used with caution in patients with
history of mania or seizures. Its safety in
pregnancy and nursing mothers is not
established.
Fluvoxamine is relatively safe in overdose. The
commonly observed adverse events associated
with fluvoxamine overdose included drowsiness,
vomiting, diarrhea and dizziness. Other notable
signs and symptoms seen with fluvoxamine
overdose
included
coma,
tachycardia,
bradycardia, hypotension, ECG abnormalities,
liver function abnormalities and convulsions. The
management of fluvoxamine overdose is mainly
supportive with gastric lavage and activated
charcoal. There are no specific antidotes. In
managing overdosage, consider the possibility
of multiple drug involvement.
Paroxetine
Paroxetine is the latest SSRI to be launched in
India. Paroxetine is indicated for the treatment of
depression, OCD and panic disorders. It is
contraindicated in patients taking MAOIs.
Paroxetine has to be used with caution in
patients with a history of mania and seizures.
There have been several reports of abnormal
bleeding (mostly ecchymosis and purpura)
associated with paroxetine treatment, including
a report of impaired platelet aggregation. There
is a risk of increased bleeding diathesis in the
face of an unaltered prothrombin time when
paroxetine is used along with warfarin. While
cytochrome P450 inhibitors like cimetidine
increase paroxetine concentration by about
50%;
hepatic
enzyme
inducers
like
phenobarbital and phenytoin, reduce paroxetine
levels by about 50%. Paroxetine inhibit TCA
metabolism leading to higher plasma TCA
concentrations. The dose of TCA may need to
be
reduced
when
co-administered with
paroxetine. There are no adequate and wellcontrolled studies establishing its safety in
pregnant and lactating women.
The commonly observed adverse events with
the use of paroxetine are asthenia, sweating,
nausea, decreased appetite, somnolence,
dizziness, insomnia, tremor, nervousness,
constipation, ejaculatory disturbance and other
male
genital
disorders
and
impotence.
Compared to other SSRIs, paroxetine is
reported to be more sedating and cause more
constipation,
weight
gain
and
sexual
dysfunction. In the treatment of depression, the
usual starting dose of paroxetine is 20 mg daily,
increased gradually, if necessary, by increments
of 10 mg to a maximum of 40 mg daily. The
recommended initial dose is 10 mg/day for
elderly patients, debilitated patients and patients
with severe renal or hepatic impairment.
Dosages may be increased if indicated but
should not exceed 40 mg.
Signs and symptoms of overdose with
paroxetine include nausea, vomiting, sedation,
dizziness, sweating and facial flushing. There
are no reports of coma and convulsions with
paroxetine overdose. Treatment of over dose is
mainly supportive. There are no specific
antidotes for paroxetine overdose. Gastric
lavage and activated charcoal are useful. In
case of ECG abnormality cardiac function may
have to be monitored. Due to large volume of
distribution of paroxetine, forced diuresis,
dialysis,
hemoperfusion
and
exchange
transfusion are unlikely to be of benefit.
SEROTONIN NOREPINEPHRINE REUPTAKE
INHIBITORS (SNRI)
Venlafaxine
Venlafaxine belongs to a new group of
antidepressants called serotonin norepinephrine
reuptake inhibitors. Venlafaxine is a potent
inhibitor of norepinephrine and serotonin
reuptake and a moderate inhibitor of dopamine
reuptake. At lower doses (<150 mg) the drug
acts essentially like an SSRI with a short half
life. At higher doses, venlafaxine appears to
recruit its noradrenergic mechanism. In this
sense it is like using an SSRI with a built in
combination treatment option accessed by
increasing the dose if the first trial is ineffective.
Venlafaxine has been indicated for the treatment
of depression, generalized anxiety disorder and
mixed anxiety and depression. There have been
reports of venlafaxine being efficacious against
resistant depression. Concomitant use of
venlafaxine in patients taking monoamine
oxidase inhibitors is contraindicated. The usual
dosage range is 75 to 225 mg given in divided
doses in a twice-daily schedule. Dosages as
high as 450 mg/day have been used in seriously
ill depressed inpatients. The extended release
form of venlafaxine gives the convenience of
14
St. John's Medical College Journal of Medicine
once a day dosing. Venlafaxine therapy is
associated with sustained increases in blood
pressure. At the higher doses, 5% to 7% of
patients may develop a modest but persisting
increase in blood pressure. It is recommended
that patients taking venlafaxine have regular
monitoring of their blood pressure. In patients
who have experienced a sustained increase in
blood pressure, the dose may be reduced or the
drug be discontinued.
The safety and side effect profile of venlafaxine
is generally similar to that of the SSRIs. Anxiety
or nervousness may emerge or worsen on
initiation of treatment. Other side effects include
nausea, insomnia, sedation, dizziness, sweating
and constipation. In patients with moderate
hepatic impairment it is advisable to reduce the
total daily dose by 50%. It is recommended that
the total daily dose be reduced by 25% in
patients with mild to moderate renal impairment
and the total daily dose be reduced by 50% and
the dose be withheld until the dialysis treatment
is completed (4 hours) in patients undergoing
hemodialysis. The safety of venlafaxine in
pregnant and nursing women has not been
established. During premarketing experience,
seizures occurred among 0.26% of venlafaxine
treated patients and mania or hypomania
occurred in 0.5% of venlafaxine treated
patients. Venlafaxine should be used with
caution in patients with a history of mania. At its
usual therapeutic dose venlafaxine has no
significant
pharmacokinetic
or
pharmaco
dynamic interactions with other drugs. This is a
significant advantage for venflaxine over other
antidepressant drugs.
Like other newer agents venlafaxine is safer in
overdose that older agents. It has a wide
therapeutic index and no mortality has been
reported in patients who have consumed many
times the therapeutic doses. Overdosages
should be managed with general supportive
measures. Use of activated charcoal or gastric
lavage should be considered.
Mirtazapine
Mirtazapine belongs to a new group of
antridepressants called the noradrenergic and
specific serotonergic antidepressants (NaSSA).
Mirtazapine has a unique dual model of action. It
antagonizes the presynaptic alpha-2-receptors
on the adrenergic and serotonergic neurons
thereby enhancing norepinephrine (NE) and 5
hydroxytryptamine (5-HT) neurotransmission.
Moreover mirtazapine also blocks 5-HT2 and 5HT3 receptors preventing many of the
undesirable side effects-seen with SSRIs and
SNRI like insomnia, nausea and sexual
dysfunction. Mirtazapine has been indicated for
use in patients with major depression, painc
disorder, generalized anxiety disorder and
chronic
post
traumatic
stress
disorder.
Mirtazapine has a faster onset of action than the
SSRIs. Mirtazapine has exhibited a lower risk of
hypomanic or manic switch from depression as
compared to TCAs or SSRIs. Studies have
found mitrazapine to be better tolerated than
TCAs, SSRIs or SNRIs. Mirtazapine has some
special
indications
like
as
an
add-on
antidepressant for patients with refractory
depression. It is also useful in patients who
cannot tolerate SSRIs because of sexual
dysfuction. The effective dose range of
mirtazapine in adults is 15-45 mg/day
administered in a single dose preferably at
bedtime. Dosage adjustment should not be
made more often than every 1-2 weeks due to
the very long half-life of mirtazapine. In elderly
patients and patients with hepatic and renal
impairment, lower initial dose and slower dose
titration is required.
The most common side effects of mirtazapine
are dose dependent drowsiness, dry mouth,
increased appetite, weight gain and dizziness.
These side effects tend to improve with time. In
premarketing clinical trials 3 out of 2,796
patients treated with mirtazapine developed
agranulocytosis. All three patients recovered
completely after mirtazapine was stopped. No
cases of agranulocytosis were reported during
the post marketing surveillance of 9000
mirtazapine treated patients in Netherlands.3 In
controlled
studies
nonfasting
cholesterol
increases to more than 20% above the upper
limit of normal were observed in 15% of patients
treated with mirtazapine compared 7% for
placebo and 8% for amitriptyline.3 Mirtazapine
should be used with caution in pregnant women
and nursing mothers. In premarketing clinical
trials with mitrazapine was assosciated with a
low incidence of seizures (1 out of 2,796
mirtazapine patients).4
However, in the absence of controlled studies in
patients with a history of seizures, it should be
used with caution. In view of its sedating
property, patients on mitrazapine should be
cautioned about engagement in' activities
15
St. John's Medical College Journal of Medicine
requiring alertness until they have been able to
assess the drug’s effect on their own
psychomotor performance. Since mirtazapine is
a weak inhibitor of hepatic enzymes it has no
clinically significant pharmacokinetic interactions
with
other
drugs.
Coadministration
of
mirtazapine with alcohol or diazepam results in
impaired cognitive and motor performances.
Mitrazapine is considered to be relatively safe in
overdose. Mortality has been reported only
when taken with other drugs. Signs and
symptoms reported with overdose included
disorientation, drowsiness, impaired memory
and tachycardia. There were no reports of ECG
abnormalities, coma or convulsions following
overdose with mirtazapine. There are no specific
antidotes for mirtazapine. The treatment
consists of general supportive and symptomatic
measures with monitoring of cardiac and vital
parameters. Gastric lavage, activated charcoal
and maintenance of airway with adequate
oxygenation may be of benefit.
Moclobemide
Monoamine oxidase inhibitors (MAOI) were
introduced in 1950s, a little earlier than the
tricyclic
antidepressants.
MAOIs
were
introduced as a treatment of depression in 1957.
The initial MAOIs like iproniazid, phenelzine.
isocaarboxazid and tranylcypromine were all
irreversible and nonselective inhibitors of
monoamine oxidase. The use of these drugs
came down due to the report of life threatening
hypertensive crisis in patients on these drugs.
By 1965 the mechanism of tyramine induced
hypertension was elucidated, thereafter this
hypertensive crisis could be avoided by the use
of dietary restrictions. They were also
handicapped in view of life threatening
interactions with other drugs.
Due to these complexities the use of MAOIs
were significantly reduced in many parts of the
world. More recently a new group of drugs RIMA
- reversible inhibitors of monoamine oxidase A
have been introduced.
Moclobemide. a
prototype of this class selectively and reversibly
inhibits MAO-A and hence has a much improved
tolerability profile. It eliminates the risk of
hypertension occurring as a result of interaction
with tyramine rich diet, hence special dietary
restrictions are not required to be followed.
Moclobemide is one of the first MAOIs to be
introduced in India. Moclobemide has similar
efficacy in both endogenous and atypical
depressions. Moclobemide appears to be as
effective as other antidepressants in the elderly
with better tolerability and safety profile.
Moclobemide is also effective in social phobia.
panic disorder and post-traumatic stress
disorder. The recommended initial dose of
moclobemide is 300 mg daily, usually
administered as two divided doses, after meals.
The dosage can be increased to a maximum of
600 mg per day depending on the severity of
symptoms.
In patients with severe hepatic dysfunction, the
daily dose of moclobemide should be
substantially reduced to one third or one half of
standard dose. In patients with moderate to
severe renal dysfunction no significant
adjustment in dosage of moclobemide is
required. Elderly patients do not require any
dosage adjustments. Strict dietary adjustment
are unnecessary but large amounts of tyraminerich food such as mature cheese, yeast extracts
and fermented soya bean products should be
avoided.
The commonly observed adverse reactions with
moclobemide were insomnia, tremors, agitation,
restlessness,
nausea
and
hypotension.
Moclobemide is better tolerated than the TCAs
and SSRIs. The safety of moclobemide in
pregnancy and lactation is not established.
Moclobemide should be used with caution in
psychotic conditions. Manic episodes can be
provoked by moclobemide in patients with
bipolar disorders. Great caution should be
exercised when moclobemide is co-administered
with TCA’s and SSRIs in view of risk of
serotonin syndrome. Pethidine can also cause
serotonin syndrome if it is administered in
patients on moclobemide. Concomitant use of
moclobemide and MAO-B inhibitors like
selegiline should be avoided or patients
receiving this combination should adhere to
strict dietary tyramine restrictions.
Moclobemide is relatively safe in overdose.
Mortality has been reported in mainly mixed
drug overdoses. Signs and symptoms of
overdosage with moclobemide include nausea.
drowsiness, mild disorientation, slurred speech,
amnesia and reduped reflexes. Treatment
consists of general supportive measures.
Gastric lavage or induction of emesis, activated
charcoal and fluid control maybe of benefit.
16
St. John's Medical College Journal of Medicine
Bupropion
Bupropion is a unicyclic antidepressant of the
aminoketone class. The primary indication of
bupropion is for the treatment of major
depression. It is comparable in efficacy to TCAs,
SSRIs and MAOIs. This drug is also beneficial in
treating patients suffering from depression
associated with psychomotor retardation, as it
has a mild stimulant rather than sedative
property. It has also been extensively used to
treat bipolar depression in view of its decreased
propensity to cause a manic or hypomanic
switch. Bupropion is also a popular combination
agent with other antidepressants like SSRIs and
venlafaxine. Other indications for bupropion are
attention deficit hyperactivity disorder in children
and adults and smoking cessation. Patients are
generally started on 100 mg twice daily with an
increase to 100 mg three times daily as
tolerated. An initial antidepressant effect
decomes apparent within 2 to 4 weeks. It has a
more favourable side effect profile than TCAs. It
is not sedating, does not produce significant
orthostatic hypotension or cardiac abnormalities
even in patients with cardiac disease. Compared
with SSRIs, bupropion has the advantage of not
being associated with sexual dysfunction.
The adverse effects observed with bupropion
are agitation, restlessness, insomnia, anxiety
and gastrointestinal disturbances. Some patients
may develop psychotic symptoms due to which
it has to be used with caution in psychotic
disorders. The primary side effect attributed to
bupropion is the increased incidence of
generalized seizures in 4/1000 patients taking a
prescribed dose up to 450 mg daily.5 There is a
tenfold increase of seizures in higher doses
between 450
and 600 mg.
Therefore a
maximum
dose of 450
mg
daily is
recommended. Bupropion is relatively safer in
overdose than TCAs. No major cardiovascular
toxicity was seen in patients with bupropion
overdose. Neurological toxicity included tremors,
lethargy and seizures. Combined use of
bupropion with MAOIs should be avoided
because of the risk of hypertensive reaction.
When used in combination, carbamazepine
decreases bupropion blood concentration and
bupropion increases valproate concentration.5
Addition of bupropion to antiparkinsonism
medication can bring down the dosage
requirement of antiparkinsonism medication. But
caution is required in this combination in view of
reports of hallucinations, confusion and
dyskinesias when bupropion was added to
previous therapeutic dosages of levodopa.5
Conclusion
The availability of the many new antidepressants
have improved the treatment options in
depressed patients. Since most of them have
comparable efficacy, the choice of medication
will be dependent on side effect profile and
prescriber’s comfort level with the medication.
Note
Since the original submission of this article, two
other selective serotonin reuptake inhibitors are
now available in the Indian market.
Citalopram: a bicyclic pthalane derivative is
usually used in the dose range of 20-40 mg per
day. The side effects reported are nausea, dry
mouth, drowsiness, insomnia, tremor, increased
sweating, diarhoea and sexual dysfunction
(ejaculatory difficulties). Caution is advised if co
administered with TCAs. It has been used in
depression, OCD, binge eating disorder and
panic disorder.6 Inspite of its low toxicity profile,
arrythmias and seizures have been reported in
overdose.7
Escitalopram : is the pharmacologically active
S enantiomer of citalopram. It is effective in the
treatment of major depression in the dose of
10-20 mg per day. It has also been used in
treatment of panic disorder. Side effects
reported with it are nausea, fatigue, insomnia,
drowsiness,
ejaculatory
dysfunction
and
increased sweating. It is contraindicated in
patients who are also taking MAOIs or with
hypersensitivity to escitalopram or citalopram.8,9
References
1.
Arana
GW
&
Rosenbaum
JF.
“Antidepressant
drugs”,
Chapter
3;
Handbook of psychiatric drug therapy.
Philadelphia; Lippincot Williams & Wilkins.,
2000. 53-113.
2.
Dollery. Therapeutic drugs, 1999 editiion.
Venlafaxine, V16-V20.
3.
Montgomery SA. Safety of mirtazapine : A
review. Int Clin Psychopharmacology 1995,
10 suppl. 4,37-45.
St. John's Medical College Journal of Medicine
4.
Stimmel GL. Mirtazapine; An antidepressant
with noradrenergic and specific serotonergic
effects. Pharmacotherapy 1997, 17(1), IQ21.
5.
Golden RN & Nathan LM. "Bupropin",
Cchapter in Comprehensive textbook of
psychiatry. Kaplan & Sadock, New York,
2000, 234-2328.
6.
Tan JY, Levin GM. 1999m Citalopram in the
treatment of depression and other potential
uses in psychiatry.
Pharmacotherapy.
Jun;19(6):675-89.
7.
Cuenca PJ, Holt KR, Hoefle JD. 2004.
Seizure secondary to citalopram overdose.
J Emerg Med.26(2): 177-81.
8.
Hirschfeld RM, Vornik LA (2004). Newer
antidepressants: review of efficacy and
safety of escitalopram and duloxetine. J Clin
Psychiatry. 65 Suppl 4:46-52.
9.
Stahl SM, Gergel I, Li D. (2003).
Escitalopram in the treatment of panic
disorder:
a randomized, double-blind,
placebo-controlled trial. J Clin Psychiatry.
64(11): 1322-7.
18
St. John’s Medical College Journal of Medicine
THE ELDERLY INDIA - a health challenge
ARVIND KASTHUR1
The term "elderly” has been defined in many
dimensions. Biologically the process if ageing
begins at least as early as puberty and is a
continuous process through adult life. Socially
the characteristics of members of society
perceived as being old vary with the cultural
setting and from generation to generation.
Economically, especially in rural areas, the
elderly are simply seen as being those who are
too old to work and earn. Chronologically
numeric age has been traditionally used in
defining the term “elderly". Even though a single
“cut off' age which would define the elderly
would vary between country and region
considering the biologic, sociologic and
economic and differences in their populations,
the United Nations in 1980 defined 60 years as
the age of transition of people to the elderly
segment of the population.1 Some authors
classify the elderly as the young old (60-70 yrs),
the old old (70-80 yrs) and the oldest old (80+
yrs).2
The global population of persons aged 60 yrs
and above is estimated at 600 million in the year
2000. Two of every three of these persons are
living in the developing world. The global
population of elderly person is expected to reach
1.4 billion in 2030. Of this rise, more than half
will be in Asia. (World Bank 1994).3
In India, the number of persons 60 years and
over was 12 million at the turn of the century.4
This has increased 6 fold to about 71 million
(expected) in 2001.
The proportion of population aged 60 years and
above is also rising. It was 5.63% in 1961, and is
expected to 7.1% in 2001 and 9.87% in 2021.
ARVIND KASTHURI M.D., D.N.B.
Associate Professor
Department of Community Health
St. John’s Medical College
Bangalore.
This makes India a “greying" nation, with the
growth rate of the elderly segment being greater
than the growth rate of the population as a
whole. It is expected that by 2021 the growth
rate of the elderly will be 1.5 times higher than
the growth rate of the general population.
The determinants of this rise in proportion of
elderly include fertility and mortality, as
measured by the Total Fertility Rate (a measure
of the number of children a woman will bear
during her lifetime), the Crude Death Rate and
the expectation of life at birth.
The Total Fertility Rate for India as a whole was
around 6 in 1971, has since reduced to 4.8 in
1981 and is projected to reach 2.6 by 2021. This
implies that the proportion of young persons will
reduce in the years to come, as the “bulge" in
the age-sex pyramid moves upward from the
base, leading to a higher proportion of people in
the older age groups. The median age, which is
defined as the age that divides the population
into two equal halves, was 20 years in 1961, and
is expected to reach 28 years in 2021.
The Crude
Death
Rate
has dropped
phenomenally from 28.5 per 1000 persons in
1951-61 to 8.7 per 1000 persons in 2001.
(Sample Registration Scheme 2001).
The expectation of life at birth was 49.3 years in
1971 and has risen to 62.2 years in 1996 and is
expected to reach 70.2 years by 2021.5 The
expectation of life at 60 years in 1970-75 was
13.8 years. This has risen to over 16 years now.
At 70 years of age, a person was expected to
live for an additional 8.9 years in 1970-1975.
This has also risen to 10.2 years currently.
The high and growing number of persons above
the age of 60 (70 million is more than 4 times
the size of the entire Australian population)
poses challenges to Indian society. The
problems faced by the elderly include social
problems, stemming from the lack of an
organized social security system as exists in
many western societies. Added to this is the
19
St. John's Medical College Journal of Medicine
changing social fabric especially in urban India,
where migration and change in value systems
leads to isolation and loneliness in old age.
Economic insecurity can lead to a renewed
poverty at the time it hurts most - old age.
Groups have been identified within the elderly
segment as those likely to face particular risk
with respect to their health or socio economic
status. Such “high risk" elderly include6
The oldest old, more than 80 years old
Elderly living alone and couples living by
themselves
3. Elderly women, especially single and
widowed
4. An elderly couple where one member is ill
5. Elderly living in institutions as opposed to
those living in families.
1.
2.
The health problems of the elderly are an
important cause of concern in this segment of
the population. It is estimated that 45% of the
elderly have chronic diseases and disabilities.
The 10 most common diseases in this segment
of population are hypertenison, cataract,
osteoarthritis, chronic obstructive pulmonary
disease, coronary heart disease, diabetes
mellitus,
benign
prostatic
hypertrophy,
dyspepsia, constipation and depression. The
five most frequent causes of death include
bronchitis and pneumonia, coronary heart
disease, cerebrovascular accidents, cancer and
tuberculosis.
2.
Specialised Geriatric Care, which
should ideally be a referral service based at an
institution which offers multidisciplinary services.
The specialized geriatric unit situated at a
hospital will serve the function of a referral
centre for a primary care unit and will look after
those elderly who are acutely or critically ill. The
specialized unit will ideally work along with the
other disciplines in a referral hospital. Other
functions which the specialized care unit could
serve include training of the primary care team
and rehabilitation and long term care, if the
infrastructure and resources permit.
India is an example of a developing country
which lacks organized services for the elderly in
the health, social or economic sectors. The
health services available for the elderly in India
are generally contained within the health
services for the general population, without any
special or specific initiatives for this group.
Such services include
1.
Services provided to persons retired from
the Government or from employment in the
organized sector - the Central Government
Health Service (CGHS) and the Employees'
State Insurance (ESI) would be examples.
2.
Services provided to patients attending
specialized Geriatric clinics / units I
departments in hospitals - this exists in a
miniscule proportion of existing medical
colleges / teaching hospitals.
3.
Services provided by private commercial
organizations to the elderly at their homes /
providing ambulances / other forms of
commercial medical service.
4.
Services
provided
by
voluntary
organisatiions, mostly on an ad hoc basis.
The health care of elderly people is envisaged at
the following levels:
1.
Primary health care including primary
medical care which includes the point of first
contact and has elements of community
education and community participation in
addition to simple health service delivery.
Primary care is organized based on the fact that
the majority of elderly people live in their own
homes or that of their relatives. Old age in itself
does not indicate a need for specialist geriatric
care.
Such primary care may be delivered by
professionals ranging from general practitioners
to nurses trained in the care of the elderly. The
components of such a service would include a
simple clinic or health centre-based outpatient
service and a domiciliary service component.
Departments / Units of Geriatric medicine have
been established at only 2 medical colleges out
of more than 150 institutions in the country. This
discipline, which places emphasis on functional
assessment, holistic care and a personalized
approach, has yet to make a mark on the Indian
health professional.
With the numbers of people above 60 years of
age in India poised to double over the next 20
years and reach a staggering 135 million, the
20
St. John's Medical College Journal of Medicine
challenge for the health sector in this country is
to make a meaningful health service available in
some form to this growing and needy segment
of the population.
4
Health care of the elderly - A manual for
trainers of physicians in Primary and
Secondary Health care Facilites - WHO,
Ministry of Health and FamilyWelfare and All
India Institute of Medical Sciences.
5.
Irudaya Rajan, S and Mohanachandran P
“Infant and Child Mortality estimates
"Economic and Political Weekly Vol XXXIII
No 19 May 9-15, 1998.
6.
WHO Technical report series 548, “Planning
and organization of geriatric service" Report
of a WHO expert committee 1974.
References
1.
WHO Technical Report series (TRS 779
“Health of Elderly" - report of a WHO expert
committee, 1987.
2.
Socio economic problems (of the elderly) Venkoba Rao, in Geriatric care in India. OP
Sharma (Ed), A n B Publishers 1999 pp 627.
3.
India’s Elderly - burden of challenge?
Irudaya Rajan, Mitra, Sankara Sarma, Sage
publications 1999.
21
St. John’s Medical College Journal of Medicine
LASER THERAPY
SUJATHA RAJ HARSHAD
The term laser is an acronym for ’light
amplification
by
stimulated
emission
of
radiation’. Lasers were first used in the early
1960’s for treatment of port wine stains, tattoos
and cutaneous tumours. Although the early
layers were effective in the treatment of these
conditions, there were considerable side effects
in the form of necrosis, scarring and hyper
pigmentation. With advances in technology,
newer lazers were developed which are much
safer and have lesser side effects.
Components of laser machine (Fig 1)
1.
2.
3.
Power Source
Lasing medium or active medium
Reflecting mirrors
Figure 1 : Schematic representation of the
component of laser machine
Types of Lasers
A variety of lasers are available: carbon dioxide,
Er:YAG, Ruby, Nd:YAG and Alexandrite etc.
They are named according to the material that
constitutes their active medium, (for example, in
the CO2 laser - active medium contains CO2)
They differ in the wavelength of light that is
emitted and in the modes of emission of the
laser beam (continuous or pulsed or Qswitched).
Indications
A wide variety of skin lesions can be treated with
laser therapy. (Table 1)
Principles of Lasers
Electrical energy from a power source excites
the atoms in the lasing/active medium. These
excited atoms are unstable and return to their
stable state releasing energy in the form of light
(laser beam). The laser beam has high energy
and is a concentrated beam of light. This laser
beam is then applied to the target to produce the
desired effects. By choosing the appropriate
wavelength, pulse duration and energy a
particular skin target can be selectively
destroyed with minimal damage to the
surrounding areas, e.g. when the target is
hemoglobin the wavelengths suitable are
418nm, 524nm or 577 nm. For melanin the 6001200nm wavelengths are suitable.1
SUJATHA RAJ HARSHAD
MD, DVD, DNB
Assistant Professor
Department of Dermatology
St. John’s Medical College Hospital
Bangalore
Pigmented lesions
Freckled, lentigines and cafe au lait macules
respond to Nd:YAG, Alexandrite and Q-switched
ruby lasers. However recurrences have been
reported.2 The treatment of melanocytic nevi
with lasers is controversial. Recurrences appear
to be common.3 The cosmetic results are better
with laser irradiation than with standard excision.
Atypical pigmented lesions should be biopsied
prior to laser therapy to rule out malignant
melanoma. The results with lasers in the
treatment
of
post-inflammatory
hyper
pigmentation
and
melasma
have
been
unpredictable. Lasers nave been shown to give
better cosmetic results in the treatment of
tattoos than conventional surgical methods.
Vascular lesions
Pulsed dye and Nd:YAG lasers have been used
to treat superficial cutaneous hemangiomas and
portwine stains.4 Other lesions which have been
reported to respond to laser therapy are
22
St. John's Medical College Journal of Medicine
telangiectasias, angiokeratomas, angiofibromas,
pyogennic granulomas, cherry angiomas and
lymphnagioma circumscriptum.
Resurfacing
Carbon Dioxide and Er:YAG lasers have been
used in resurfacing of skin for treatment of acne
scars and photoageing. The Er:YAG causes less
thermal damage, less scarring and faster wound
healing and therefore ita is considered more
efficient than the CO2 laser.
Benign superficial tumours
Pre-operative checklist
It is important to discuss the expectations,
limitations, outcome, risks and cost of the
procedure with the patient.
•
•
Obtain written informed consent for the
procedure
Check for medications being taken by the
patient, history of drug allergies or
infections.
Post laser care
Neurofibromas,
syringoma,
xanthelasma,
trichoepithelioma and a number of other benign
dermal tumours have been successfully
removed with the help of lasers.
Regular dressings and antibiotics need to be
prescribed along with sunscreens.
Inflammatory
The laser is beneficial if used properly. However,
side effects can occur. The common side effects
are hyper or hypopigmentation and scarring.
Post-operative erythema and infection may be
other limiting factors.
Lasers have proven to given better access than
conventional surgery in treating intertriginous
areas like the axilla and groin. The conditions in
which there has been reported benefit include Hailey-Hailey disease. Darier's disease and
hidradenitis suppurativa.
Hair removal
Several lasers are available for removal of hair
Viz.: alexandrite, Nd:YAG, ruby and diode
lasers. Temporary removal of hair does occur.
Permanent hair growth reduction has been
reported. Response rates are variable and
multiple sessions are required for the same
5.6
area. •
Miscellaneous
CO2 lasers have been used for treatment of
plantar and periungual warts resistant to
conventional
modes
of
therapy
like
electrodessication, cryotherapy and chemical
cautery. High cure rates have been reported.
The wart virus (Human Papilloma Virus) has
been well documented in the laser smoke plume
and the laser staff should take adequate
precautions against contracting the infection.
Hair transplantation7 and punch grafting (for
vitiligo) have been aided by laser therapy. The
advantages are that there is reduced bleeding
from the site and the time required for surgery is
shortened. The thermal damage to the recipient
site may result in poor graft survival.
Side effects
Precautions to be taken
Use of face mask, gloves and eye protection is a
must for persons within the operating room.
Use of the suction/smoke evacuator is
necessary to minimize the risk of viral particle
exposure to staff in the operating room.
Recent Advances
Lasers are also being used for diagnostic
purposes such as imaging and for photodynamic
therapy. Thus the different forms of laser and its
use in skin disorder continue to evolve and the
future seems exciting.
References
1.
Lask GP, Lowe NJ. Lasers in cutaneous and
cosmetic surgery. Pennsylvania, Churchill
Livingstone, 2000.
2.
Grossman ME, Anderson RR, Farinelli W et
al. The treatment of cafe au lait macules
with lasers. Arch Dermat 1995; 131:14161420.
3.
Grevelink JM, Van Leewuwen RL, Anderson
RR et al. Clinical and histological responses
23
St. John's Medical College Journal of Medicine
of congenital melanocytic nevi after single
treatment with Q-switched lasers. Arch
Dermat 1997;133(3):349-353.
4.
Spicer MS, Goldberg DJ. Lasers
dermatology. JAAD 1996;34:1-25.
5.
Dietrickx CC, Grossman ME, Farinelli WA.
Permanent hair removal by normal mode
Ruby laser. Arch Dermat 1998;134:837-842.
6.
Roger CJ, Glaser DA, Siegfrid EC. Hair
removal using topical suspension assisted
Q-switched Nd:YAG and long pulsed
Alexandrite lasers: A comparative study.
Dermatol Surg 1999;844-850.
7.
Chu EA, Rabinov CR, Wong BJF et al.
Laser-assisted
hair
transplantation:
Histologic comparison between CO2 and
Ho:YAG
lasers.
Dermat
Surg
2001;27(4):335-342.
8.
Knoell KA. Treatment of vitiligo with the
Ultrapulse Carbon dioxide laser in patients
concomitantly receiving oral psoralen plus
UV-A
therapy.
Arch
Dermat
1997;133(12):1605-1606.
9.
Thissen M, Westerhof W. Laser therapy for
further depigmentation in vitiligo. Int J
Dermat 1997;365(5):386-388.
in
Table 1
Types of lasers and their common clinical uses
Laser
Wavelength
(nm)
Pulsed dye
Laser
510,577
Common Uses
Advantages
/Disadvantage
Hb
Superficial vascular
lesions,
hypertrophic
scars
Transient purpura, scarring,
dyspigmentation
Target
Ruby
694
melanin
Pigmentation - epidermal
and dermal, tattoos, hair
Transient hyper or
hypopigmentation,
epidermal atrophy
Alexandrite
755
melanin
Pigmentation — epidermal
and dermal, tattoos, hair
Hypopigmentation
Nd:YAG
1064
No
specific
target
Pigmentation — epidermal
and dermal, lattoos, hair,
vascular
Deep tissue penetration
Erbium
YAG
2940
water
Resurfacing
Quicker wound healing,
less scare, less erythema,
poor hemostasis
Carbon
Dioxide
10,600
water
Resurfacing, excision
Delayed wound healing,
hemostasis good
24
St. John's Medical College Journal of Medicine
MANAGEMENT OF EPILEPSY
SARMA G.R.K.
Management of Epilepsy
The management of epilepsy is a complex
process and requires a basic understanding of
the pathogenesis, clinical features and natural
history of various epilepsy syndromes as well as
a logical and individualized approach to each
patient. Certain special patient groups like
pregnant women and the elderly require
additional care and skill in the management.
Decision- making is called for at every stage of
management including the decision to initiate
therapy, the choice of the most appropriate drug,
the duration of drug treatment, the decision to
withdraw anti-epileptic drugs and the decision to
consider surgical management in difficult cases.
These issues are discussed in detail in the
subsequent sections.
1.
However, there is no substantial evidence to
support this hypothesis. The decision to treat
depends on a balance of benefits versus
drawbacks of therapy and should be
individualized. Though there are no strict rules,
general guidelines for starting anti epileptic
therapy are:
1.
Diagnosis of epilepsy must be firm. Syncope
and non-epileptic attacks (pseudo-seizures)
are frequently mistaken for epileptic attacks.
There is no place at all for a trial of
treatment to clarify the diagnosis, because it
seldom clarifies. A good first hand account is
essential as diagnostic tests are often non
confirmatory.
2.
Risk of recurrence of seizures must be
sufficient. Most would accept that 50-80% of
all patients with a first non-febrile seizure
would have further attacks, the greatest risk
being in the first 6 months after the first
seizure. •
The risk of recurrence is
influenced by
Etiology, greater risk in structural cerebral
disease and least in acute symptomatic
epilepsy. In patients with learning disability
or cerebral damage, the risk approaches
100%.
EEG: There is consensus that, the risk of
recurrence is high if the first EEG shows
spike and wave discharges. However, the
predictive value of a normal EEG or EEG
with mild abnormalities is less clear.
Age: the risk of recurrence is higher in those
under 16 or over 60 years.
Seizure type: partial seizures are more likely
(94%) to recur than generalized seizures.
3.
Seizures must be sufficiently troublesome.
Type of seizures: some benign epilepsy
syndromes have excellent prognosis without
therapy (e.g. benign rolandic epilepsy) and
do not require long-term therapy. Some
types of seizures have minimal impact on
quality of life (e.g. partial, absence or sleep
attacks). So the benefits of treating such
seizures even if happening frequently can
NEWLY DIAGNOSED PATIENTS
The decision to initiate therapy in newly
diagnosed patients is critical. In addition to its
biological effects, therapy confers illness status,
confirms the state of being epileptic and can
effect the self-esteem, social relationships,
education and employment. Chronic subtle side
effects are not easily detected and weigh heavily
on decision to treat. For example, the potential
adverse effects of anti-epileptic drugs (AED) on
learning
in
children
are
an
important
consideration
in treatment of childhood
epilepsies. However, the benefits of therapy
include, lower risk of recurrence of seizures,
potential injury and death, psychological and
social benefits of more security. One hypothesis
is that early therapy will prevent establishment of
chronic epilepsy and improve the long-term
outcome.
G.R.K. SARMA MD, DM.
Associate Professor
Department of Neurology
St. John’s Medical College Hospital
Bangalore
25
St. John’s Medical College Journal of Medicine
sometimes
be
outweighed
by
its
disadvantages.
Frequency and timing of seizures: if the
baseline
frequency
is
low,
the
disadvantages of treatment can be high. It
would be unwarranted to treat a person
having less than one seizure a year,
especially if this was confined to sleep and a
minor or a partial seizure,
Precipitation of seizures: occasionally,
seizures
occur
only
in
specific
circumstances or with certain precipitants
(photosensitivity, fatigue, alcohol). Avoiding
these circumstances may avoid the need for
drug treatment. For example, photosensitive
seizures can be prevented by using a small
screen, using remote control, using 100Hz
television screen with liquid crystal display,
using polarizing glasses, keeping screen
contrast and brightness low, avoiding
exposure when sleep deprived and avoiding
looking at flickering pattern.3
4.
Good compliance must be likely.
5.
Patient must be fully counseled and patient’s
wishes must be fully accounted for. The role
of physician is to explain the relative
advantages and disadvantages of therapy
and the final decision must be left to the
patient.
Protocol for treatment of newly diagnosed
epilepsy patients
1.
Establish diagnosis
2.
Identify precipitating factors
3.
Decide upon the need for antiepileptic drug
therapy
4.
Counsel the patient regarding therapy
5.
Start monotherapy with the chosen first line
drug, initially at low dosage and titrate up to
a low maintenance dose. Loading dose is
needed only in cases presenting with status
epilepticus.
6.
If the seizures continue, titrate to higher
doses
7.
If maximal doses fail, alternate monotherapy
has to be started and once the
recommended doses have been reached,
the previous drug has to be gradually
tapered.
8.
If seizures continue, reassess the diagnosis
and patient compliance.
9.
If seizures continue, a combination therapy
of two or even three drugs will be needed.
Starting AED
The goal of therapy is to achieve complete
control without adverse effects. In most cases,
this is achieved with initial first line therapy. In
others, it may take time to find the right
medication and in others, seizure control may be
possible only at the expense of side effects and
in still others, the goal may not be realized.
Monotherapy versus combination therapy
Single drug therapy will provide optimal seizure
control in about 80% of patients.4 Its advantages
are better tolerability, simpler regimen, no
interactions and less risk of teratogenicity.
Combination therapy is needed in 20% patients,
but carries the disadvantages of increased side
effects, increased risk of pharmacokinetic
interactions and teratogenicity.
Classify seizure type
This is very important in choosing the best drug.
The first and second line drugs in different
seizure types5 are shown in the Table 1.
Serum Antiepileptic
Monitoring
Drug
Concentration
This is very useful in monitoring phenytoin
therapy and moderately useful in monitoring of
carbamazepine and phenobarbitone therapy and
is of very little use in valproate and vigabatrin
therapy.
Its
usefulness
in
monitoring
gabapentine and lamotrigine therapy is not
established.6
The major indications for serum AED
concentration monitoring are to check on
compliance with
prescribed
therapy,
to
determine whether symptoms or signs are likely
to be dose related adverse effects of the
prescribed therapy, to monitor pharmacokinetic
interactions to guide dosing of AED, to monitor
patients who are acutely ill, pregnant and those
with renal or hepatic disease.7
26
St. John’s Medical College Journal of Medicine
Table 1. Choice of anti-epileptic drugs in
various seizure types
Seizure
Type
First line
drugs
Second line
drugs
Simple &
complex
partial seizures
primary &
secondarily
generalized
tonic clonic
seizures
Carbamazepine
phenytoin
valproate
Phenobarbitone
topirmate
lamotrigine
clobazam
clonazepam
gabapentin
Absence
seizures
Valproate
ethosuximide
Clobazam
clonazepam
phenobarbitone
lamotrigine
Atypical
absence, tonic
seizures, clonic
seizures
Valproate
Ethosuximide
clonazepam
clobazam
carbamazepine
lamotrigine
phenobarbitone
Myclonic
seizures
Valproate
Clonazepam
clobazam
lamotrigine
phenobarbitone
PATIENTS WITH EPILEPSY IN REMISSION
Epilepsy is said to be in remission when
seizures have not recurred for long periods of
time, which is arbitrarily defined as 2-5 years in
different centers. In such patients, routine
hematological and biochemical monitoring is not
required.
Discontinuation of therapy: It must be
understood that withdrawal of therapy is never
risk-free. The decision to withdraw therapy then
depends on the level of risk the individual patient
is prepared to accept.
Assessing the risk of seizure recurrence after
drug withdrawal: the factors with increased risk
of recurrence of seizures are shown in Table 2.
Table 2. Factors which increase the risk of
recurrence of seizures
❖
❖
❖
❖
❖
♦♦♦
Age over 16 years
Need for 2 or more drugs to control seizures
Seizures after starting treatment
Secondarily generalized seizures
Myclonic seizures
EEG with spike and wave discharges
Short period of freedom from seizures
Type and severity of epilepsy
Mental retardation
Neurological deficit
Family history of epilepsy
The above risk factors are additive and when
two or more adverse factors are present, the risk
of recurrence is over 70%. Most recurrences
after drug withdrawal occur within the first six
months and this should be clearly explained to
the patient. The risk of recurrence of seizures
after stopping AED varies.89 Certain childhood
epilepsy syndromes like childhood absence
epilepsy,
benign
rolandic
epilepsy and
uncomplicated
febrile
conclusions
have
particularly good outcome after withdrawal of
AED. In a recent prospective study in children,
there was a 36% recurrence rate following
withdrawal of drug after a mean seizure free
period of 2.9 years.10 In general withdrawal of
drugs may be attempted after a 2 year seizure
free period. After a single attack, 6 months of
therapy may suffice. The risks of recurrence
should be explained to the patient. Only one
drug at a time must be withdrawn.
Process of drug withdrawal: This needs care.
Sudden reduction in dose or withdrawal of
antiepileptic drugs can result in a severe
worsening of seizures or status epilepticus. The
fastest recommended rates of reduction of
doses of standard drugs are shown in Table 3.11
Table 3. Recommended rates of withdrawal
of anti-epileptic drugs
Drug
Dose decrement
per month (mg)
Carbamazepine
Phenytoin
Phenobarbitone
Valproate
Clobazam
Clonazepam
Gabapentin
Lamotrigine
Topiramate
200
50
30
200
io
1
400
100
100
EPILEPSY IN THE ELDERLY
The incidence of epilepsy is surprisingly high in
the elderly. About 30% of new cases of epilepsy
occur in the people over 65 years. The
prevalence of epilepsy in those over 70 years is
double that in children. Epilepsy is the third most
common neurological condition in the elderly
after dementia and stroke. The chief cause of
epilepsy in the elderly is cerebro-vascular
disease.12 They have a serious impact on the
patients. The risk of fractures, head injury and
St. John's Medical College Journal of Medicine
sudden death are increased. Self-esteem and
independence are further compromised.
The differential diagnosis of epilepsy in the
elderly is wide and includes syncope,
hypoglycemic episode, transient ischemic
episode, transient global amnesia, vertigo and
nonspecific dizziness.
Use of antiepileptic drugs in the elderly
In the elderly, protein binding is reduced due to
lower serum albumin levels and drug clearance
is decreased due to renal or hepatic disease.13
As they are on multiple co-medications, risks of
drug interactions are increased. It should be
noted that most drugs have not been subjected
to trials in the elderly. Drug compliance is also
low due to failing memory and confusion.
Adverse effects of drugs may manifest in
unfamiliar forms in the elderly. They may include
confusion, general ill health, motor or
behavioural disturbances. The side effects may
be noted even with the drug levels being in the
therapeutic range.
Phenytoin has complex pharmacokinetics and
has to be given in low initial maintenance doses
(200 mg/day) and increments should be of 50
mg each time. Drug level monitoring may be
necessary
in
difficult
cases.
Similarly,
carbamazepine has to be started at low doses
(100mg/day) and increased by 100 mg every
fortnightly as its clearance is reduced by 40% in
the elderly. There are no such guidelines for the
use of phenobarbitone and it is rational to follow
the same principles of starting with low doses
and continuing with small increments. Valproate
clearance is reduced by 65% in the elderly.
Encephalopathic side effects are more common
in the elderly with valproate. It may be started at
200 mg/day and increased to 600 mg/day
gradually. Gabapentin is a safe drug in the
elderly because it is not metabolized, there is
minimal protein binding and there are no
significant interactions. The only limiting factor is
its relatively low efficacy in controlling severe
epilepsy. Lamotrigine is extensively metabolized
and is protein bound. It should be used with
caution in the elderly.
MANAGEMENT OF EPILEPSY IN WOMEN
Certain special issues need to be addressed
while treating women with epilepsy.14,15
1. Fertility
Fertility rates have been found to be nearly 20%
lower in women with epilepsy than in the general
population in various studies. There are
undoubtedly social effects namely, lower rates of
marriage, late marriages, social isolation and
stigmatization. Some avoid having children
because of the risk of epilepsy in the offspring
and some to avoid the teratogenic effects of
antiepileptic drugs. Other patients have impaired
cognition and personality disorders. In addition,
biological factors include drug effects and
genetic factors. Thus women with epilepsy are
at disadvantage due to lowered fertility. If there
are any potentially treatable causes for the
infertility, these should be sought.
2. Oral contraception
Enzyme inducing drugs like phenytoin,
phenobarbitone, carbamazepine reduce
the
efficacy of oral contraceptives, especially the low
estrogen (< 50pg) preparations. Non-enzyme
inducing drugs like valproate, gabapentin,
vigabatrin and benzodiazepines do not carry this
risk. In one study, the failure rate of OCP
containing at least 50pg estradiol are needed
and sometimes 60, 80 or 100 pg will be needed.
Since estrogen metabolism is increased in these
patients, risk of adverse effects of high dose
estrogen is unlikely to be increased.
3. Injectable contraceptives
The blood levels of depo-provera are not
affected by hepatic enzyme induction because
its rate-limiting step is hepatic blood flow. Thus
injectable contraceptives are unaffected by
concomitant use of AED.
4. Menstruation and catamenial epilepsy
Estrogen is mildly epileptogenic and the high
estrogen levels during the follicular phase are
responsible for the propensity for seizures
during this phase. Premenstrual tension and
water retention are other possible contributory
factors. It is believed that up to 10% of women
with epilepsy have exacerbations of their
seizures in relation to menstrual cycle. If this
tendency is strong, it is called catamenial
epilepsy.1 Special therapeutic regimens have
been tried in these women. Intermittent
clobazam taken for 5-7 days in the high-risk
period is the most effective regimen with a
responder rate of nearly 80%. However, in
routine clinical practice, this is not completely
effective because of the irregularity of the
menstrual cycle and also to the tolerance to
28
St. John's Medical College Journal of Medicine
clobazam. Thus, most neurologists treat this
group with long-term antiepileptic administration.
Teratogenicity of antiepileptic drugs
There is now conclusive evidence that
antiepileptic drugs increase the risk of congenital
malformations. The most common of these are
cleft lip, cleft palate, cardiac malformations,
neural tube defects and skeletal abnormalities.
As many of the patients are on multiple drugs,
individual risks of AED are not known with
certainty. However, in general the risk is
maximal with these drugs in descending order,
valproate,
carbamazepine,
phenytoin and
phenobarbitone. The background population risk
for spina bifida is 0.2-0.5%. With use of
valproate, it is 1-2% and with carbamazepine, it
is 0.5-1.0%. Learning disability is 2-7 times more
common in off springs of epileptic mothers. All
these risks are greatest in those taking high
doses of multiple drugs. Folate administration
decreases the risk of neural tube defects by
72% and must be given to all pregnant women
and to women planning pregnancy along with
antiepileptic drugs in doses of 5 mg/day.17 No
statement regarding newer drugs can be made,
as experience with them is short and limited.
Vigabatrin has caused cleft palate and fusion
defects in rabbits and reports of children with
spina bifida, cleft palate, absent diaphragm and
Siamese twins exists in humans. Topiramate in
animal models caused right sided limb and
vertebral and rib anomalies. Gabapentin caused
hydro-ureter and hydronephrosis in rabbits.
Currently, the recommendation is to avoid the
use of any of these newer drugs in pregnancy
until more definite advice can be given.
the fetus is uncertain. In the latter stages of
pregnancy, a convulsion carries a risk of trauma
to the placenta and the fetus. Seizures can
result in maternal and fetal hypoxia. First
trimester seizures can increase the risk of fetal
malformations. Status epilepticus can result in
significant maternal and fetal morbidity and
mortality.
Table 4.
Complications
patients
•
•
•
•
•
•
•
•
•
•
•
Pregnancy has random effects on epilepsy.
About one third of patients experience increased
frequency of seizures due to hormonal changes,
noncompliance
and
inappropriate
dose
reductions, changing drug metabolism and
distribution, vomiting and sleep deprivation. A
small number of women notice decreased
frequency of seizures. The effect of seizures on
pregnancy
in
epileptic
Bleeding
Premature separation of placenta
Toxemia of pregnancy
Miscarriage
IUGR, low birth weight
Still birth
Premature labour
Breech and abnormal presentations
Forceps delivery, precipitant labour
Psychiatric disorders
Seizures and status epilepticus
Guidelines for management of epilepsy in
pregnancy
1.
Establish whether antiepileptic therapy is
indeed required.
2.
Rational uses of the drugs with the goals of
using the minimum effective doses and
minimize multi-drug regimens.
3.
Dose adjustments must be made based on
serum levels.
4.
Dose increments may be needed especially
in the last trimester due to fall in drug levels.
5.
Folic acid supplements must be given in all
women who are or have recently been
taking antiepileptic drugs.
6.
Screening for fetal malformations by serial
ultrasound examinations at 10, 18 and 24
weeks, measurement of serum alpha
fetoprotein and amniocentesis.
7.
The neonate should receive 1 mg of vitamin
K i.m. at birth, as they are deficient in this
vitamin if the mother has been on enzyme
inducing drugs.
Pregnancy
The usual complications of pregnancy are
increased up to 3 times in epileptic women
(Table 4). The peri-natal mortality is increased
two fold. The likely causes are seizures during
the delivery and the adverse effects of
antiepileptic drugs.
of
29
St. John's Medical College Journal of Medicine
8.
The treatment of new ont et epilepsy in
pregnancy follows the same principles as in
the non-pregnant patients.
9.
A history of status epilepticus
indication for caesarean section.
10.
If seizures occur during labour, parental
drugs like phenytoin have to be given.
11.
During puerperium,
antiepileptic drug
dosage has to be reduced if this was
increased during pregnancy based on serum
levels.
12.
Most drugs can be continued during breast
feeding
except
phenobarbitone
and
benzodiazepines, which can reach very high
levels in the infant's blood. Neonatal
lethargy, irritability and feeding difficulties
are the signs to be watched for.
is
an
MANAGEMENT OF CHILDHOOD EPILEPSY
SYNDROMES
Neonatal Seizures
While there is no doubt that most neonatal
seizures are epileptic, some subtle and some
tonic seizures are not associated with EEG
changes and may be sub-cortical in origin,
resulting from abnormal brainstem release
mechanisms.18 The most common causes are
hypoxic ischemic encephalopathy, intra-cranial
hemorrhage, neonatal infections and metabolic
disorders (for example - hypocalcaemia,
hypomagnesaemia and hypoglycaemia). The
development of neonatal seizures is an ominous
sign, not only because they often indicate
cerebral disease, but also because the seizures
themselves damage the developing brain.
If the seizures are considered non-epileptic,
drug treatment may not be indicated. Indeed
drug treatment may worsen the phenomenon by
decreasing the level of cortical inhibition over
sub-cortical structures. Opinions vary about the
need to treat infants with EEG evidence of
seizure activity without overt clinical signs. There
is disagreement about the duration of therapy.
Many neonatal seizures are self-limiting and
prolonged therapy carries its own risk. For all
other seizures treatment is urgent. EEG
monitoring is desirable and artificial ventilation
often required. The underlying cause has to be
corrected. Hypoglycaemia requires correction
with 2-4 ml/kg of 25% dextrose intravenously.
Hypocalcaemia needs slow intravenous injection
of 2-5% calcium gluconate with ECG monitoring.
Hypomagnesaemia requires 2-8 ml of 2-3%
magnesium sulfate intravenously or 0.2 ml/kg of
50%
solution
intramuscular.
Pyridoxine
deficiency, although rare, responds to 50-200
mg of pyridoxine. Emergency antiepileptic drugs
are indicated in all except isolated seizures. A
loading dose of 20 mg/kg phenobarbitone is
given to achieve blood level of 20 mg/ml,
followed by maintenance dose of 3-4 mg/kg/day
i.v. or i.m. Phenytoin is a second line drug and is
given in loading dose of 15-20 mg/kg i.v. at a
rate not exceeding 1-2 mg/kg/min and a
maintenance dose of 3-4 mg/kg/day to obtain a
plasma level between 15-20mg/ml. It is
mandatory to monitor blood levels because of
abrupt changes in half-life in the first 2-3 weeks
of life.
Febrile Seizures
3-5% of children will have at least one attack of
febrile seizures. The important risk factors
appear to be an acute temperature rise and
attainment of high fever. In majority of the cases,
viral infection is the underlying cause of fever.
8% are caused by viral or pyogenic meningitis.
Hence all the children with first episode of febrile
seizure must be subjected to lumbar puncture.
30-50% of susceptible children will have second
attack and 10% have three or more. Prolonged
febrile seizure can result in cerebral damage
with consequential focal neurological deficit,
intellectual deficits and HHE syndrome
(hemiplegia, hemi atrophy and epilepsy
syndrome). Therefore febrile seizures require
emergency therapy if they continue for 15
minutes or more. Between 6-18% of children
may show subsequent learning difficulties,
probably reflecting an underlying cerebral
dysfunction. Years later, between 6-12 years of
age, epilepsy may develop in less than 10%.
Emergency treatment includes administration of
diazepam 0.5 mg/kg per rectally, given if the
seizure has continued for 15 min or more or if
there is a past history of prior prolonged
seizures. Child should be cooled by external
measures including cooling blankets and other
means. Emergency prophylactic treatment can
be given by rectal diazepam or oral diazepam as
soon as fever develops. Suitable doses include
0.3-0.5mg/kg twice a day rectally or 5mg orally
for children less than 3 years and 7.5 mg orally
30
St. John's Medical College Journal of Medicine
for those over 3 years. Measures to lower
temperature should also be taken, including
tepid
sponging,
removing
clothing
and
administering
paracetamol.
Unfortunately,
seizure occurs before the fever is apparent in
one third of cases and prophylaxis is not feasible
in these patients.
The need for long-term prophylaxis is debated. It
is now restricted for those at a particularly high
risk of frequent or complex febrile seizures in
view of long term adverse effects and risk to
learning
and
development.
Either
phenobarbitone 15 mg/kg/d or valproate 20-40
mg/kg/day in two divided doses are most
commonly used drugs.
West Syndrome
It is a severe epileptic encephalopathy
characterized by regression of acquired
milestones,
infantile
spasms
and
hypoarrhythmia pattern in the EEG.1 The
prognosis depends on the etiology, which
includes hypoxic injury, metabolic disorders,
neuronal migration disorders, neuro-cutaneous
syndromes,
degenerative
diseases
and
idiopathic cases. Urgent treatment of the
underlying disorder must be initiated wherever
possible Hormonal therapy with ACTH is
probably more effective than conventional anti
epileptic drugs, though there are no case
controlled studies. Low dose regimen with 1 U of
ACTH/kg/day should be tried and if this fails,
high dose regimen with 60-80 U/kg/day should
be given. Pyridoxine has been reported to be
very effective in some cases and may be tried in
refractory cases. Vigabatrin is found to be very
effective in cases of West Syndrome due to
tuberous sclerosis, where it is more effective
than ACTH. In a few cases where focal
abnormalities can be demonstrated, surgery is
very effective in abolition of seizures, but it is not
certain if this improves cognitive function. 7096% of the children have learning difficulty and
in 30-50% cases chronic epilepsy develops.
Lennox-Gastaut Syndrome.
Its etiology is same as that of the West
Syndrome. The prognosis for control of seizures
and intellectual development is poor.20 Currently,
the usual drugs preferred are sodium valproate
and benzodiazepines. Valproate is particularly
effective against atypical absences, myoclonic
or atonic seizures. Clinical trials of lamotrigine
and
topiramate
have
shown
significant
reductions in multiple seizure types, though very
few became completely seizure free. Awareness
and responsiveness also improved with use of
these newer drugs. Ketogenic diet has a
dramatic effect on the seizure frequency but is
very
complicated
and
needs
utmost
understanding and motivation of the parents.
Surgical therapy includes corpus callosotomy
and hemi-cortical resection to control the
generalized seizures.
EPILEPSY IN PATIENTS WITH ADDITIONAL
HANDICAPS.
Epilepsy in patients with learning difficulty is
often severe and resistant to drug therapy. Its
treatment demands the knowledge of some
additional principles. Vigilance for side effects is
particularly important. In the presence of
cerebral damage, drug induced side effects
occur more frequently and at lower levels. These
include confusion, behavioral effects, mental
deterioration, encephalopathy, weight gain and
hyperactivity. Cluster attacks and status
epilepticus can be precipitated by seemingly
trivial insults such as inter-current infections and
environmental changes. Overmedication in the
face of intractable epilepsy has to be avoided so
as to prevent cognitive side effects. Surgical
option can be considered in refractory cases and
the presence of handicap by itself is not a
contraindication for surgery.
STATUS EPILEPTICUS
Status epilepticus is defined as a condition in
which seizures occur with such a frequency that
the patient fails to recover consciousness in
between the attacks. It is also defined as a
seizure, which lasts longer than 30 minutes. It
may be classified based on the seizure type as
tonic clonic, simple partial, complex partial and
absence status epilepticus. It occurs in 1-4% of
patients with epilepsy and is commonest in
patients with partial epilepsy.
Tonic clonic status epilepticus is the commonest
and its management will be discussed in detail.
The guidelines are provided by the Working
Group on status epilepticus of the Epilepsy
Foundation of America in 1993.21 General
measures include maintenance of airway,
oxygenation, blood pressure, fluid electrolyte
status, blood glucose estimation, correction of
hypo or hyperglycemia, control of hyperthermia
31
St. John's Medical College Journal of Medicine
and identification and
precipitating factors.
correction
of
the
Pharmacological measures:
Diazepam and lorazepam are the most common
initial drugs in status epilepticus. Diazepam is
distributed rapidly in the adipose tissue and has
a short duration of action (less than one hour)
though it acts very rapidly (within 5-10 minutes).
It is given in doses of 0.15-0.25 mg/kg in adults
and 0.1-1.0 mg/kg in children. Lorazepam has a
longer duration of action (12-24 hours) and is
given in doses of 0.1 mg/kg in adults and 0.050.5 mg/kg in children.
Phenytoin and phenobarbitone are the drugs
available for perenteral administration in status
epilepticus. Their loading doses are 15-20 mg/kg
and maintenance doses are 3-5mg/kg/day.
Fosphenytoin is a prodrug of phenytoin, which
has advantages including less local toxicity, less
hypotension and solubility in any aqueous
solution. If the seizures are refractory to these
drugs, pentobarbital (15-20 mg/kg loading dose
and 1-2 mg/kg/hr of maintenance dose) or
thiopentine (5-10 mg/kg loading dose and 2
mg/min maintenance dose) have to be
administered to induce a burst suppression
pattern in the EEG.
The management of simple and complex partial
status epilepticus is similar but can be less
aggressive since vital functions like respiration
are not compromised in these seizures.
MEDICALLY INTRACTABLE EPILEPSY ’
Drug therapy fails in 10-20% cases which are
called refractory. There are over ten widely used
anti-epileptic drugs and far more combinations.
All combinations cannot be therefore tried. The
chances of a new drug controlling seizures after
two drugs have been tried are less than 5%.
Therefore, the practical definition of intractable
epilepsy is one which is uncontrolled with two
mono-therapy regimens and at least one poly
therapy regimen. The initial steps in the
management of refractory epilepsy are:
1.
Review diagnosis: In any uncontrolled
epilepsy patient, it is important to ascertain if the
diagnosis of epilepsy is correct. It is not
uncommon to treat non-epileptic phenomenon
like syncope or pseudo-seizures for prolonged
period of time with multiple anti-epileptic
medication with disastrous results. A review of
the history from an eyewitness, review of EEGs
and other investigations are essential.
2.
Establish the etiology: It is essential to
ascertain the possible cause of epilepsy and to
exclude a progressive pathology.
3.
Review compliance: This is one of the
most important and often missed reasons for
treatment failure.
If the above factors are taken care of, then
appropriate patients have to be selected for
referral for epilepsy sugery.22 The indications
and contraindications for epilepsy surgery are
tabulated below. (Table 5)
Table 5
Indications
and
epilepsy surgery
contraindications
for
Indications
Intractable seizures
Seizures must significantly
reduce the quality of life
3. A localized seizure focus by
EEG and MRI.
1.
2.
Contra-indications include
Benign self-limited epilepsy
syndromes
2. Severe mental retardation or
psychosis
3. Neuro-degenerative and
neuro-metabolic disorders
4. Severe family dysfunction
1.
SURGICAL PROCEDURES
1. Temporal lobe seizures
Temporal lobe resection is an effective
procedure in patients with uncontrolled complex
partial seizures _of temporal lobe origin. The
amount of tissue removed is determined by
intra-operative corticography and stimulation
studies. The remission rates with this procedure
vary from 70-80% (either complete seizure
control or significant improvement). The
potential risks of the procedure include
quadrantanopic field defect, cerebrovascular
accident, 3rd nerve palsy and memory and
language deficits.
- 31
St. John’s Medical College Journal of Medicine
2. Non-temporal lobe seizures
The most common procedure is extra-temporal
resection usually involving the frontal lobe. The
outcome is less satisfactory than temporal
resection and the chances of achieving seizure
free state or significant reduction in seizure
frequency is only 50%.
3. Hemispherectomy
This drastic procedure is used in patients with
severe unilateral motor seizures who already
have hemiparesis and non-functional hand.
Examples include Rasmussen encephalitis and
Sturge-Weber syndrome, cerebral infarctions,
hemi-megalencephaly and trauma. 75% of
patients have gratifying reduction in seizure
frequency. The main risks of this procedure are
superficial
hemosiderosis,
bleeding
into
hemispherectomy cavity or fatal brain-stem shift.
4. Corpus callosotomy
In this procedure, spread of seizures is
restricted. This is particularly usefuf in patients
with very frequent seizures, particularly drop
attacks due to rapid generalization.
5.
Mattson RH. Selection of antiepileptic
drug therapy. In: Levy RH, Mattson RH,
Meldrum BS, eds. Antiepileptic drugs, 4th ed.
New York: Raven Press 1995.
6.
Patsalos PN, Sander JWAS, Oxley JR,
Lascelles PT. Immediate anticonvulsant drug
monitoring in management of epilepsy. Lancet
1987; 2:39.
7.
Mattson
RH.
Antiepileptic
drug
monitoring: a reappraisal. Epilepsia 1995; 36
(Suppl 5): S22-S29.
8.
MRC antiepileptic drug withdrawal study
group. Randomized study of antiepileptic drug
withdrawal in patients in remission Lancet
1991 ;337: 1175-1180.
9.
MRC antiepileptic drug withdrawal study
group 1993. Prognostic index for recurrence of
seizures after remission of epilepsy. Br Med J
1993;306: 1374-1378.
NONPHARMACOLOGIC MODALITIES
10.
Shinnar S, Berg AT, Moshe SL et al.
Discontinuing antiepileptic drugs in children with
epilepsy: A prospective study. Ann Neurol 1994;
35:534-545.
These
include vagus
nerve stimulation,
ketogenic diet, behavioral therapy, biofeed back
are all useful modalities and are currently under
evaluation.
11.
Duncan JS, Shorvon SD, Trimble MR.
Discontinuation of phenytoin, carbamazepine
and sodium-valporate in patients with active
epilepsy. Epilepsia 1990a; 31: 584-591.
References
1.
Hart YM, Sander JWAS, Johnson AL,
Shorovon SD. The National General Practice
Study of Epilepsy: Recurrence after a first
seizure. Lancet 1990; 1271-1274.
2.
Sander JWAS, Hart YM, Johnson AL,
Shorovon SD. The National General Practice
Study of Epilepsy: Newly diagnosed epileptic
seizures in a general population. Lancet 1990a;
336:1276-1277.
3.
Fish DR, Quirk JE, Smith SJM, Sander
JWAS, Shorvon SD. Vidoegames and epilepsy.
Final Report 1994, HMSO, London.
4.
Reynolds
EH,
Shorvon
SD.
Monotherapy or polytherapy for epilepsy?
Epilepsia 1981; 22:1-10.
12.
Shorvon SD, Gilliat RW, Cox TCS Yu
YL. Evidence of vascular disease from CT
scanning in late onset epilepsy. J Neurol
Neurosurg Psychiatry 1984; 47: 225-230.
13.
Schener ML. Drug treatment
in the
elderly. In: Engel J, Pedley TA, eds. Epilepsy a
comprehensive
textbook.
Philadelphia:
Lippincot-Raven, 1997.
14.
Delgado-Escueta AV and Janz D.
Consensus
guidelines:
preconception
counseling, management and care of pregnant
women with epilepsy. Neurology 1992; 42(Suppl
5) 149-160.
15.
Yerby MS. Treatment of epilepsy during
pregnancy. In Wyllie E, ed. The treatment of
epilepsy: principles and practice, 2nd ed.
Baltimore: Williams and Wilkins, 1997.
16.
Rosciszewska
D.
Epilepsy
menstruation. Epilepsia 1987; 12:373-378.
and
33
St. John's Medical College Journal of Medicine
17.
Medical Research Council Vitamin
Study Ressearch Group. Prevention of neural
tube defects: results of Medical Research
Council vitamin study. Lancet 1991; 338:131137.
20.
Pravet C, Genton P. Lennox-Gastaut
Syndrome and other childhood epileptic
encephalopathies. In: Engel J, Pedley TA, eds.
Epilepsy:
A
comprehensive
textbook.
Philadelphia: Lippincot-Raven, 1997.
18.
Volpe J J. Neonatal seizures: current
concepts and classification. Paediatrics 1989;
84: 422-428.
21.
Treatment
of
convulsive
status
epilepticus: recommendations of the Epilepsy
Foundation of America’s working group on
status epilepticus. JAMA 1993; 270: 854-859.
19.
Holmes GL, Vigerano F. Infantile
spasms. In: Engel J, Pedley TA, eds. Epilepsy:
A comparenhensive textbook. Philadelphia:
Lippincot-Raven, 1997.
22.
Engel J. Surgery for seizures. N Engl J
Med 1996; 334:647-652.
34
St. John's Medical College Journal of Medicine
THE IMCI AN IMPORTANT INITIATIVE FOR THE SICK CHILD
REYNOLD G. WASHINGTON
What is IMCI?
What is the aim of the IMCI?
IMCI is a strategy, which expanded reads:
Integrated Management of Childhood Illness.
The IMCI strategy is targeted towards improving
health and thus growth and development among
children under the age of five years. In terms of
measurable outcomes the IMCI aims at:
Whose initiative is the IMCI?
The IMCI is a collaborative initiative of the WHO
and UNICEF. The WHO division of Child Health
and Development (CHD) has collaborated with
UNICEF, the World Bank and other agencies for
the development of the IMCI.
1.
Reducing deaths in children under the age
of five years.
2.
Reducing the frequency and severity of
illness and disability in this age group.
3.
Improving practices both
facilities and at home.
What is the rationale behind the IMCI?
Every year 11.6 million deaths occur among
children in developing countries before they
reach their fifth birthday. Seventy percent of
these deaths are due to five main causes. Death
may result from any of these causes
independently or in combination in a given child.
These causes include Acute Respiratory
Infections (ARI mainly pneumonia), diarrhoea,
measles, malaria and malnutrition.(Fig 1) Three
out of four children seeking care at a health
facility also present with one or more of these
conditions.
IMCI is an integrated strategy which focuses on
the child as a whole who may present with more
than one apparent disease condition. IMCI
strategy is appropriate in any country where the
infant mortality rate is more than 40 per
thousand live births and where transmission of
falciparum malaria is common. The Infant
Mortality Rate in India is currently 71 per 1000
live births (UNICEF 2000) and falciparum
malaria is endemic in many parts of the country.
By these criteria, India is a country which
qualifies for the adoption of the IMCI.
REYNOLD G. WASHINGTON MD, DNB
Associate Professor
at the health
Potentially fatal illnesses in children are often
brought to the attention of health workers at first
level primary health care facilities. The initial
focus of the Integrated Management of
Childhood Illness (IMCI) therefore is on:
1.
Improving the performance of primary health
care workers through training and support.
To consolidate gains made earlier and to
progress towards greater and better infant
and child health, staff in primary health care
facilities who are already managing and
treating some of these conditions need to
now be trained to deal with individual
children who may present with more than
one condition.
2.
Improvement in the health system required
for management of childhood illness, not
merely administration of immunization or
distribution of ORS or Cotrimoxazole.
3.
Improvement in family and community
practices through education and counseling
focused mainly on the primary care givers of
children under five at home.
Department of Community Health
St. John's Medical College
Bangalore.
35
St. John's Medical College Journal of Medicine
Have we not had programs for the under five
before? So, what is different about IMCI?
3.
In the past WHO and UNICEF have focused on
disease specific programs. Prominent among
these are:
1.
The Expanded Program of Immunization
(1978), expanding the number of antigens
included in the program, the coverage of
immunization and the definition of the target
group.
2.
The Universal Immunization Program (1985)
focusing on universal immunization of all
infants and pregnant women against the 'six
killer diseases
*
of childhood.
3.
4.
Diarrheal disease control program (modified
1992) which took into consideration other
conditions such as malnutrition, dysentery,
persistent diarrhoea and fever (malaria), as
part of standard case management.
Acute Respiratory Infections (ARI) standard
case management (modified 1995) which
added management protocols on ear
discharge and sore throat to the already
existing protocols aimed at classifying and
treating children based on age and on
whether they had severe disease, severe
pneumonia, pneumonia or no pneumonia.
The
disease-specific
standard
case
management protocols have been useful in
contributing to reduction in the mortality
associated with these diseases in children
under five years of age. The limitations of these
disease specific approaches was that they failed
to take into account the following facts:
1.
2.
Diseases occur in combination: a child may
present simultaneously with both ARI and
diarrhoea. Managing this child using two
different disease specific protocols could be
confusing to a health worker.
Symptoms in the under five especially are
not system or disease specific. Both
pneumonia and malaria may present with
fever, cough and chest waif indrawing.
Depressed conciousness may be due to
diarrhoea
with
severe
dehydration,
meningitis,
severe
malaria,
severe
hypoglycaemia, severe hypoxia or other
conditions.
Immunization programs targeted at universal
coverage aimed only at prevention of the six
killer diseases. Not much in terms of
guidelines were issued with regard to
management of disease in the event of
vaccine failure, or failure to administer the
vaccine. Further, a fatal outcome of the six
killer diseases is often not due to the
disease per se but due to complications
arising out of the disease (e.g., pneumonia
following measles).
The development of IMCI guidelines will perhaps
counter these limitations of disease specific
programs.
What are the components of the IMCI?
Components of the IMCI include both curative
and preventive interventions.
These include:
Case Management
Interventions
•> Pneumonia
❖ Diarrhoea
Dehydration
Persistent diarrhoea
Dysentery
❖ Meningitis, sepsis
❖ Malaria
Measles
❖ Malnutrition
❖ Anaemia
❖ Ear infection
Preventive
Interventions
❖ Immunization during
sick child visits to
reduce missed
opportunities
<• Nutrition counseling
❖ Breast feeding support
including assessment
and correction of breast
feeding technique
What is new in the IMCI strategy?
The new inclusions in the IMCI strategy include:
1.
Improved case management by integration
of disease specific guidelines.
2.
The use of more specific clinical signs, such
as use of palmar pallor for detecting anemia
in children.
3.
The inclusion of periodic doses of
mebendezole to counter anemia as a result
of worm infestation.
4.
Specific guidelines to make a clinical
diagnosis of measles and administration of a
dose of Vitamin A to all children diagnosed
36
St. John’s Medical College Journal of Medicine
to have measles. In addition, case
management of complications that can lead
to death or disability following measles are
paid attention to.
5.
Simplification of the clinical signs for the
classification
of dehydration due to
diarrhoea. Dry mouth and tongue and
absence of tears have now been excluded.
6.
Inclusion of the current WHO case
management strategies for pneumonia and
ear infection, diarrhoea with dehydration,
dysentery,
persistent
diarrhoea
and
malnutrition.
7.
Simplification of the classification of nutrition
status to detect malnutrition even in early
stages before it becomes overt.
8.
Emphasis on the nutritional therapy of
persistent
diarrhoea,
stressing
the
importance of feeding and micronutrient
supplementation.
9.
Counselling of the mother or primary care
giver at home to ensure proper care at
home.
use of IMCI. It is only appropriate if trainers
practice what they teach.
Doctors, nurses and ANMs and literate health
workers need both technical and higher care
facility supports. An appropriate referral system
for prompt referral of children and for provision
of continuing education is an essential
prerequisite for better effectiveness of the IMCI
approach. Mutual trust and appreciation of all
partners in the implementation process and the
referral system is essential to the successful
implementation of the IMCI.
What are the steps in the use of IMCI
guidelines?
The case management process as laid out in the
charts involves the following steps:
1.
The health worker must first assess the
child. This is done by identifying if the child
has any of the danger signs and asking
about the four main symptoms in all children
(cough or difficult breathing, diarrhoea, fever
and ear problem). The health worker then
carries out further assessment if a main
symptom is reported. She/he will also review
the nutritional and immunization status in all
children.
2.
The health worker must then classify the
child’s illness. The classification of illness is
based on a colour-coded triage system.
Health workers are already familiar with this
through use of the WHO case management
guidelines
for
diarrhoea
and
acute
respiratory infections (ARI). The disease
classification tables from the chart on the
assessment and classification of the sick
child aged 2 months to 5 years are shown in
(Fig. 2); the left and middle columns show
how the signs are used to classify the child's
illness, while the right column indicates the
treatments.
For whom is the IMCI?
IMCI guidelines have been developed primarily
for outpatient health facilities. Personnel
included in its implementation therefore include
doctors, nurses, auxiliary nurse midwives and
literate health workers. In addition to health
personnel, the logistic and laboratory support
that is available in a given facility will also
determine the ability to implement IMCI
guidelines. A doctor can do little more than a
trained literate health worker in health facilities
which lack logistic support or laboratory facilities
to manage children with severe illness.
IMCI guidelines have been adapted even for
inpatient care. Instructions for counseling
mothers to deliver proper care at home prior to
discharge are particularly relevant.
It is essential that doctors including general
practitioners and specialist in the field of
Paediatrics and Community Medicine are
reoriented to the IMCI approach. This will in
addition facilitate training of the nurses, ANMs
and literate health workers in the appropriate
Each illness if classified
whether it requires:
according
to
urgent referral
specific medical treatment and advice;
or
simple advice on home management
Action oriented classifications are used
rather than exact diagnoses
37
St. John's Medical College Journal of Medicine
3.
4.
After classification, the health worker
identifies the specific treatments that need
to be administered. If the child has to be
referred to a hospital, the health worker
gives only essential treatment before
departure. An integrated treatment plan is
developed since most children have more
than one illness classification.
2.
1995: WHO’ Program for Control of Acute
Respiratory Infections: “Management of the
child with ARI".
3.
1997: WHO, “Integrated Management of
Childhood Illness": a WHO/UNICEF initiative
- Supplement No. 1 to Volume 75 of the
Bulletin of the WHO.
The health worker then carries out practical
treatment instructions. This includes
instructions to the mother on the
administration of oral drugs, on the need to
increase fluid intake during diarrhoea and on
the treatment of small ailments at home. The
mother is advised on the signs which
indicate that the child should immediately be
brought back to the clinic. She is also
instructed on when she must return for
routine follow-up.
4
1999: WHO, "IMCI Information".
5.
2000: UNICEF. “The State of the World’s
Children 2000".
5.
The health worker assesses feeding and
counsels the mothers on feeding problems
as necessary.
6.
Follow up
instructions for various
conditions are given when the child returns
to the clinic.
Fig 1 Causes of death among children under
5 years of age in developing countries, 1995.
Conclusion
IMCI must go hand in hand with measures to:
1.
Increase and sustain immunization coverage
levels by raising immunization activities and
avoiding missed opportunities.
2.
Increase the coverage of Vitamin A
supplementation by using sick child
encounters to give supplements in areas
with Vitamin A deficiency.
3.
Improve infant and child feeding and growth
by nutritional counseling.
IMCI requires action at the level of the health
facility, home and community. It requires you to
act and to act now.
References
1.
1992: WHO, Program for Control of
Diarrhoeal diseases: “Management of the
child with diarrhoea".
* Approximately 70% of all childhood deaths are
associated with one or more of these 5 conditions.
Reprinted with permission in Integrated
Management of Childhood Illness: A
WHO/UNICEF Initiative - Bulletin of the
WHO. Suppl. 1 (75) 1997.
38
St. John's Medical College Journal of Medicine
Integrated management of childhood illness by outpatient health workers
Fig. 2. Classification tables for integrated management of childhood Illness, based on four main symptoms and
nutritional status.
SIGNS
CLASSIFY AS
TREATMENT
(Urgent pre-referral treatments are in bold print.)
Classify
COUGH or
DIFFICULT
BREATHING
• Any general danger
sign or
• Chest indrawing or
• Stridor in calm child
SEVERE
PNEUMONIA
or VERY
SEVERE DISEASE
► Give an appropriate antibiotic for 5 days.
• Fast breathing
PNEUMONIA
If the child It:
• 2 months up
lo 12 months
• 12 months
to 5 years
Fast breathing is:
■' 50 breaths per
minulo
> 40 breaths per
SIGNS
NO PNEUMONIA:
COUGH OR COLD
CLASSIFY AS
TREATMENT
Two of the following signs:
• Lethargic or unconscious
• Sunken eyes
• Not able to drink or drinking
poorly
• Skin pinch goes back very slowly.
► Soothe the throat and relieve the cough with
a safe remedy.
► Advise mother when to return immediately.
► Follow-up in 2 days.
► If coughing more than 30 days, refer for
assessment.
► Soothe the throat and relieve the cough with
a safe remedy.
► Advise mother when to return immediately.
► Follow-up in 5 days if not improving.
No signs of pneumonia
or very severe disease
minute
► Give first dose of an appropriate antibiotic.
► Refer URGENTLY to hospital.
SEVERE
DEHYDRATION
► If child has no other severe classification:
— Give fluid for severe dehydration (Plan C, see Fig. 4).
OR
If child also has another severe classification:
— Refer URGENTLY to hospital with mother giving
frequent sips of ORS on the way.
Advise the mother to continue breastfeeding.
► If child Is 2 years or older and there is cholera in
your area, give antibiotic for cholera.
Two of the following signs:
► Give fluid and food for some dehydration (Plan B,
• Restless, irritable
• Sunken eyes
• Drinks eagerly, thirsty
• Skin pinch goes back slowly.
see Fig. 4).
► If child also has a severe classification:
— Refer URGENTLY to hospital with mother giving
frequent sips of QRS on the way.
Advise mother to continue breastfeeding.
SOME
DEHYDRATION
► Advise mother when to return immediately.
► Follow-up in 5 days if not improving.
Not enough signs to classify as
some or severe dehydration.
• Dehydration present.
• No dehydration.
NO
DEHYDRATION
► Give fluid and food to treat diarrhoea at home (Plan A,
see Fig. 4).
► Advise mother when to return immediately.
► Follow-up in 5 days if not improving.
SEVERE
PERSISTENT
DIARRHOEA
► Treat dehydration before referral unless the child has
another severe classification;
► Refer to hospital.
PERSISTENT
DIARRHOEA
► Advise the mother on feeding a child who has
PERSISTENT DIARRHOEA.
► Follow-up in 5 days.
DYSENTERY
► Treat for 5 days with an oral antibiotic recommended
for Shigella In your area.
• Blood In the stool.
► Follow-up in 2 days.
39
St. John's Medical College Journal of Medicine
S. Gove et al.
Fig. 2. Continued
SIGNS
CLASSIFY AS
• Any general danger sign or
* Still neck.
VERY SEVERE
FEBRILE
DISEASE
TREATMENT
► Give quinine for severe malaria (first dose).
► Give first dose of an appropriate antibiotic.
► Treat the child to prevent low blood sugar.
► Give one dose of paracetamol in clinic for high fever
(38.5 *C or above).
► Refer URGENTLY to hospital.
► If NO cough with fast breathing, treat with oral antimalarial.
• Fever (by history or leels
hot or temperature
’ 37 5
*C).
MALARIA
OR
If cough with fast breathing, treat with cotrimoxazole for 5 days.
► Give one dose of paracetamol In clinic lor high fever
(38.5 *C or above).
► Advise mother when to return immediately.
► Follow-up in 2 days if fever persists.
► If fever is present every day for more than 7 days, refer for assessment
• Any general danger sign or
• Stiff neck.
► Give quinine for severe malaria (first dose) unless no malaria risk.
DISEASE
► Give first dose of an appropriate antibiotic.
► Treat the child to prevent low blood sugar.
► Give one dose of paracetamol In clinic for high fever
(38.5 *C or above).
► Refer URGENTLY to hospital.
MALARIA
► If NO cough with fast breathing, treat with oral antimalarial.
OR
If cough with fast breathing, treat with cotrimoxazole for 5 days.
► Give one dose of paracetamol In clinic for high fever
(38.5 °C or above).
► Advice mother when to return immediately.
► Follow-up In 2 days if fever persists.
VERY SEVERE
FEBRILE
• NO runny nose and
NO measles and
NO other cause of fever
► If fever is present every day for more than 7 days,
refer for assessment
► Give one dose of paracetamol In clinic for high fever
• Runny nose PRESENT or
• Measles PRESENT or
• Other cause of fever
PRESENT.
FEVER
MALARIA
UNLIKELY
(38.5 °C or above).
► Advice mother when to return immediately.
► FoDow-up in 2 days if fever persists.
► If fever is present every day for more than 7 days.
refer for assessment
• Any general danger sign or
• Clouding of cornea or
• Deep or extensive mouth
ulcers.
• Pus draining from the eye or
• Mouth ulcers
• Measles now or within the
last 3 months.
40
SEVERE
COMPLICATED
MEASLES
MEASLES WITH
EYE OR MOUTH
COMPLICATIONS
MEASLES
► Give Vitamin A.
► Give first dose of an appropriate antibiotic.
► If clouding of the cornea or pus draining from the eye, apply
tetracycline eye ointment
► Refer URGENTLY to hospital.
► Give Vitamin A.
► If pus draining from the eye, treat eye infection with tetracycline
eye ointment
► If mouth ulcers, treat with gentian violet
► Follow-up in 2 days.
► Give Vitamin A.
St. John's Medical College Journal of Medicine
Integrated management of childhood illness by outpatient health workers
Fig. 2. Continued
SIGNS
CLASSIFY AS
TREATMENT
MASTOIDITIS
► Give first does of an appropriate antibiotic.
► Give first dose of paracetamol for pain.
► Refer URGENTLY to hospital.
• Tender swelling behind the ear.
Classify
EAR PROBLEM
• Pus is seen draining from the
ear and discharge is reported
for less than 14 days, or
• Ear pain.
ACUTE EAR
INFECTION
► Give paracetamol for pain.
► Dry the ear by wicking.
► Follow-up in 5 days.
• Pus is seen draining from the
ear and discharge is reported
for 14 days or more.
CHRONIC EAR
INFECTION
► Dry the ear by wicking.
► Follow-up in 5 days.
• No ear pain and
No pus seen draining from the
ear.
NO EAR
INFECTION
SIGNS
Classify
NUTRITIONAL
STATUS
• Visible severe wasting or
• Severe palmar pallor or
• Oedema ol both feet.
CLASSIFY AS
SEVERE
MALNUTRITION or
No additional treatment.
TREATMENT
► Give Vitamin A.
► Refer URGENTLY to hospital.
SEVERE ANAEMIA
• Some palmar pallor or
• Very low weight for age.
ANAEMIA
or VERY
LOW WEIGHT
• Not very low weight-for-age and
no other signs of malnutrition.
► Give an antibiotic for 5 days.
NO ANAEMIA
and NOT VERY
LOW WEIGHT
► Assess the child's feeding and counsel the mother on feeding
according to the FOOD box on the COUNSEL THE MOTHER chart
— If feeding problem, follow-up in 5 days.
► If pallor;
— Give iron.
— Give oral antlmalarlal If high malaria risk.
— Give mebendazole if child is 2 years or older and has not had
a dose In the previous 6 months.
► Advice mother when to return immediately.
► If pallor, follow-up In 14 days.
If very low welght-for-age. follow-up in 30 days.
► If child Is less than 2 years old, assess the child's feeding and
counsel the mother on feeding according to the Food box on
the Counsel the Mother chart
— If feeding problem, follow-up in 5 days.
► Advise mother when to return immediately.
41
St. John's Medical College Journal of Medicine
NEONATAL RESUSCITATION
FULTON D’SOUZA
Introduction
Secondary Apnea
3-5% of the 26 million infants born in this country
experience asphyxia at birth. Birth Asphyxia is
the leading cause of neonatal death in India.
Asphyxia is characterized by
• Progressive hypoxia
• Hypercapnia
• Metabolic acidosis (due to hypoperfusion)
Physiology of Asphyxia
When hypoxia continues the gasping respiration
is weaker and weaker until the infant takes a last
gasp and enters secondary apnea. The heart
rate and arterial pressure falls and death occurs
unless effective resuscitation is initiated
promptly.
Assume secondary apnea
1*
FlMXt
Infants who become asphyxiated undergo a
sequence of events. There is an initial period of
rapid breathing, then respiration ceases and
heart rate begins to fall and primary apnea
follows.
1C:
<■<!,* NW
v/>
*»A*'**
It may be difficult to distinguish primary from
secondary apnea. Therefore apnea at birth
should be treated as secondary apnea and
resuscitation should be initiated promptly as
apnea may begin in utero and. continue after
delivery.
Clearing of lung fluid
Fulton D’Souza MD
Assistant Professor
Department of Paediatrics
St John’s Medical College Hospital
Bangalore
Fetal lung fluid must be cleared if air is to fill the
lungs. To clear fetal lung fluid and expand the
lungs may require two to three times the
pressure of a normal breath.2
Problems in clearing the lung fluid occur in
•
•
•
•
Infants apneic at birth
Infants with weak initial respiratory effort
Premature infants
Infants depressed by asphyxia, maternal
drugs and anaesthesia.
- 42
St. John's Medical College Journal of Medicine
Pulmonary circulation
At birth pulmonary blood flow must increase for
proper oxygenation. This is accompanied by
arterioles in the lungs opening up and getting
filled with blood previously diverted away from
the lungs through the ductus arteriosus.
Decreased Pulmonary Perfusion
In the asphyxiated newborn, hypoxemia and.
acidosis maintain a fetal pattern of circulation
with diminished pulmonary blood flow.2
Decreased Cardiac Function: Early in asphyxia,
blood is shunted to the brain and the heart. With
increasing hypoxemia and acidosis, myocardial
function fails, cardiac output decreases and
blood flow even to these vital organs is
diminished.
Being prepared for resuscitation
Two major factors for prompt effective
resuscitation are
• Anticipation of need for resuscitation
• Adequate preparation of equipment and
personnel.
1.
2.
3.
4.
5.
Is the amniotic fluid clear of meconium?
Is the baby breathing or crying?
Is there good muscle tone?
Is the baby’s colour pink?
Is the baby term?
Apgar score
The Apgar score is generally allotted at 1 minute
and again at 5 minutes of age. However,
assessment of the infant should begin
immediately at birth. So it is helpful only for
assessing the infant’s condition and the
effectiveness of the resuscitative efforts.
The ABC’s of resuscitation
The steps in resuscitating newborn infants follow
the well-known TABC of resuscitation
T- temperature regulation
A - establish an open airway
B - initiate breathing
C - maintain circulation
Initial steps in resuscitation
1.
Preventing heat loss : (Fig 2)
Anticipation
Delivery room staff should be prepared to
handle problems and consider every delivery as
a high risk one.
Preparation
To allow for the unexpected case, minimum
preparation for every delivery should include:
•
*
•
A radiant warmer heated and ready for use
is preferred. However a room heater or 60100 watt bulb can be used for the same
purpose.
All resuscitation equipment immediately
available and in working order
At least one skilled person is required to
perform a complete resuscitation including
endotracheal intubation and administration
of medicines.
Heat loss is prevented by2,6
a.
b.
2.
Placing the infant under a heated radiant
warmer.
Quickly drying the infant and removing the
wet linen.
Open airways
a.
Positioning - The neonate is placed on
his / her back with neck slightly
extended (Fig3)
/J»StT«CM»VC
OP
JrtfAh’ •
Signs to evaluate
The following five questions differentiate the
baby in need of assistance from the baby who
can receive routine care.3
43
St. John's Medical College Journal of Medicine
Tactile stimulation
If an infant does not breathe, tactile stimulation
may be used briefly in an attempt to initiate
breathing. These are only by (Fig 5)
atio»/
Tactic
MAiKTAH
th<
-Solx
come* foirt’r*
b.
Suctioning - Suction the mouth first and
then the nose. (Fig 4).
Slapping or flicking the soles of feet
Evaluation
Now monitor for three vital signs2
Respiratory rate
Heart rate
Colour
Respiration : Evaluate infant’s respiration. If
normal, go to next sign. If not, positive pressure
ventilation.
Heart rate: If >100, then go to the next step.
Coiour: If central cyanosis present provide free
flow oxygen by blowing oxygen over the infants
nose so that the infant breathes oxygenenriched air. If using tubing for delivery of free
flow of oxygen, then the tubing should be
attached to the oxygen flow meter with 5 litres of
oxygen/min.
Deliver oxygen to the infant as follows:
Tubing away from the nostril: Low Flow Oxygen
Tubing close to nostril: High Flow Oxygen
Meconium
If thick and particulate or thin meconium stained
amniotic fluid is present one should suction the
mouth and pharynx as soon as the baby’s head
is delivered and before the delivery of the
shoulders.
After delivery, the hypopharynx should be
suctioned to remove residual meconium. Then,
in case of thick meconium, trachea should be
intubated if baby is depressed, to remove any
residual meconium using the meconium
aspirator. The tracheal suctioning is done by
applying the suction directly to an endotrachael
tube. If the meconium is thin and watery and the
infant is active after a thorough suctioning, no
endotrachael suctioning (ET) is required. If the
baby is active and vigorous ET suction need not
be done even in thick meconium stained
amniotic fluid.4,5
44
St. John's Medical College Journal of Medicine
a.
b.
c.
Infant is apneic or gasping
Heart rate <100
Infant has central cyanosis and apneic after
the initial resuscitation.
First select the appropriate equipment.
Obtain a resuscitation bag and connect it to an
oxygen source.
Select a mask of proper size — covering nose
and mouth and not eyes.
Position: Infants neck should be slightly
extended to ensure an open airway.
The pressure needed to inflate the lungs will
vary depending on the infant's size, the
condition of the lungs and whether the infant has
previously taken a breath.5
Meconium in Amionitic fluid
l
Intra partum suctioning of mouthy pharynx and nose
Thin
J
Infant active
""
Thick
Infant depressed
{
i
i
I
Observe
,______ Suction trachea____
Resuscitation PRN
First breath - The initial lung inflation following
delivery may require a pressure of 30-40 cm
H2O.
Succeeding breaths - pressure of 15-20 H2O
Pulmonary disease - pressure of 20-40 cm H2O
Resuscitation PRN
Bag and mask ventilation : Equipment
1.
2.
3.
4.
5.
6.
7.
After placing the mask in position and checking
seal and ventilation observe for appropriate rise
of chest.
Resuscitation bags
a. Anaesthesia bag
b. Self inflating bag
If chest does not rise
Pressure gauge
Oxygen reservoir
Mask - circular and anatomical
Oxygen source
Flow meter
Oxygen tubing
Indication: Bag and mask
indicated whenever (Fig 6)
ventilation
is
Action
Condition corrected
1. Reapply mask
2. Reposition infants head
3 Check for secretions,
suction if present
4. Ventilate with mouth
slightly open
5. Increase pressure slightly
inadequate seal
blocked airway
blocked airway
blocked airway
inadequate pressure
Normal rate 40 -60 breaths / min.
When to stop
When the heart rate is above 100.
Check heart rate: after infant received 100%
oxygen for 15-30 seconds, check heart rate for 6
seconds.
Heart rate
Action
>100
observe respiratory rate and colour
<60
continue to ventilate.
begin chest compression
<100 but >60
continue ventilation alone
Signs of improvement
•
•
•
Increasing heart rate
Spontaneous respiration
Improving colour
45
St. John's Medical College Journal of Medicine
Orogastric tube is passed in infants
receiving bag and mask resuscitation to
prevent distention of abdomen and
aspiration. (Fig 7).
Chest compressions
Indications: It is based on neonate’s heart rate. It
is necessary when despite 15 to 30 seconds of
ventilation with 100% oxygen, the heart rate is
below 60 beats per minute? 3,4
Infants position : neck slightly extended. Firm
support for the back so that heart can be
compressed between sternum and the spine.
Position of compression: While one person
continues ventilation, quickly locate the lower
third of the sternum. (1 cm below the line joining
the two nipples) or area just above xiphoid?
(Fig 8)
LOCATION
CHtsr
46
St. John's Medical College Journal of Medicine
•
Technique
2
1, Two finger method: The tips of the middle and
index or ring fingers should be used for
compression
2. Thumb method: The balls of the thumb should
be used for compression. (Fig 9).
Check: After 30 seconds of compression and
ventilation, check the heart rate for 6 seconds.
<60 ->continue compressions and ventilation
>60
stop chest compression but continue
ventilation. Even if heart rate is found to be 0
compression and ventilation should continue
until a medical decision is reached to
discontinue resuscitation.
Endotracheal intubation
Preparing for endotracheal intubation
1.
ET tube: Size 2.5, 3.0, 3.5, 4.0 mm2
Tube Size
(mm)
Weight
(gm)
Gestational
Age (Wks)
2.5
3.0
3.5
3.5-4.0
<1000
1000-2000
2000-3000
ABOVE 3000
below 28
28-34
34-38
ABOVE 38
2.
Insert stylet to appropriate distance if
required. (However try to avoid stylet
unless there is difficulty in intubation)
Laryngoscope:
Attach blade
No. 0 for preterm
No. 1 for term infant
Check light
Additional features:
- Cut strip of tape
- Prepare suction equipment
- Prepare oxygen tube with 100% O2
- Prepare resuscitation bag and mask
Rate: Sternum should be compressed to a
depth of 1/3 of anterior posterior diameter of
chest with three compressions and one
ventilation occurring in a 2 second cycle.5
This provides 90 compressions and 30
ventilations per minute.
Position infant flat on the back with neck slightly
extended. Insert laryngoscope. Stand at the
head end of the infant.
Be sure that
laryngoscope blade is locked in operating
position and the light is bright. Hold the
laryngoscope in left hand. Introduce the blade
into the mouth and advance it to just beyond the
base of the tongue. This should position the
blade with vallecula
Visualize Glottis: Lift the blade and observe for
landmarks. As you lift the blade epiglottis and
glottis should come into view.
47
St. John's Medical College Journal of Medicine
Fig. 10
When you visualize glottis
a.
b.
c.
What landmarks do you see? If the blade is
in too far, not far enough or off to one side
take corrective action.
If view of glottis obscured by secretions,
suction secretions
Apply tracheal pressure if you are not able
to visualize glottis.
Inserting ET tube: When the glottis can be seen
introduce the ET tube into right side of mouth
and into glottic opening.
Insert the tip of the tube until the vocal cord
guide is at the level of the vocal cords.
When the tube is positioned withdraw the
laryngoscope and then the stylet and observe
for the tube position by ventilation.
1.
2.
After initial confirmation by above methods fix
the tube to the infants face. The above can also
be obtained by inserting tube to following
distance from angle of mouth.
correct
FiMftr
1C6 : fl CHNlQUfc
Observe the chest and abdomen. Look for
good chest expansion
Bilateral breath sounds are of equal
intensity.
If unilateral withdraw tube
appropriately. If no air entry withdraw and
resuscitate, then re-intubate.
Of VSlNfij
LAiS YN'
Weight (kg)
Depth of insertion
(cms from angle of mouth)
1
2
3
4
7
8
9
10
Now obtain a chest x-ray.
Medications
Mechanism of action
Stimulates the heart
Increases tissue perfusion
Restores acid base balances
Routes of administration
fOf.K.FCI
(X'SITlOrt
Of
LACfrxix’IX r« *
a.
b.
Umbilical vein through a catheter which is
inserted into the vein until there is a free flow
of blood.
Peripheral vein
48
St. John's Medical College Journal of Medicine
c.
Expected signs: Heart rate should rise to 100
beats/min or above within 30 seconds after
infusion.
Endotracheal instillation (Fig 11)
Directly or using 5F catheter.
Follow up: If heart rate remains below 100
beats/min
consider
epinephrine
(re
administration) - may be repeated every 3 to 5
minutes if required.
2. Volume Expanders
Indications for use : Evidence or suspicion of
acute blood loss with signs of hypovolemia.
Types of volume expanders:
ENBOTRACKEAU
Four volume expanders may be administered.
• Whole blood (O-ve blood cross-matched
with the mothers blood)
• 5% albumin - saline solution
• Normal saline
• Ringers lactate
cp
Administration :
Indications
1.
2.
The neonates heart rate remains below 60
beats/minute despite adequate ventilation
(with
100%
oxygen)
and
chest
compressions for a minimum period of 30
seconds2,3,4
Heart rate is zero
Effects:
a.
b.
Medications used
1.
Dosage: 10 ml/kg
Route: Intravenous
Rate: give over 5-10 mins, by syringe or
intravenous drip.
Increase vascular volume
Decrease metabolic acidosis by increasing
tissue perfusion
Epinephrine
Expected signs
Blood pressure should
increase, pulse becomes stronger and pallor
should improve.
Preparation
- Recommended concentrations 1:10,000
- Concentration available 1:1000
Preparing syringes - Prepare 1 ml in a syringe
Follow-up : May be repeated
hypovolemia persist.
Dosage
and
route:
Intravenous
endotracheal 1:10,000; 0.1-0.3 ml/kg
3.
and
Rate: Given rapidly
Mechanism of action
a.
b.
Increases strength and rate of cardiac
contractions
Causes peripheral vasocontraction
if signs of
Sodium Bicarbonate
Indications for use:
1.
2.
Prolonged arrest that does not respond to
other therapy
Documented metabolic acidosis
Note: Sodium bicarbonate should be used only
after ventilation is established.
Preparations
Recommended
0.5mEq/ml = 4.2% solution.
concentration
49
St. John's Medical College Journal of Medicine
Administration:
syringes.
Prepare two
10 ml prefilled
Dosage: 2 mEq/kg.
Route: intravenous
Rate: Give slowly, over at least 2 minutes
(1mEq/kg/mt)
to
minimize the
risk of
intraventricular hemorrhage.
Effects:
a. Corrects metabolic acidosis by raising the
pH of the blood in the presence of adequate
ventilation
b. Provides some volume expansion resulting
from the hypertonic solution of sodium.
Expected signs : Heart rate should rise to 100
beats/mt or above within 30 seconds after
infusion is completed.
Follow up : Heart rate below 100 - consider
readministration of epinephrine and continue
with volume expanders, ventilation and chest
compression. If persistent hypotension is
present, consider administration of dopamine.
4.
Naloxone Hydrochloride
Indications for use:
a. Severe respiratory depression in the
newborn AND
b. A history if maternal narcotic administration
within the past 4 hours.
Preparation : Concentration available 0.4mg/ml
or 1 mg/ml solution. Prepare 1 ml in a syringe.
Administration:
Dosage : 0.1mg/kg (100pg/kg)
Routes: Endotracheal, intravenous preferred..
Intramuscular, subcutaneous .: Acceptable but
delayed onset of action.
Rate: Inject rapidly.
Effects: Narcotic antagonist.
Signs: Spontaneous respiration.
Follow-up : Monitor respiration and heart rate
closely. Re-administer naloxone if respiratory
depression recurs.
Note: The duration of action of naloxone is 1 to 4
hours. The duration of the narcotic often
exceeds that of naloxone, necessitating
repeated doses of naloxone.
5.
Dopamine Hydrochloride
Indications : After prolonged resuscitation if the
infant has poor peripheral perfusion and thready
pulse and continues to show evidence of shock.
Preparation : Dopamine is administered only as
a continuous infusion. An intravenous solution
containing dopamine must be prepared.
The concentration of the solution to be prepared
will vary based on
- Dosage desired
- Infants weight
- Volume of fluid considered safe to administer.
Dosage: Begin at 5 pg/kg/min (May increase
upto 20pg/kg/min if necessary) since dopamine
is given as a continuous infusion the dosage is
always expressed as the amount of dopamine to
be infused per kilogram per minute.
Preparing solution : Commonly used formula 6x infants wtt in kg x desired dose/pg/kg/mt
---------------------------------------------------------------- --- |\/|g of desired
amount of fluid in ml/h
dopamine per
100ml. sol
Multiplying 6 times infants’s weight in kilograms
with desired dose of dopamine in pg/kg/min and
dividing by desired amount of fluid to infuse in
ml/hr will provide you, the amount of dopamine
in mg to add to each 100 ml of solution
prepared.
Effects:
Strengthens cardiac contractions
Increases cardiac output
Raises blood pressure
Expected signs:
Blood pressure should rise
Heart rate should stabilize
Infusion rates are usually increased in
increments of 3-5 pg/kg/min if the blood
pressure and perfusion do not improve.
Follow-up:
After 15 minutes: check heart rate and blood
pressure at least every 3-5 minutes until the
blood pressure is stabilized.
Caution: If an infant has an insufficient response
to 20pg/kg/min of dopamine it is highly unlikely
that raising the dose further will make a
difference.
50
St. John's Medical College Journal of Medicine
References
1.
Operationalisation of essential Newborn
care at District level: Resource Book National Neonatology Forum & Government
of India.
2.
Kattwinkel J, Niermeyer S., et al. ILCOR
advisory statement from the Pediatric
working group of the International Liaison
committee on Resuscitation. Circulation
1999; 1927-1938.
3.
Deorari A. Newer Guidelines for Neonatal
Resuscitation - How my practice needs to
change? Indian Pediatrics 2001; 38:496499.
4.
Gupta P. Guidelines 2000 for Neonatal
Resuscitation- Indian Paediatrics 2000;
37:1229-1233.
5.
Kattwinkel J. Text Bool of Neonatal
Resuscitation, 4th Edition Elk Grove Village,
Illinois, American Academy of Paediatrics
and American Heart Association, 2000.
6.
International
Guidelines
for
Neonatal
Resuscitation: An expert'from the guideline
2000 for Cardiopulmonary Resuscitation and
Emergency
Cardiovascular
care:
International
consensus
on
Science
2000;106:e29.
51
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