Standard Treatment Guidelines

A Manual for Medical Practitioners


STANDARD TREATMENT GUIDELINES

MESSAGE

The Tami Nadu Health System Project (TNHSP) is undertaking several initiatives to improve the
quality of service in all the secondary care hospitals in the state. Improved quality of care in all the
Government Medical Institutions will help significantly in improving the health outcome in the state.
Following a standard treatment protocol in treating the patients, is one way to improve the quality of
care.

This edition of the Standard Treatment Guidelines for various diseases will enable the Medical
Officers to follow an established standard in treating the patients in the Government health facilities.
This will ensure that the treatment is effective and done at least cost, too.

The Health and Family Welfare Department of the Government of Tamil Nadu is a front-runner in
the provision of health care. It has taken many innovations to enable the best health outcome for the
people in the state. The Standard Treatment Guidelines is another indication of the innovation by the
state, to sustain the momentum of improving the health outcomes.

I congratulate the experts, for their valuable contribution and the officers of the TNHSP in bringing
out the guidelines.
STANDARD TREATMENT GUIDELINES

FOREWORD

The management of quality in health care provision and assuring the quality in service provision in
public health institutions are critical in ensuring the health outcome of the people.

The Tamil Nadu Health System Project (TNHSP), launched in March 2005, is enabling an
architectural correction in the health care delivery in the state. It has taken many steps to improve the
health care provision in the state.

The publication of the Standard Treatment Guidelines has been prepared with contributions from
several experts. This guideline will assist Medical Officers and other health care providers to provide
appropriate and standard health care for clients who visit the public health facilities. This will help us
to move towards ensuring and sustaining a good standard in provision of health care thus helping us
to realise the best health outcome for the people in the state.

The Health and Family Welfare Department appreciates this initiative of TNHSP in formulating this
Standard Treatment Guidelines for implementation in the public health facilities in the state. I
recommend this document to all the Medical Practitioners and the health experts in the state and I
suggest they utilise this guideline to ensure quality health care in the state.

Principal Secretary to Government
Department of Health & Family Welfare
Government of Tamil Nadu
STANDARD TREATMENT GUIDELINES

PREFACE

Guidelines enable the setting of standards for service provision, help in assessing services, improve
them, reduce costs and importantly they enable client satisfaction. These are goals that health
systems strive towards.

I am happy to note that the Tamil Nadu Health System Project (TNHSP) has published a Standard
Treatment Guideline for provision of health care in public health facilities in the state. This is the
first initiative of its kind in the state. This guideline will help doctors to provide a standard treatment
to all clients. This will ensure that any client, with similar episode of illness, will obtain the same
standard of treatment in any public health facility, across the state.

I congratulate the Editorial Committee, the contributors, the reviewers, the publisher and staff of
TNHSP for their efforts, in publishing this guideline. I request feedback from the health personnel,
which will significantly help us to improve this, further.

Prof. Dr. Thirumalaikolundu Subramanian M.D
Formerly Director and HOD
Institute of Internal Medicine
Madras Medical College & Government General Hospital
Chennai – 600003.

TAMIL NADU HEALTH SYSTEM PROJECT

STANDARD TREATMENT GUIDELINES

INTRODUCTION

The Tamil Nadu Health System Project (TNHSP), Health and Family Welfare Department,
Government of Tamil Nadu has taken many steps to improve the quality of care in public health
facilities in the state.

The Standard Treatment Guidelines (STG), is a profile of thematic presentation of various medical
conditions and existing treatment modalities practiced worldwide. It is a systematically developed
method to assist Medical Practitioners and other health care providers in making decisions for
specific clinical episodes.
Its use contributes significantly in attaining Total Quality Management (TQM) in health care. It also
helps the Medical Practitioners to be apprised of recent advancements in the provision of care.

This initiative by TNHSP is an important component of its efforts at improving quality in health
care. A team of experts from renowned Medical Colleges of Tamil Nadu have contributed
significantly in compiling this document, especially the various anecdotes, clinical methodology,
diagnostic tools, cross references and current practices. An Algorithimic approach to the
management of the common clinical conditions will help significantly to save precious time in
decision making. The aim of this document is to enable uniformity and rational prescriptions and an
attitudinal change to tackle emergencies, epidemics and other health related issues across the state in
a better manner.

The guidelines have been peer-reviewed by the faculty at Christian Medical College, Vellore and
suggestions were incorporated with the concurrence of the STG Committee.

STG is the first step. Although it is intended to be comprehensive, the users are requested to refer the
publications mentioned in the guideline for a comprehensive knowledge. A CD version of the
guidelines will be made available through the HMIS (Health Management Information System) of
TNHSP. The feedback form in enclosed and the comments and suggestions from the users will help
to improve the future editions of this guideline.

It gives me immense satisfaction and joy in introducing the Standard Treatment Guidelines for the
benefit of the Medical Practitioners and health care providers in Tamil Nadu.

I also take this opportunity to thank the experts and the staff of TNHSP in enabling the preparation of
this guideline.


Project Director
TNHSP









STANDARD TREATMENT GUIDELINES – TAMIL NADU
EDITORIAL BOARD


Category Name and Designation Office Address Contact Nos
Principal Advisor Thiru. V.K.Subburaj, I.A.S.,
Secretary to government
Health & Family Welfare Department
Secretariat, Chennai -9.
Ph : 25671875
Fax : 25671253
Chairman –
Editorial Board
Dr.S.Vijayakumar,I.A.S.,

Special Secretary to Government,
Health and Family Welfare
Department and Project Director
Tamil Nadu Health Systems Project
And Project Director, Tamil Nadu
AIDS Control Society
And
Ph : 044 – 24345990
Fax : 044 -24345994
Chief Coordinator (Capt) Dr.M.Kamatchi

Expert Advisor
TNHSP
Ph : 044 – 24345991
Fax : 044 -24345992
Advisors Dr.S.Vinayagam,
Dr.P.Nandagopalsamy,
Dr.S.Elango,

Director of Medical Education
Director of Medical and Rural Health
Services
Director of Public Health and
Preventive Medicine

Ph : 28364502
Fax : 28364500
Ph : 2434 3271
Fax : 24343271
Ph : 24320802
Fax : 24323442
Editor Dr.P.Thirumalaikolundu
subramanian,

formerly Director & Professor,
Institute of Internal Medicine, MMC
& GGH
Ph : 25305534
Fax : 25305115
Sub Editors

Dr.M.S.P.Saravanan,
Dr.G.Sasikala
Medical Officers
TNHSP
Ph : 044 – 24345991

Fax : 044 -24345992



STANDARD TREATMENT GUIDELINES – TAMIL NADU
Contributors and Reviewers

Topic Name and Designation Department / Institution Contact Details
General
Medicine


Dr.K.Raghavan
Dr.V.K.Rajeswari
Dr.M.Jubilee
Dr.D.Rajasekaran
Dr..S.G..Siva Chidambaram

Dr. Natarajan (SMC)
Dr.Rajendran (SMC)

Dr.Rajendran(KMC)
Madras Medical College





Stanley Medical College


Kilpauk Medical College
Mobile : 98840 60066
Mobile : 98400 96120
Mobile : 94444 12289
Mobile : 98402 00750
Mobile : 98410 87216

Mobile : 98410 72858


Toxicology

Dr.C.Rajendran(MMC) MMC GGH Mobile : 94443 84964
98410 17720
Medicine



Dr.D.Ranganthan
Dr.Geetha Lakhsmipathy
Dr..M.Jayakumar
Dr.Alagesan
Dr.P.Padmanaban
Dr.N.Rajendiran
Dr.V.Natarajan
Dr.B.Parveen
Dr.Jayaraman
Dr.V.S.Dorairaj
Dr. Kannamma Sabapathy
Dr. Sathyanathan
Dr. Nammalvar
Dr.B.Krishnaswamy
Dr. Anuradha
Dr.V.Vedamoorthy
Dr. R.Muthuselvan
Dr. T.S.Swaminathan
Dr.Kumaran
Dr.Porkodi
Dr.Jayanthi
Respiratory Diseases
General Nervous System
Kidney & Urinary Tract Diseases
Cardiology
Medical Gastroenterology
Diabetalogy
Neurology
Skin Diseases
Skin Diseases
Sexually Transmitted Diseases
Hematology
Psychiatry
Community Psychology
Geriatric Medicine
Medical Genetics
Medical Oncology
Injection Safety
Radiology
Radiology
Rheumatology
Medical Gastroenterology (SMC)
Mobile : 94441 40773
Mobile : 93823 42419
Mobile :
Mobile : 98841 27563
Ph : 22457259
Mobile : 98400 42898
Mobile :
Mobile : 98402 54112
Mobile : 94441 19274
Mobile : 94441 29606

Mobile : 98410 19910
Mobile : 99949 92229
Mobile : 94440 71976
Mobile : 94443 40166
Mobile :
Mobile : 94444 72728
Mobile : 98402 73232
Mobile : 98403 94961

Mobile
Pediatrics &
Neonatology

Dr.R.Kandasamy
Dr.P.Ramachandran
Dr. Saradha Suresh
Pediatrics & Neonatology
Pediatrics & Neonatology
Pediatrics & Neonatology
Mobile : 94449 50432
Mobile : 98404 71901
Mobile : 94440 21321
Surgery



Dr. Dorairajan
Dr.R.Veerapandian
Dr.S.Ammamuthu
Dr.V.Velayutham
Dr. Muthukumar
Dr.K. Harsha Vardhan
Dr.Srikumari Damodaran
Dr. Jayaraman
Dr.M.Chandrasekaran

General Surgery
Geriatric Surgery
ENT Diseases
Eye Diseases
Neuro Surgery
Cardio Thoracic Surgery
Surgical Gastroenterology
Urology
Surgical Endocrinology
Surgical Oncology
Mobile : 98400 83583
Mobile : 94448 44972
Mobile : 94444 37059
Mobile :
Mobile : 94433 53463
Mobile : 98410 13542
Mobile : 98410 76231
Mobile :
Mobile : 92821 07070
Mobile :
Dr.M.P.Namasivayam
Dr.Vidyasagaran
Plastic Surgery
Vascular Surgery
Mobile : 98402 65592
Mobile : 94442 96952
Orthopedics Dr.Mayilvahanan
Natarajan
Orthopedics Mobile : 98410 70743
Obstetrics
and
Gynaecology
Dr. Revathy
Dr.Vasantha N.Subbaiah
Obstetrics and Gynaecology
Obstetrics and Gynaecology
Mobile : 94443 57957
Mobile : 94444 54666
Anesthesiolo
gy
Dr.Venkatachalam Anesthesiology Mobile : 94440 07550
Dentistry Dr.K.S.Gamal Abdul
Nasser
Dentistry Mobile : 94440 27123
Bio Medical
Waste
Management
Dr. K.Vinay Kumar
Ms.Jaisee Swetha
Deputy Director, TNHSP
Programme officer, TNHSP
Mobile : 94450 30722
Mobile : 94450 30716
Searching
Medical
Literature
Dr.J. Mariano Anto
Bruno Mascarenhas
Co Ordinator, Management
Information System and
Technical Associate, Cadaver
Transplant Programme, Govt of
Tamil Nadu
Mobile : 98421 11725
Internal
Reviewers
Dr Gurusamy (CEO)
Dr.Julia Hopper(DD
Training & HRD)
Dr.Gunasekaran (DD
Tribal Health)
Dr.Kumaresan (DD
Procurement)

Dr.P.K.Amarnath Babu
Dr B.Bharathi
Dr M.Raja
Dr.A.Muthu Sundari
Mr. Pradeep

TNHSP
Peer
Reviewers
Professors and Associate
Professors and
Faculty of Specialty
Departments
Christian Medical College,
Bagayam, Vellore.

Support Staff
Assistants
with
Computer
Knowledge
Mrs. S.Jayanthi
Mr.M.Hari Harasudhan
Mr.M.Amarnath

TNHSP
Support Staff
Computer
Operators
Mrs. R.Shanthi
Ms.Amala Mary
Mr.Chandrasekar
TNHSP



Ph: 044-24345994

Acknowledgment


The Tamilnadu Health Systems Project, Health and Family Welfare
Department, Government of Tamilnadu has a taken a major initiative to improve the
quality of care in all Government institutions in the state. Standard Treatment
Guidelines (STG), a manual for Medical Practitioners to be used at different points of
the therapeutic process is one among the components of the Project in its Quality
enhancement strategy.

This manual was mode possible with the encouragement of the Secretary,
Health and Family Welfare Department, Government of Tamilnadu, Project
Director,Tamilnadu Health Systems Project and Chairman of the Standard Treatment
Guidelines committee Dr.S.Vijayakumar I.A.S., for his valuable guidance. We are
indebted to all our former Project Directors of Tamilnadu Health Systems Project for
their timely contributions towards STG.

We express our gratitude to all the contributors, Reviewers, Clinical and
Managerial experts in the making of this guidelines.

We are grateful to our Chief Coordinator and Expert Advisor
(Capt).Dr.Kamatchi and Prof. Thirumalaikolundu Subramanian, formerly Director and
Head, Institute of Internal Medicine, Madras Medical College / Government General
Hospital, Chennai who have been the main guiding force behind the STG committee.

We express our thanks to the printers M/s Ikon Press, Chennai for their
expertise and special word of thanks to Mr.Karthi of Hybrid screens, Chennai for
computer processing.





Statements
 This guidelines is designed to provide concise information and not intended to provide
comprehensive scientific information
 For detailed and up to date information as well as to know the current developments, users
are requested to go through textbooks, monograms, original articles, review papers, case
reports, websites, etc.,
 For administration of each drug, users are requested to go through the latest product
information leaflets provided by the manufactures. Moreover dosage schedule are being
constantly revised and new side effects are recognized. Hence, users have been reminded to
recall the indications dosage, side effects consider the contraindications and interaction
before using any drug
 The Editors, the Coordinators, the Contributors, the Reviewers , Publishers and the Funding
agency do not assume any liability for any injury and / or damage to person or property
arising out of this publication
 Every effort was taken to print the version with appropriate information. However, it is
possible that errors might have crept in. Hence users are requested to offer their remarks and
suggestions to the following e- mail address < mail@tnhsp.net> tnhsproject@gmail.com for
revising the future edition.













1
Common Conditions
and General Topics
Chapter 1
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
● Fever
● Management of Trauma
● Cardiot horacic Trauma
* Blunt I nj uries
* Penet rat ing I nj uries
* Chest Wall I nj uries
* Pleuropulmonary I nj uries
* Mediast inal I nj uries
● Principles of Surgery
● Examinat ion of Surgical Pat ient s
● Pre Operat ive Assessment and Preparat ion
● Anaest hesia in Surgical Pract ice
● Post Operat ive Care
● Wound Care
● Sut ures and Wound Dehiscence
3
Fever
Def inition
Fever
An elevat ion of normal body t emperat ure t hat
exceeds t he normal daily variat ion and occurs in
conj unct ion wit h an increase in t he hypot halamic set
point - for example, from 37°C t o 39°C.
Hyper t her mi a
● An unchanged set t ing of t he hypot halamic set
point in conj unct ion wit h an uncont rolled increase
in body t emperat ure t hat exceeds t he body’s abil-
it y t o lose heat
● Heat st roke
* Thermoregulat ory failure in associat ion wit h a
warm environment
● Malignant hypert hermia
* Hypert hermic and syst emic response t o ha-
lot hane and ot her inhalat ional anest het ics in
pat ient s wit h genet ic abnormalit y
● Neurolept ic malignant syndrome
* Syndrome of hypert hermia, aut onomic dys-
regulat ion, and ext rapyramidal side effect s
caused by neurolept ic agent s (e.g., haloperi-
dol)
Hyper pyr exi a
● Temperat ure > 41.5°C (> 106.7°F) 1
● Can occur wit h severe infect ions, but more com-
monly occurs wit h cent ral nervous syst em (CNS)
hemorrhages or hypert hermia
Symptoms
Temper at ur e
● The mean normal oral t emperat ure is 36.8° ±
0.4°C (98.2° ± 0.7°F), wit h low levels at 6 a.m.
and high levels at 4–6 p.m.
● The normal daily t emperat ure variat ion is t ypi-
cally 0.5°C (0.9°F). (However, in some individuals
recovering from a febrile illness, daily variat ion
can be as great as 1.0°C.)
* During a febrile illness, diurnal variat ions are
usually maint ained, but at higher levels.
* Daily t emperat ure swings do not occur in pa-
t ient s wit h hypert hermia.
* Rect al t emperat ures are generally 0.4°C
(0.7°F) higher t han oral readings. (Lower oral
readings are probably at t ribut able t o mout h
breat hing, a part icularly import ant fact or in
pat ient s wit h respirat ory infect ions and rapid
breat hing.)
* Lower-esophageal t emperat ures closely re-
flect core t emperat ure.
* Tympanic t hermomet er measurement s, al-
t hough convenient , may be more variable
t han direct ly det ermined oral or rect al values.
Some f ebr i l e di seases have char act er i st i c
pat t er ns.
● Wit h relapsing fevers, febrile episodes are sepa-
rat ed by int ervals of normal t emperat ure.
● Tert ian fevers are associat ed wit h paroxysms on
t he first and t hird days. Plasmodium vivax caus-
es t ert ian fevers.
● Quart an fevers are associat ed wit h paroxysms
on t he first and fourt h days. P. malariae causes
quart an fevers.
● Ot her relapsing fevers are relat ed t o Borrelia in-
fect ions and rat-bit e fever, which are bot h associ-
at ed wit h days of fever followed by a several-day
afebrile period and t hen a relapse.
● Pel-Ebst ein fever, wit h fevers last ing 3–10 days
separat ed by afebrile periods of 3–10 days, is
classic for Hodgkin’s disease and ot her lympho-
mas.
● I n cyclic neut ropenia, fevers occur every 21 days
and accompany t he neut ropenia.
● There is no periodicit y of fever in pat ient s wit h
familial Medit erranean fever.
Si gns
Si gns of hyper t her mi a
● Hallucinat ions
● Delirium
● Dry skin
● Pupil dilat ion
● Muscle rigidit y
4
Di f f er ent i al Di agnosi s
Fever vs hypert hermia
● I t is import ant t o dist inguish bet ween fever and
hypert hermia.
* Hypert hermia can be rapidly fat al and charac-
t erist ically does not respond t o ant ipyret ics.
● There is no rapid way t o make t his dist inct ion.
● Hypert hermia is oft en diagnosed on t he basis of
event s immediat ely preceding elevat ion of core
t emperat ure.
* Heat exposure
* Treat ment wit h drugs t hat int erfere wit h t her-
moregulat ion
● I n addit ion t o clinical hist ory, physical aspect s of
some forms of hypert hermia may alert t he clini-
cian.
* I n heat-st roke syndromes and in t he set t ing
of drugs t hat block sweat ing, t he skin is hot
but dry.
* Ant ipyret ics do not reduce elevat ed t empera-
t ure in hypert hermia.
» I n fever and hyperpyrexia, adequat e doses
of aspirin or acet aminophen usually result
in some decrease in body t emperat ure.
Causes of hypert hermia syndromes
● Heat st roke: t hermoregulat ory failure in associa-
t ion wit h a warm environment
* Exert ional: caused by exercise in high heat or
humidit y
» Even in healt hy individuals, dehydrat ion or
common medicat ions (e.g., over-t he-coun-
t er ant ihist amines wit h ant icholinergic side
effect s) may help t o precipit at e exert ional
heat st roke.
* Nonexert ional: occurs in high heat or humidit y
» Typically affect s very young, elderly, or
bedridden individuals, part icularly during
heat waves
» Also affect s pat ient s t aking ant icholinergic
agent s (e.g., phenot hiazines), ant iparkin-
sonian drugs, diuret ics
● Drugs
* Monoamine oxidase inhibit ors (MAOI s)
* Tricyclic ant idepressant s
* Amphet amines
* Cocaine
* Phencyclidine
* “ Ect asy” (met hylenedioxymet hamphet amine)
* Lysergic acid
* Diet hylamide
* Salicylat es
* Lit hium
* Ant icholinergic agent s
● Malignant hypert hermia
* Elevat ed t emperat ure, increased muscle me-
t abolism, muscle rigidit y, rhabdomyolysis, aci-
dosis, and cardiovascular inst abilit y develop
rapidly.
* Occurs wit h use of inhalat ional anest het ics or
succinylcholine
* Oft en fat al
● Neurolept ic malignant syndrome
* Charact erized by “ lead-pipe” muscle rigidit y,
ext rapyramidal side effect s, aut onomic dys-
regulat ion, and hypert hermia
* Occurs in t he set t ing of:
» Neurolept ic agent use
» Phenot hiazines
» But yrophenones, including haloperidol
and bromperidol
» Fluoxet ine
» Loxapine
» Tricyclic benzodiazepines
» Met oclopramide
» Domperidone
» Thiot hixene
» Molindone
» Wit hdrawal of dopaminergic agent s
● Serot onin syndrome
* Seen wit h select ive serot onin upt ake inhibi-
t ors (SSRI s), MAOI s, t ricyclic ant idepressant s,
and ot her serot onergic medicat ions
* Has many overlapping feat ures, including
hypert hermia, but is dist inguished by di-
arrhea, t remor, and myoclonus
● Endocrinopat hy
* Thyroxicosis
5
* Pheochromocyt oma
● CNS damage
* Cerebral hemorrhage
* St at us epilept icus
* Hypot halamic inj ury
Di agnost i c Appr oach
● Few signs and sympt oms in medicine have as
many possible diagnoses as fever.
● The t empo and complexit y of t he workup will de-
pend on t he pace of t he illness, diagnost ic con-
siderat ions, and t he pat ient ’s immune st at us.
● I f findings are focal or if t he hist ory, epidemio-
logic set t ing, or physical examinat ion suggest s
cert ain diagnoses, t he laborat ory examinat ion
can be focused.
● I f fever is undifferent iat ed, t he diagnost ic net
must be cast furt her.
● A met iculous hist ory is most import ant .
● At t ent ion must be paid t o :
* Prescript ion and nonprescript ion drugs (in-
cluding supplement s and herbs)
* Surgical or dent al procedures
* Exact nat ure of prost het ic mat erials and/ or
implant ed devices
* Occupat ional informat ion concerning expo-
sure t o:
» Animals
» Toxic fumes
» Pot ent ially infect ious agent s
» Possible ant igens
» Febrile or infect ious individuals in t he
home, workplace, or school
* Geographic area in which t he pat ient has lived
* Travel hist ory (including milit ary service)
* I nformat ion on:
» Unusual hobbies
» Diet ary proclivit ies (e.g., raw or poorly
cooked meat , raw fish, unpast eurized milk
or cheeses)
» Household pet s
» Sexual orient at ion, including precaut ions
t aken or omit t ed
» Use of t obacco, alcohol, and marij uana or
ot her illicit drugs
» Trauma
» Animal bit es
» Tick or ot her insect bit es
» Transfusions
» I mmunizat ions
» Drug allergies or sensit ivit ies
» Et hnic origin
» Blacks are most likely t o have hemo
globulinopat hies.
» Turks, Arabs, Armenians, and
Sephardic Jews are especially likely t o
have familial Medit erranean fever.
* I nformat ion on family members wit h:
» Tuberculosis
» Ot her febrile or infect ious diseases
» Art hrit is or collagen vascular disease
» Unusual family sympt omat ology, such as
deafness, urt icaria, fevers and polyserosi-
t is, bone pain, or anemia
● Physical examinat ion should include:
* Det erminat ion of oral or rect al t emperat ure
* Look for Focus of I nfect ion
» Drain Pus, if present
» Check for I nt ravenous canulae and cat h-
et ers and remove t hem and if t hey cannot
be removed, replace t hem. Treat as per
Cult ure / Sensit ivit y Report
» Check for Nosocomial I nfect ion and t reat
accordingly
* Examinat ion of:
» Skin
» Lymph nodes
» Eyes
» Nail beds
» Cardiovascular syst em
» Chest
» Abdomen
» Musculoskelet al syst em
» Nervous syst em
6
» Rect um
* I n men: examinat ion of penis, prost at e, scro-
t um, and t est es
» The foreskin, if present , should be ret ract-
ed.
* I n women: pelvic examinat ion, looking for
causes of fever such as pelvic inflammat ory
disease and t ubo-ovarian abscess
I nvesti gati ons
Labor at or y Test s
● I f hist ory, epidemiologic sit uat ion, or physical
examinat ion suggest s more t han a simple viral
infect ion, t he following t est s may be indicat ed:
* Complet e blood count
* Different ial count
» Perform manually or wit h an inst rument
sensit ive t o t he ident ificat ion of eosi-
nophils, j uvenile or band forms, t oxic gran-
ulat ions, and Döhle bodies
* Blood smear
» Appropriat e if t here is a hist ory of expo-
sure or possible exposure t o a variet y of
pat hogens, including: Malaria parasit es,
Babesia Ehrlichia, Borrelia, Trypanosomes
* Eryt hrocyt e sediment at ion rat e
» Ext remely high values (> 100 mm/ h) may
suggest a primary rheumat ologic disorder,
vasculit is, or malignancy.
* Urinalysis, wit h examinat ion of urinary sedi-
ment
* Chemist ries
» Elect rolyt es
» Glucose
» Blood urea nit rogen
» Creat inine
» Liver funct ion
» Creat ine phosphokinase (elevat ed in
hypert hermia) or amylase
* Microbiologic t est s
» Rapid st rept ococcal t est or t hroat cult ure if
t here is pharyngit is
» Cult ures of blood and urine
» St ain, fluid analysis, and cult ure of sam-
ples from specific sit es of concern ident i-
fied by hist ory and examinat ion
» Sput um analysis in pat ient s wit h
s uspect ed pneumonia
» Joint fluid analysis in pat ient s wit h
art hrit is
» Cerebrospinal fluid analysis in pat ient s
wit h suspect ed meningit is
» HI V t est in pat ient s at epidemiologic risk
I magi ng
● Chest x-ray : Part of t he evaluat ion of any signifi-
cant febrile illness
● Ot her imaging st udies: guided by sympt oms and
signs
Di agnost i c Pr ocedur es
● Lumbar punct ure : I ndicat ed in pat ient s wit h pos-
sible bact erial meningit is
● Aspirat ion and drainage of possibly infect ed col-
lect ions or abscesses : Oft en done wit h radiologic
guidance
● Bone marrow biopsy (not simple aspirat ion) for
hist opat hologic st udies (as well as cult ure) : I ndi-
cat ed in febrile syndromes when marrow infilt ra-
t ion by pat hogens or t umor cells is possible
Tr eat ment Appr oach
1. I f t here is Cardio Respirat ory Compromise à Shift
Pat ient t o Higher Cent re wit h I CU Facilit ies / Shift
Pat ient t o I CU
2. I f t he Core Body Temperat ure is More t han 41
deg Celsius (105 deg F) à Treat as Hypert hermia
and Refer t he Pat ient t o a Higher Cent re wit h I CU
Facilit ies / Shift Pat ient t o I CU.
3. Take Smear for Malaria
● Based on whet her t he Area is High Risk (refer
t o t he chapt er on Malaria for more det ails about
High Risk Areas) or Low Risk
» I n High Risk Area, 25 mg/ kg of chloroquine
base for 3 days (10mg/ kg on day 1 and
day 2 and 5 mg/ kg on day 3) wit h a single
dose of Primaquine 0.75mg/ kg on t he first
day.
» I n Low Risk Area, presumpt ive t reat ment
wit h Chloroquine 10 mg/ kg single dose
7
d. Furt her Management as per Result s of Blood
Smear Examinat ion
5. Tab Ciprofloxacin 10 mg/ kg in 2 divided doses
upt o a maximum of 750 mg t wice daily for 10 –
14 days
6. I f associat ed wit h Cough / Evening Rise of Tem-
perat ure / Loss of Appet it e / Loss of Weight ,
Check Sput um for AFB
Treatment
Tr eat ment of f ever
● Obj ect ives
* To reduce t he elevat ed hypot halamic set point
* To facilit at e heat loss
● Treat ment t o reduce fever is recommended for:
* Pat ient s wit h cardiac, cerebrovascular, or pul-
monary insufficiency
* Pat ient s wit h organic brain disease
* Children wit h a hist ory of febrile or nonfebrile
seizures
* There is no correlat ion bet ween absolut e t em-
perat ure elevat ion and onset of a febrile sei-
zure in suscept ible children.
● Ant ipyret ic t reat ment should be given on a regu-
lar schedule rat her t han int ermit t ent ly.
* I nt ermit t ent t herapy aggravat es chills and
sweat s.
* Chronic high-dose t herapy wit h ant ipyret ics
(such as aspirin or nonst eroidal ant i-inflam-
mat ory drugs [ NSAI Ds] used in art hrit is) does
not reduce normal core body t emperat ure.
Tr eat ment of hyper t her mi a
● Obj ect ives
* To facilit at e heat loss
* To reduce heat product ion in endogenous
hypert hermia
Speci f i c Tr eat ment of f ever
● Ant ipyret ic t reat ment
* Aspirin, NSAI Ds, and glucocort icoids are ef-
fect ive ant ipyret ics.
* Acet aminophen is preferred because it :
» Does not mask signs of inflammat ion
» Does not impair plat elet funct ion
» Does not adversely affect t he GI t ract
» I s not associat ed wit h Reye’s syndrome
* Treat ing fever and it s sympt oms does no harm
and does not slow t he resolut ion of common
viral and bact erial infect ions.
* Reducing fever wit h ant ipyret ics also reduces
syst emic sympt oms of headache, myalgias,
and art hralgias.
● I n hyperpyrexia, t he use of cooling blanket s fa-
cilit at es t he reduct ion of t emperat ure.
* However, cooling blanket s should not be used
wit hout oral ant ipyret ics.
Speci f i c Tr eat ment of Hyper t her mi a
● Ant ipyret ics are of no use in hypert hermia.
● Physical cooling should be init iat ed immediat ely.
* A sponge bat h wit h cool wat er, coupled wit h
t he use of fans, is oft en sufficient .
* Cooling blanket s and ice bat hs are effect ive
but not well t olerat ed.
* I nt ravenous fluid administ rat ion
* I nt ernal cooling by gast ric or perit oneal lav-
age wit h iced saline in severe cases
* I n ext reme cases, hemodialysis or cardiopul-
monary bypass
● Malignant hypert hermia
* Cessat ion of anest hesia
* Administ rat ion of dant rolene (1–2.5 mg/ kg
q6h for at least 24–48 hours) plus
* Procainamide administ rat ion because of risk
of vent ricular fibrillat ion
● Neurolept ic malignant syndrome
* Discont inuat ion of offending agent s
* Pharmacot herapy not well st udied
» Efficacy has been quest ioned.
» Pot ent ial agent s include:
» Dant rolene (0.25–2 mg/ kg q6–12h I V)
» Bromocript ine (2.5–10 mg PO or via na
sogast ric t ube q6–8h)
» Amant adine (200 mg PO or via nasogas
t ric t ube q12h)
8
Moni t or i ng
● Monit oring of pat ient s wit h fever depends on t he
underlying cause.
● Pat ient s wit h hypert hermia generally require ad-
mission t o a monit ored-care set t ing unt il cooling
measures have rest ored normot hermia.
Compl i cat i ons
● Complicat ions are relat ed t o t he underlying cause
of fever.
● Hypert hermia is oft en fat al.
Pr ognosi s
● Fever
* I n most cases, eit her t he pat ient recovers
spont aneously or t he hist ory, physical exami-
nat ion, and init ial screening laborat ory st udies
lead t o a diagnosis.
* When fever cont inues for 2–3 weeks and re-
peat examinat ions and laborat ory t est s are
unrevealing, t he pat ient is provisionally diag-
nosed as having fever of unknown origin.
● Hypert hermia
* The prognosis for hypert hermia depends on
t he rapidit y of cooling.
Pr event i on
● Fever
* No common prevent ive measures
● Hypert hermia
* Avoid excessive act ivit y in hot or humid envi-
ronment s.
* Maint ain adequat e int ake of fluids before, dur-
ing, and aft er st renuous act ivit y or exposure
t o ext reme heat .
* Maint ain proper vent ilat ion t o promot e cooling
from sweat evaporat ion.
I CD-10
R50 Fever of ot her and unknown origin
Management of trauma
Trauma is t he leading cause of deat h in t he younger
age group Deat hs occurring aft er t rauma can be
prevent ed by immediat e t reat ment in some cases
Trauma or inj ury is charact erized by a sudden
alt erat ion or physiological imbalance result ing from
an acut e exposure t o physical, chemical, t hermal or
mechanical energy t hat exceeds t he t olerance level of
t he body
I n all t rauma cases t ransfer of energy occurs t o body
t issues result ing in t issue damage.
The Golden Hour: The crit ical first period following
inj ury in which lifesaving measures must be undert aken
and definit ive management should be st art ed t o ensure
best chance of survival and t o reduce morbidit y.
The component s of maj or t r auma management
ar e
● Recept ion of t he vict im
● Primary survey
● Resuscit at ion phase
● Secondary survey
● Definit ive t reat ment phase
● Follow up and rehabilit at ion
Recept i on and document at i on
● Pre hospit al care of t he inj ured - Ret rieval resus-
cit at ion and t ransfer of t he vict im t o t he hospit al
is an import ant fact or in t he out come of t reat-
ment
● Follow maj or Trauma Guidelines in order or si-
mult aneously depending on t he nat ure and ur-
gency of t he sit uat ion
● Assessment , invest igat ion and management must
proceed simult aneously in maj or t rauma cases
● Record t he det ailed event s of t he accident includ-
ing from where, by whom and how t he vict im was
brought t o t he hospit al I t is import ant in medico-
legal cases and ident ifying unconscious pat ient
Pr i mar y Sur vey:
I s a rapid assessment of vit al funct ions t o ident ify
life t hreat ening condit ions and allow t heir immediat e
correct ion (ABCDE)
Airway and cervical spine cont rol
Breat hing and Vent ilat ion
Circulat ion wit h cont rol of bleeding
Disabilit y assessment and Deformit y
Exposure and Examinat ion
9
Airway
● Maint anence of airway is t he first and t he most
import ant fact or in t he management of t he t rau-
ma pat ient
● Clear airway, mout h, nose and t hroat of blood,
vomit us and secret ions by suct ion
● Maint ain airway by chin lift or j aw t hrust , suct ion,
oropharyngeal airway or orot racheal int ubat ion
● I mmobilize cervical spine in neut ral posit ion by
semi rigid collars
● I nt ubat e (ETT) whenever required and vent ilat e
I nt ubat i on pr ocedur e
● Oxygenat e wit h 100% oxygen t hrough mask or
airway
● Cricoid pressure and ET t ube held by t he assist ant
( size of t he t ube is roughly t he size of t he lit t le
finger)
● Lift Tongue wit h t he laryngoscope
● Visualize t he vocal cord
● I nt roduce t he E T Tube int o t he t rachea
● Confirm t ube posit ion by auscult at ion
● I nflat e cuff t o prevent aspirat ion.
Br eat hi ng and Vent i l at i on
● Oxygenat e, int ubat e, vent ilat e, I f Respirat ory
Rat e is < 10, > 30
● Do not allow t he effect s of head inj ury, shock or
t issue damage t o be compounded by hypoxemia
● Administ er high flow oxygen up t o 10 l/ min by
face mask or assist ed vent ilat ion
● Treat t ension pneumot horax - immediet ely. ( I t is
a clinical diagnosis, do not wait for chest X ray),
by insert ing wide bore canula/ I CD
● Drain large hemot horax.
● Occlusive dressing (air t ight ) and I CD for open
pneumot horax
Ci r cul at i on
● Arrest act ive bleeding by direct pressure or sut ur-
ing
● Replace volume wit h fluids
● Transfuse fully cross mat ched blood when avail-
able
● Reduce of fract ures-early
● Surgical hemost asis for uncont rolled bleeding
Causes of per si st ent hypot ensi on
● I nadequat e resuscit at ion
● Occult bleeding (pelvis,abdomen,chest or femur)
Ai r way obst r uct i on
● Pneumo and hemot horax
● Pericardial t amponade
● Spinal inj ury
● Pump failure
● Drugs (bet a blockers, nit rat es, ant ihypert ensives)
and alcohol
● Manage persist ent hypot ension by adequat e re-
suscit at ive measures
● Plan urgent surgery when resuscit at ive measures
10
fail t o st abilize t he pat ient
Di sabi l i t y
● Assess pat ient ’s level of consciousness
● Pupil size and react ion t o light
● Glasgow coma scale (Eye opening, Mot or Re-
sponse and Verbal response) and APACHE for
grading of progression or det eriorat ion of pa-
t ient ’s condit ion
● Hypovolemia may produce severe brain dysfunc-
t ion, hence should be correct ed first .
Exposur e and Exami nat i on
● Expose t he part s
● Evaluat e inj uries complet ely
● Record findings
Resusci t at i ve Phase
The init ial st eps of resuscit at ion are:
● Est ablishment and maint enance of secure airway
● Assist ed vent ilat ion if necessary wit h high con-
cent rat ion oxygen
● Arrest of bleeding and rapid rest orat ion of blood
volume
● Maint ain Breat hing and circulat ion, blood volume
and vit al paramet ers
● Record findings at regular int ervals before pro-
ceeding t o t he next phase.
Secondar y Sur vey
● Examine in a syst emat ic manner from head t o
t oe t o ident ify all occult inj uries, aft er addressing
life t hreat ening emergencies
● Remove all clot hing before examinat ion
● Pay special at t ent ion t o pat ient ’s back, axillae and
perineum
● Examine oral cavit y, nose, ears and scalp
● Digit al rect al examinat ion if necessary
● I nvest igat e-essent ial radiology
* X-ray chest , abdomen, cervical spine, pelvis,
skull and ot her part s as and when required
* Sonography (FAST),
* CT brain for head inj ury pat ient s.
● Avoid missing inj uries and disabilit ies during sec-
ondary survey, since missed inj uries are common
in t rauma pat ient s, eg. Fract ure phalanx or t oe
maybe missed in a case wit h head inj ury or mul-
t iple fract ures.
● Plan for emergency surgery if necessary
Def i ni t i ve Tr eat ment phase
● I nit iat e appropriat e t reat ment immediat ely de-
pending on t he nat ure of t he inj uries.
● Priorit ize inj uries - t rauma surgeon coordinat es
and t akes decisions
● Undert ake simult aneous surgery/ repair coordi-
nat ing wit h all specialist s concerned when mult i-
ple organs or syst ems are affect ed.
● Tet anus and ant ibiot ic prophylaxis
● Pain relief
● Alleviat ion of anxiet y and fear of t he pat ient and
relat ives- an int egral part of t rauma care
11
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12
● Hand over t he pat ient t o ER/ OT st aff
● Give det ails of inj uries, t reat ment and out come
expect ed and alleviat e anxiet y of t he pat ient and
relat ives wherever possible.
● Record t he propert ies of t he pat ient including t he
j ewels worn, clot hing and ot her belongings and
hand over t o aut horit ies and inform police if no
at t ender is available.
I n t he Emer gency War d
● Follow t he t rauma management guidelines
● Primary survey (ABCDE) and resuscit aion
● Maint ain airway, breat hing and circulat ion
● Record hist ory wit h dat e and t ime, received t ime
and examinat ion t ime during resuscit at ion
● Mode and det ails of inj uries should be not ed.
● Life t hreat ening emergencies should be at t ended
first
● Secondary survey for det ailed examinat ion and t o
avoid missing inj uries
● Priorit ize inj uries, coordinat e and undert ake sur-
gery aft er resuscit at ive measures.
● Record clinical condit ion, t reat ment inst it ut ed,
invest igat ion result s, expert opinions obt ained in
chronological order wit hout and delay.
● Avoid overwrit ing and correct ions
● Get consent from relat ives, if not available from
RMO/ ot her medical officers.
● Undert ake surgeries simult aneously in mult iple
inj uries.
● Early surgery and repair of inj uries/ arrest of
bleeding should be done depending on t he na-
t ure of t he inj ury
● Record t he operat ive findings, procedure done
and Post-operat ive condit ion of t he pat ient .
● Record clinical condit ion at reasonable int ervals
in t he Post-operat ive period
● Follow medico legal requirement s and hospit al
rules at all t imes
● I nform pat ient ’s relat ives about t he condit ion of
t he pat ient at regular int ervals and alleviat e t heir
fears.
● I ssue t he discharge cert ificat e wit h required de-
t ails and also issue and cert ificat es required for
legal acion
Management of t he t r auma vi ct i m
on ar r i val of t he pat i ent at casual t y depar t ment
● Examine t he pulse, BP, level of consciousness,
orient at ion t o t ime, place and person and general
condit ion of t he vict im.
● I nit iat e life saving measures first
● Maint ain airway, breat hing and circulat ion
● Draw blood for invest igat ions (blood grouping,
cross mat ching, blood sugar et c.)
● Expose and examine wounds t horoughly
● I V access and fluid replacement should be init i-
at ed.
● I nj ect ion TT and dressing/ sut uring of obviously
bleeding inj uries.
● Transfer t o emergency room wit h paramedics
● Record event s:
* Record hist ory and event s simult aneously/
during t reat ment
* Record t he pulse BP, Level of consciousness,
orient at ion t o t ime, place and person and
general condit ion of t he vict im.
* Record t he Dat e, Time, and by whom t he pa-
t ient was examined wit h name in capit al let-
t ers and designat ion
* Record t he dat e t ime, place and det ails of
accident , and t he person bringing t he vict im
(relat ive/ at t endant / police)
* Sit e, size, dept h, number and t ype of wounds
should be recorded.
* I f t he vict ims breat h smells of alcohol/ under
t he influence of alcohol, it should be recorded.
* I f referred from some ot her hospit al/ Nursing
home/ clinic, t he referral not e should be at-
t ached and t he fact should be not ed in t he
accident regist er.
* Sign t he Accident Regist er wit h t he dat e and
name in capit al let t ers.
* Record t ransfer det ails and sign
* I nform RMO/ higher aut horit ies about VI Ps or
mass casualt ies
Dur i ng Tr ansf er
● Always accompany t he pat ient during t ransfer
● Cont inue fluid resuscit at ion during t ransfer
13
● Always sign t he records wit h dat e and name in
block let t ers.
Ot her Ser vi ces
● Arrange t ransport for t he vict im while referring or
during discharge (ambulance)
● I ssue necessary cert ificat es wit hout delay (AR
copy, wound cert ificat e et c.)
● Discuss wit h t he pat ient ’s relat ives and provide
psychological support t hroughout t reat ment
● Brain deat h cert ificat ion and possible organ do-
nat ion in brain deat h cases.
● Complet e formalit ies expedet iously when t he pa-
t ient expires
● Provide psychological support t o aggrieved family
members
● Arrange post mort em in medicolegal cases
● Send t he body t o t he mort uary wit hout delay
● Explain procedures t o be followed
● Handing over bodies t o right relat ives in case of
disput e wit h help of police and revenue officials
● Help in embalming if t ransport at ion t o a far off
place (embalming is done by anat omy depart-
ment aft er Post mort em by forensic medicine de-
part ment
● Arrange t ransport (mort uary van)
● I nform social organizat ions for cremat ion and last
rit es if needed by relat ives
Requi r ement f or Tr anspor t i ng bodi es by ai r
● Valid cert ificat ion from aut horit ies - hospit al and
police
● Embalming of t he body and embalming cert ifi-
cat e from professor of anat omy
● Needs special air t ight coffins specially made for
air lift ing bodies
Cardio - Thoracic Trauma
Causes
● Blunt inj uries
* Road Traffic Accident s
* Fall from height
* Assault
* Crush inj uries
● Penet rat ing inj uries
* St ab inj uries
* Gunshot wounds
* Missile inj uries
● Chest wall inj uries
* Rib fract ures
» Simple
» Mult iple
» Flail chest
* St ernal fract ure
* Shoulder Girdle fract ure
* Thoracic Spine I nj ury
● Pleuro Pulmonary I nj uries
* Pneumot horax
» Simple pneumot horax
» Tension pneumot horax
* Haemot horax
* Lung cont usion
* Lung lacerat ion
● Mediast nal I nj uries
* Cardiac Tamponade
* Aort a, large blood vessel inj ury
* Tracheo – bronchial inj ury
14
Chest wall injuries
Rib fracture
Symptoms
ł Chestpain
ł Dyspnea
ł Tachycardia
ł Cyanosis
Investigations
ł Chest X-ray PA view-
ł To detect fracture site, number of ribs involved to
diagnose associated pneumothorax, hemothorax
Treatment
ł Adequate Analgesia
ł Chest Physiotherapy
ł Intercostal drainage in case of pneumo or he-
mothorax
Sternal fracture
Symptoms
ł Chest pain
ł Dyspnea
ł Tachycardia
ł Hypotension if underlying cardiac injury
Investigations
ł Chest X-ray Lateral view
ł To detect fracture site, displacement
ł CT chest for definitive diagnosis
Treatment
ł Adequate Analgesia
ł Isolated sternal Fracture: If chest X-ray, ECG are
normal and if patient is stable,patient can be
discharged.
Shoulder Girdle Injury
Symptoms
ł Shoulder pain
ł Deformity
ł Tachycardia and Hypotension if Underlying sub-
clavian /axillary injury
Investigations
ł Chest X-ray PA view
ł To detect fracture site, involvement of ribs, diag-
nose associated pneumothorax.
ł Vascular opinion, if distal pulses not felt.
Treatment
ł Refer for ortho consultation after immobiliz-
ing and ruling out life threatening associated
Injuries
Thoracic Spine Injury
Symptoms
ł Back pain
ł Weakness of both lower limbs,
Flail chest mechanics
15
● Neuorgenic shock (don’t overload wit h fluids,
give vasopressors), asso.
● Associat ed rib fract ures.
I nvesti gati ons
● X-ray DL spine AP / lat eral.
● To diagnose fract ures, dislocat ion, associat ed rib
fract ures.
● MRI spine-t o assess ext ent of spinal cord inj ury
Treatment
● Rule out cervical spine inj ury,t ension pneumot-
horax.
● I n primary care cent re-immobilize spine and
referral t o t ert iary cent re for Ort hopedic consul-
t at ion
Pleuro - Pulmonary injuries
Symptoms
● Any of t he above inj uries l may occur alone or
co-exist wit h ot her chest and abdominal inj uries.
* Chest pain
* Dyspnea
* Tachycardia
* Cyanosis.
● I n Tension Pneumot horax:
* Hypot ension
* Cyanosis
* Tracheal hyper resonance.
● Persist ent hypoxia wit h low SaO2, low pO2: sus-
pect pulmonary cont usion
Pneumot hor ax
I nvesti gati ons
● Chest X-ray PA view
* To ident ify collapsed lung borders
* Hemot horax
* Tension pneumot horax (look for mediast inal
shift )
Treatment
● Urgent Needle decompression in 2nd int er cost al
space in mid-clavicular line in t ension Pneumot-
horax
● I CD for Pneumo - hemot horax
Pneumothorax - CT
Spontaneous Pneumothorax types
16
Hemot hor ax
I nvesti gati ons
● Chest X-ray PA view-I rregular opacit y in t he pleu-
ral cavit y if significant collect ion.
● CT Chest-sensit ive for minimal hemot horax.
Treatment
● I nt ercost al Drainage t o drain t he blood
● Emergency Thoracot omy
● I nit ial drain of 1500ml or persist ent drain >
200ml / hr.
Pul monar y cont usi on
I nvesti gati ons
● Suspect in any chest t rauma wit h persist ent
hypoxia.
● Chest X-ray PA view - less sensit ive, pat chy
homogenous opacit y in any lung zones
● CT Chest - definit ive for ext ent or sit e of cont u-
sion.
Treatment
● I nt ubat ion and mechanical vent ilat ion-key t o
management
● Ant ibiot ics t o prevent infect ion.
● I nt ercost al drainage, if hemot horax is present .
Mediastinal injuries
Car di ac Tamponade
Symptoms and si gns
● Hypot ension
● Muffled Heart sounds
● Dist ended neck veins
● Elevat ed JVP
I nvesti gati ons
● Chest X-ray: Widening of cardiac silhouet t e
● Ult rasound: Blood in pericardial cavit y
● ECG: less sensit ive, low volt age QRS, ST-T chang-
es.
Treatment
● Fluid resuscit at ion
● Pericardiocent esis under Ult ra sound guidance
● Direct Surgical Decompression: ensures clot re-
moval and complet e hemost asis.
Cardiac and Aortic injury
Symptoms
Cardiac cont usion can vary from clinically occult
and t ransient cardiac depression t o fat al rupt ure,
arrhyt hmias, LV failure
Mort alit y 80-90%
I nvesti gati ons
Diagnosis considered in all pat ient s sust aining
decelerat ing inj ury or st ernal impact ion. 2D ECHO is
t he best met hod.
Treatment
● Fluid resuscit at ion
● Pericardiocent esis under Ult rasound guidance.
● Direct Surgical Decompression: ensures clot re-
moval and complet e hemost asis.
Tracheo - bronchial injury
Symptoms
● Hemopt ysis
● Dyspnea
● Subcut aneous and mediast inal emphysema
● Pneumot horax and air leak.
I nvesti gati ons
Pulmonary contusion
17
● Chest X-ray: Pneumomediast inum, Pneumot ho-
rax, Pleural effusion.
● Bronchoscopy: import ant in diagnosis and in se-
lect ive endobronchial int ubat ion.
Treatment
Early surgical correct ion is needed and immediat e
referral t o a specialist , once vit als are st abilized. I t is
import ant t o maint ain vent ilat ion in t he wait ing period
by using endobronchial t ubes or high frequency j et
vent ilat ion.
Principles of surgery
“ The surgeon should have an eagle’s eye, a lion’s
heart and lady’s fingers”
The aim of surgery is t o cure pat ient s and provide
relief from pain and disabilit ies.
The maj or principle is t o make surgery safe and
beneficial t o pat ient s
The safet y and success of surgery depend on t he
following
● Early correct diagnosis
● Thorough preoperat ive assessment and good
preparat ion
● Smoot h conduct of anaest hesia
● Correct surgical t echnique
● I nt ensive Post-operat ive care
● Ant icipat ing complicat ion (s) and early int er-
vent ion (s)
● Cont inued follow up and rehabilit at ion
● Dedicat ed t eam
Ear l y cor r ect di agnosi s and deci si on maki ng
● Confirm clinical diagnosis by invest igat ions
● Observe cont inuously and examine frequent ly t o
diagnose and t o underst and t he progression or
det eriorat ion of t he pat ient ’s condit ion.
● Offer t he best opt ion (beneficence), when mult i-
ple modalit ies of t reat ment are available (surgical
and non-surgical).
● Discuss t he medical problem wit h t he pat ient /
relat ives/ family physician. Always respect t he
pat ient ’s preference (aut onomy) in t he t reat ment
● Weigh t he course of t he disease and t he out come
of surgery, benefit s and complicat ions of surgery
before planning a procedure
● Prefer minimal access, endo surgery and non-
invasive procedures wherever possible for t he
convenience and rapid recovery of t he pat ient
Pr eoper at i ve assessment and cor r ect i on of co-
mor bi di t i es
● Examine t he pat ient complet ely t o diagnose t he
problem and assess t he physical condit ion for an-
aest het ic fit ness and surgery.
● Assess t he condit ion of t he heart , lung, kidney
and CNS funct ions.
● Treat co-morbid condit ions (diabet es, hypert en-
sion, cardiac and pulmonary ailment s et c) and
bring t he pat ient t o near normal condit ion (fluid
and elect rolyt e abnormalit y, t reat ment of sept i-
cemia et c) before anaest hesia and surgery.
I nvesti gati ons
● Assess t he physical condit ion by necessary inves-
t igat ions t o correct any abnormalit y
● Record t he dat e of invest igat ions and result s in
t he case sheet .
● Avoid unnecessary and repeat ed invest igat ions.
Good pr eoper at i ve pr epar at i on
● Prepare t he pat ient physically and ment ally for
anaest hesia and surgery.
● Plan preoperat ive st rat egy, t iming of surgery, se-
lect ion of t eam and Post-operat ive requirement of
inst rument s,equipment s,vent ilat ors,blood, int en-
sive care, et c.
● Discuss t he procedure, t he problems expect ed
and t he out come of t he procedure before surgery
wit h t he anest het ist and t he surgical t eam and be
prepared t o t ackle t he unexpect ed on t able
● Discuss frankly about t he problem, procedure
and explain t he possible risks involved in surgery
and anaest hesia wit h t he pat ient / relat ives and
obt ain a det ailed informed consent
● Writ e preoperat ive inst ruct ions clearly in t he case
sheet wit h t he provisional diagnosis, t he surgical
procedure planned and sign.
Oper at i on t heat r e pr i nci pl es
● Maint ain t heat re discipline st rict ly
● Pract ice asept ic t echniques always
18
● Administ er premedicat ion preferably in t he t hea-
t re under t he supervision of t he Anest het ist .
● Reassure t he pat ient again when he / she is shift-
ed t o t he operat ion t able.
● Reconfirm t he correct pat ient , t he diagnosis and
t he sit e of lesion before giving anaest hesia and
surgery
● Posit ion t he pat ient on t he t able properly before
washing up.
Cor r ect sur gi cal t echni que
● Maint ain st rict asepsis t hroughout t he surgical
procedure.
● Plan incision t o give adequat e exposure.
● Perform t he correct procedure required aft er as-
sessing t he condit ion on t he t able.
● Handle t issues gent ly, use diat hermy t o t he mini-
mum.
● Select proper sut ure mat erials.
● Close wound in layers, place drains if needed.
● Keep blood loss t o t he minimum.
● Avoid single unit t ransfusion, st rict ly follow blood
t ransfusion norms.
Post -oper at i ve car e
1. I mmediat e - I n t he operat ion t heat re
* Ensure complet e recovery of t he pat ient from
anaest hesia.
* Record t he operat ive procedures in det ail and
t he condit ion of t he pat ient before leaving t he
operat ion t heat re
* Writ e Post-operat ive inst ruct ions clearly.
* Send t issues/ biopsy mat erial t o hist o pat ho-
logical and microbiological examinat ion aft er
proper labelling and writ ing requisit ion clearly
wit h proper clinical pict ure.
2. I n t he Post-operat ive ward
* Monit or closely during t he Post-operat ive pe-
riod.
* Maint ain fluid, elect rolyt e balance and glyc-
emic cont rol.
* Ant icipat e problems and int ervene if required.
* Care wound and drains properly.
* Maint ain psychological support t o t he pat ient by
t he surgical t eam, st aff nurses,counselors,social
workers and t he relat ives t hroughout t he
hospit al st ay.
Fol l ow-up and r ehabi l i t at i on
● Follow-up and rehabilit at ion is essent ial in case of
mut ilat ing surgeries, amput at ions and in elderly.
● Refer pat ient s t o higher cent ers for possible re-
const ruct ive/ cosmet ic surgery, t o enable t hem t o
lead an independent and normal life.
● Rehabilit at e / provide art ificial limb for amput ees
t o make t hem independent .
● Explain t he available welfare measures offered
t o t hem by government al and non-government al
organizat ions.
I mpor t ant Not e
● Weigh t he benefit s, complicat ions and nat ural
course of t he disease before embarking on sur-
gery.
● Avoid unnecessary surgery.
● Provide emergency care always and inst it ut e life-
saving measures immediat ely.
● Refer pat ient s t o specialist s / higher cent er for
minimal access surgery/ non invasive t reat ment if
available / required.
● Ensure safet y in emergency surgery and do t he
minimum necessary procedure.
● Be prepared for t he unexpect ed in surgery all t he
t ime.
● Follow medical et hics, moral values and legal for-
malit ies st rict ly.
● Do good and do no harm, always t reat pat ient s
wit h t ender loving care.
“All surgeons know how t o operat e, a good surgeon
knows when t o operat e, but a great surgeon knows
When not t o operat e.
Examination of surgical patients
● Elicit complet e hist ory before proceeding t o ex-
amine t he surgical pat ient .
● Examine t he pat ient complet ely from head t o t oe.
● Physical examinat ion includes General and Local
examinat ion.
● Record findings wit h dat e and t ime in t he case
sheet and sign.
19
● A good hist ory may lead t o t he diagnosis in most
of t he pat ient s or it may direct t he surgeon t o t he
diseased organ or syst em
Gener al assessment of t he sur gi cal pat i ent
Ment al st at us
Record ment al st at us (level of consciousness) in
all pat ient s, especially in geriat ric, neurological, head
inj ury and in medico-legal pat ient s
Five st ages of level of consciousness:
3. Conscious wit h orient at ion t o t ime, place and
person.
4. Conscious but not orient ed
5. Drowsy (semi consciousness).
6. St upor (unconscious), responds t o painful st imuli.
7. Coma (unconscious), no response t o painful st im-
uli.
Bui l d and st at e of nut r i t i on:
Build and st at e of nut rit ion of t he pat ient will give
clue t o t he
Clinical diagnosis
Cachexia in malignancy.
Chronic nat ure of t he disease.
Requirement of preoperat ive nut rit ional support
(wound healing).
Nut rit ional st at us includes hydrat ion.
Faci es
By looking at t he face t he ment al st at e and
int elligence, t he severit y of pain, diseases and effect of
t reat ment can also be gauged. There are some t ypical
facies such as:
‘Facies hippocrat ica’ in generalized perit onit is
‘Risus sardonicus’ in t et anus
‘Adenoid facies’ in hypert rophied adenoids
At t i t ude and decubi t us
The at t it ude and posit ion of t he pat ient in bed is
informat ory.
Example:
The pat ient wit h cerebral irrit at ion lies curled up
on his side away from light .
Perit onit is pat ient s wit h pain lie st ill.
Colicky pain pat ient s become rest less and t oss
on t he bed.
Meningit is of t he neck will show neck ret ract ion
and rigidit y.
Fract ure neck of femur, t he lower limb may be
lying in helpless eversion.
Vi t al Si gns
Pulse
I ndicat es cardiovascular condit ion and severity of illness
Examine all peripheral pulses for
● Rat e – fast ,eg: t hyrot oxicosis and ap
pendicit is slow t hready pulse,
eg. hypot ension and shock
● Rhyt hm – regular or irregular, in cases of
at rial fibrillat ion
● Condit ion of art erial wall – t hickening (e.g) art e -
riosclerosis et c.
Respi r at i on
Type:
● Thoracic- in females, massive ascit is, huge ab-
dominal mass et c.
* Abdominot horacic – in males
Rat e:
Tachypnoea - Fast breathing eg: in fever,
shock, hypoxia,
* cerebral dist urbances, met abolic acidosis,
t et any, hyst eria et c.
* Slow and deep respirat ion is an ominous sign
in cerebral compression.
* Dyspnoea (difficult y in breat hing) is an omi-
nous sign and has t o be at t ended first before
* at t empt ing t o do a complet e examinat ion
Temper at ur e:
Normally t aken in t he mout h, axilla or rect um
Rect al or core t emperat ure is usually 1 F more t han t he
peripheral, axillary t emperat ure
Post-operat ive t emperat ure is an import ant
paramet er.
Fever is an early indicat or of sepsis
Local exami nat i on
“ Eyes do not see what t he mind does not know”
I nspect i on
● Make t he pat ient comfort able and examine com-
plet ely.
20
● Ensure adequat e privacy and expose t he part s t o
be examined.
● Observe t he pat ient in good light , preferably in
daylight .
● Examine t he female pat ient s in t he presence of a
female st aff nurse.
● Compare wit h t he corresponding normal side
wherever possible.
● Post pone det ailed examinat ion in acut ely and se-
verely ill pat ient s.
● Look for any abnormalit ies such as presence of
swellings, ulcers, sinus, scars, engorged veins,
pigment at ion et c specially look for pulsat ions and
perist alsis in t he abdomen
Pal pat i on
● Confirm t he inspect ion findings
● Feel for t he warmt h and t enderness
● Palpat e gent ly when t he lesion is t ender
● Follow det ailed and met hodical palpat ion.
Per cussi on
To find out t he presence of gas, fluid in t he abdomen
(ascit is, effusion, perforat ed hollow viscus) To
different iat e bet ween a solid or hollow viscus (liver,
st omach, colon) To access t he enlargement of solid
organs (upward enlargement of liver)
Auscul t at i on
Auscult at e chest and abdomen t o make out
abnormalit ies in heart and breat h sounds and t he
presence of perist alsis, murmurs, bruit s et c.
Movement s
Record range of movement and abnormal movement s
in ort hopaedic cases and in nerve inj uries
Measur ement s
Record measurement s of abdominal girt h in
int est inal obst ruct ion (progression) swellings, ulcers
( reduct ion of size during t reat ment ) inj uries in
medicolegal cases (lengt h, breadt h dept h, sit e, nat ure)
fract ures in ort hopedic cases ( reduct ion of limb lengt h )
I mpor t ant Not e
Local examinat ion is never complet e wit hout t he
examinat ion of t he draining lymph nodes and t he
examinat ion of t he draining area is import ant when
t here is lymph node enlargement . eg; oral examinat ion
in a case of cervical adenit is.
Gener al exami nat i on
I n chronic cases, examine t he pat ient as a
whole, aft er complet ing t he local examinat ion.
General examinat ion is required mainly for t he following
purposes:
● Arrive at a complet e diagnosis
● Assess t he physical condit ion and co-morbid con-
dit ions
● Decide t he t reat ment modalit y et c.
● Select t he t ype of anaest hesia
● Det ermine t he nat ure of t he operat ion
● Det ermine t he prognosis
1. Head and neck
Examine
* Eyes,
* Oral cavit y,
* Cranial nerves,
* Neck nodes,
* Neck veins,
* Carot id pulsat ions,
* Posit ion of t rachea and neck movement s.
2. Thorax
Examine t he t ype of chest ,
* Crowding of ribs,
* Winging of scapula,
* Kyphoscoliosis,
* Chest movement s,
* I nt ercost al t enderness
* Presence of any dilat ed vessels and pulsa-
t ions,
* Apex beat ,
* Heart and lungs,
* Upward enlargement of t he liver,
* Oblit erat ion of liver dullness.
3. Abdomen
* Examine wit h pat ient lying comfort ably in t he
couch fully exposed wit h hips and legs flexed
and abdominal muscles relaxed and pat ient
breat hing easily.
21
* I nspect t he t ype of abdomen: scaphoid-boat
shaped (normal) or dist ended (generalized or
localized)
* Abdominal wall – posit ion of t he umbilicus,
presence of scars, dilat ed vessels, abdominal
reflexes, visible perist alsis or pulsat ion.
* Hernial orifices, lymph nodes.
* Abdominal examinat ion is incomplet e wit h-
out t he examinat ion of scrot um, perineum,
inguinal region, back and rect al examinat ion.
4. Examine t he back including t he spinal column
5. Gynaecological examinat ion should be done in
female pat ient s
6. Upper and lower limbs
* General examinat ion of t he arms and hand
wit h part icular reference t o t heir vascular sup-
ply and nerve supply (power, t one, reflexes
and sensat ions), axillae and lymph nodes,
j oint s, finger nails – clubbing or koilonychia
* General Examinat ion of legs and feet – wit h
part icular reference t o t he vascular supply
and nerve supply (Power, t one, reflexes and
sensat ion), varicose vein, edema, j oint s.
7. Ot her examinat ions:
Examine Sput um, vomit , urine, and st ool by naked eye
and under microscope, if required.
Physi cal f i ndi ngs i n r el at i on t o di sease condi t i on and r i sk
Organ /
Syst em
Finding Disease/ Condit ion Risk
Eyes Jaundice Liver disease Bleeding, encephalopat hy
Skin Pallor
Cyanosis (peripheral and cent ral)
Lesions
Scars
Turgor
Anemia
Poor perfusion, Frost bit e
Dermat osis
Prior Surgery
Reduced, lost
Heart failure
I schemia
I nfect ion
adhesion, alt ered
anat omy,
dehydrat ion
Nails Clubbing
Cyanosis
Koilonychia
Lung disease
Lung disease
Anemia
Respirat ory reserve
reduced
Heart failure
Heart Hypert ension
Hypot ension
Bradyarrhyt hmia
Tachyarrhyt hmia
Murmur
Bruit
Mult iple et iologies
Mult iple et iologies
Coronary art ery disease
CAD, Hypert hyroidism
Valvular disease,
At herosclerosis
Heart failure
Lung Rales
Wheeze
CHF, COPD,
Pulmonary infect ion
COPD, ast hma
Respirat ory reserve
reduced
Abdomen Hepat omegaly
Mass Lymphadenopat hy
Liver disease,
cancer, infect ion
Encephalopat hy
Delayed healing
Musculo-
skelet al
St iff neck
Rest rict ion of movement s
Art hrit is
Art hrit is
I mmobilit y
I ncreased falls
Gait Unst eady
waddling
Trendelenberg
Alcoholism
Bilat eral dislocat ion of hip
coxavera
muscle dyst rophies, polio,
pert he’s art hrit is
I ncreased fall
Nervous Sensory impairment
Focal deficit s
Mult iple et iologies
CVA, ot hers
I nj ury
Paralysis, convulsion
22
I mpor t ant Not e
● Undert ake life-saving measures first before com-
plet e examinat ion in emergency.
● Modify t he order of examinat ion in children / eld-
erly / in emergency
● Explain and get pat ient ’s permission before phys-
ical examinat ion (rect al, vaginal Examinat ion)
● Always examine t he female pat ient in t he pres-
ence of a st aff nurse and ensure privacy
● Never forget t o peruse t he old records or exam-
ine t he pat ient complet ely including t he draining
lymph nodes, rect al examinat ion et c
Preoperative assessment and
preparation
Perioperat ive care is a t erm which encompasses t hree
main component s of surgical management , which are
int erlinked and t o be followed st ep by st ep met iculously
t o achieve t he best result s following surgery.
Preoperat ive Phase
PERI OPERATI VE CARE
I nt raoperat ive Phase
Post operat ive Phase
Assessment Preparat ion
Anaest hesia Operat ion
Early/ Lat e Post
Operat ive Care
Rehabilit at ion and
followup
Pr eoper at i ve assessment
Preoperat ive assessment is done t o:
● Evaluat e t he physical st at us of t he pat ient
● I dent ify t he co-morbid condit ions
● Plan t reat ment modalit y, assess operabilit y
● Opt imise pat ient ’s condit ion preoperat ively
Preoperat ive preparat ion depends on t he follow-
ing:
* The diagnosis (condit ion, st age of t he dis-
eases)
* Proposed surgical int ervent ion and nat ure
(elect ive/ emergency, maj or/ minor)
* Pat ient ’s healt h, associat ed risk fact ors and
pat ient ’s preferences
Pr eoper at i ve assessment consi st s of t he
f ol l owi ng
● Comprehensive hist ory including medicat ion re-
view
● Physical examinat ion
● Nut rit ional assessment
● Surgical risk assessment and decision making
Hi st or y and medi cat i on r evi ew
● Elicit t horough hist ory from t he pat ient in his own
words.
● Elicit hist ory from mot hers for children and from
relat ives/ caregivers for elders.
● Record present ing complaint s and t he onset of
sympt oms and progression of t he disease in
chronological order.
● Elicit personal hist ory which includes smoking,
alcoholism, previous illnesses like recent myo-
cardial infarct ion, pulmonary t uberculosis, COPD,
seizures, j aundice, AI DS, cancer, diabet es, previ-
ous surgery and drug allergies.
● Obt ain list of medicat ions, over-t he-count er
drugs, herbal preparat ions and ingest ion of as-
pirin, NSAI D, diuret ics, oral hypoglycemic agent s,
sedat ives, et c
Physi cal Exami nat i on
● Assess t he physical condit ion and ident ify co-
morbid condit ions.
● Focus on det ailed, met hodical examinat ion, in-
spect ion, palpat ion, percussion, auscult at ion,
mobilit y and fixit y et c, t o arrive at t he anat omical
diagnosis.
● Proceed t o find out t he pat hological diagnosis
such as congenit al, inflammat ory, neoplast ic or
degenerat ive, met abolic or hormonal pat hology.
● Cont inuous/ frequent serial observat ion over a
period of t ime, is somet imes helpful in achieving
t he diagnosis.
● Examine regional lymph nodes for any enlarge-
ment . When lymph nodes are enlarged, draining
area should be examined and examinat ion of t he
lesion is not complet e wit hout examinat ion of re-
gional lymph nodes.
● I dent ify Cardiovascular or respirat ory signs such
as t achycardia, hypert ension, JVP elevat ion, ar-
23
rhyt hmias, murmurs, S3 gallop, edema, cyano-
sis, rales and rhonchi, bronchospasm and chest
deformit y
Nut r i t i onal Assessment and Pr epar at i on :
● Assess t he st at e of nut rit ion clinically (Body Mass
I ndex) and biochemically.
● Assess fluid st at us along wit h t he nut rit ional st a-
t us.
● Est imat e serum albumin level (> 6mg/ dl normal).
● Poor nut rit ion causes poor wound healing (wound
dehiscence, infect ion, development of pressure
sores, weakness and loss of funct ion).
● Consider parant eral nut rit ional supplement a-
t ion. TPN is useful in gast ric out let obst ruct ion,
pancreat it is, alcoholism, malnut rit ion and Post-
operat ive pat ient s. Parent ral nut rit ion is cost ly.
● Prefer ent eric rout e as soon as possible t o pre-
vent Gut Bact erial Translocat ion
Cogni t i ve and Funct i onal Assessment
● Record t he preoperat ive level of act ivit y and
baseline ment al st at us in t he elderly/ neurologi-
cal pat ient s.
● Ment al st at us allows t he physician t o recognize
delirium.
● To predict pot ent ial problems and t o plan int er-
vent ions.
● Poor funct ional st at us carries a high surgical risk.
I nvest i gat i on
● To confirm t he diagnosis
● To assess t he physical condit ion of t he pat ient for
fit ness for anaest hesia and surgery.
● Assess t he necessit y, benefit s, complicat ions and
cost of invest igat ion
● Avoid unnecessary and repeat ed invest igat ions.
● Biochemical -blood urea and sugar; serum creat i-
nine and lipid profile
● Clinical pat hological complet e urine analysis and
blood count
● Radiological -X-ray chest PA view and ult ra-sono-
gram abdomen
● Cardiological -ECG
Special invest igat ions may be carried out depending
upon t he pat ient s’ condit ion and indicat ions
* For diagnosis: endoscopy, barium meal, en-
ema st udies, art eriography, FNAC
* To assess t he st at us of cardiovascular, respira-
t ory, neurological, renal, hepat ic and t hyroid
funct ions
* For maj or and high-risk surgery e.g echocar-
diography, angiography, CT, MRI , ult rasono-
gram, ABG enzyme analysis et c,.
* St udy t he invest igat ion report s and correlat e
wit h t he clinical pict ure of t he pat ient and
writ e t he remarks in t he medical record be-
fore ordering furt her invest igat ion or init iat ing
t reat ment
Di agnosi s
Preoperat ive diagnosis and planning is import ant for
t he smoot h conduct of surgery.
I n emergency, life-saving sit uat ions, explorat ion
and rest orat ion of vit al funct ions are more import ant .
eg: head inj uries, t horaco abdominal inj uries, t hen
peripheral and skelet al inj uries
Tissues removed should be sent for hist opat hological
examinat ion properly preserved and labeled for
pat hological diagnosis.
Sur gi cal r i sk assessment and deci si on maki ng
● The benefit of surgery should be weighed against
t he possible complicat ions and risks.
● Surgical risk assessment also includes t he anaes-
t het ic risk.
● Anest het ist should assess t he surgical pat ient
preoperat ively and his opinion and suggest ions
should be carried out t o bring t he pat ient t o near
normal levels pre- operat ively.
American societ y of anest hesiologist (ASA) physical
st at us classificat ion has been used successfully t o
st rat ify operat ive risk.
ASA cl assi f i cat i on
1. Normal healt hy pat ient s
2. Pat ient wit h mild syst emic disease
3. Pat ient wit h severe syst emic disease t hat limit s
act ivit y but it is not incapacit at ing
4. Pat ient has incapacit at ing disease t hat is a con-
st ant t hreat t o life
5. Moribund pat ient not expect ed t o survive 24
24
hours wit h or wit hout an operat ion
Car di ovascul ar syst em
● The capacit y t o increase t he cardiac out put in re-
sponse t o int ra and Post-operat ive challenges is a
fundament al det erminant of survival of t he pa-
t ient .
● Acut e fall in vent ricular preload leads t o
hypot ension; acut e increase leads t o vent ricular
and pulmonary congest ion and should be avoid-
ed.
Hi gh r i sk pat i ent s
● Hist ory of ischemic heart disease, conges-
t ive cardiac failure, cerebrovascular disease,
t hromboembolism, and hyperlipidemia
● Preoperat ive serum creat inine higher t han 2 mg
/ dl
Preoperat ive t reat ment wit h insulin
Per i -oper at i ve st r at egi es
● Complet e cardiac work up: ECG, ECHO, st ress
t est .
● Cardiologist opinion and t reat ment .
● Wait for 4 t o 6 weeks aft er myocardial infarct ion
for elect ive surgery.
● St op ant i-plat elet drugs one week prior t o sur-
gery.
● Bet a-blocker and aspirin significant ly reduces
mort alit y and morbidit y in cardiac pat ient .
Respi r at or y syst em
Evaluat e t he pulmonary funct ions for t horacic,
abdominal and maj or surgeries.
I nvesti gati ons
Necessary t est s include forced expirat ory volume
at one second (FEV1) t he forced vit al capacit y
and t he diffusing capacit y of carbon monoxide.
Ri sk f act or s f or Post -oper at i ve pul monar y
compl i cat i ons:
● Thoracic, upper abdominal surgery and maj or
surgeries.
● Preoperat ive hist ory of COPD, purulent produc-
t ive cough, cigaret t e smoking.
● Anaest hesia t ime more t han 3 hrs.
● Geriat ric, obese and hypoprot einemic pat ient s.
Per i oper at i ve st r at egi es
● St op smoking
● Pre and Post-operat ive chest physiot herapy
● Vigorous pulmonary t oilet t e and rehabilit at ion
● Cont inue bronchodilat or t herapy
● Use of epidural anaest hesia
Renal syst em
● I dent ify cardio vascular, circulat ory, haemat ologic
and met abolic derangement s secondary t o renal
dysfunct ion
● Treat anaemia wit h eryt hropoiet in.
● Evaluat e coagulat ion - uremia may t rigger coagu-
lopat hies.
● Preoperat ive dialysis for chronic end-st age renal
disease pat ient s.
● Avoid nephrot oxic agent s and maint ain adequat e
int ravascular volume t o prevent secondary renal
insult
● Use narcot ics for Post-operat ive pain cont rol may
have a prolonged effect in spit e of hepat ic clear-
ance in pat ient s wit h renal impairment .
Hepat obi l i ar y syst em
I nvest igat ion for liver dysfunct ion
● Serum albumin
● Prot hrombin
● Fibrinogen
● CBC
● Serum elect rolyt es
Malnut rit ion is common in cirrhot ic pat ient s; advice
appropriat e ent eral supplement at ion.
Endocr i ne syst em
● Pat ient s wit h diabet es mellit us, hyper or hypot hy-
roidism, or adrenal insufficiency have increased
physiological st ress during anaest hesia and sur-
gery
● I dent ify complicat ion of diabet es mellit us and
maint ain glycemic st at us adequat ely
● Est imat e blood sugar t wo hours prior t o surgery
25
● Swit ch over t o insulin from oral hypoglycemic
drugs for bet t er glycemic cont rol
● Supplment st eroid for a presumed abnormal ad-
renal response t o periperat ive st ress in case of
st eroid use (eg: prednisolone< 5 mg).
● I dent ify t ype and degree of endocrine dys func-
t ion and t reat accordingly
Vulnerable groups Expect ed problems
● Children
● Pregnancy
● I mmuno com-
promised
● Elderly
● Hy pot her mi a, bl ood
loss and fluid
imbalance
● Abort ion, drugs cross-
ing placent al barrier
● Florid infect ion, poor
wound healing
● Loss of funct ional re-
serve and complica-
t ions
Cent r al ner vous syst em
CNS problesm such as dement ia and delirium are
associat ed wit h poor prognosis special considerat ion
should be given t o vulnerable groups
Preoperat ive check list :
● Consent for surgery
Record t he consent in t he casesheet which rep-
resent s t he result of discussion (s) wit h t he pa-
t ient and family members regarding t he risks and
benefit s of t he proposed surgery.
● Get consent preferably writ t en and signed by t he
pat ient aft er making him underst and t he implica-
t ions of anaest het ic and surgical risks
● Counseling
The surgeon should gain t he confidence of t he pa-
t ient wit h his kind approach and frank discussion on
t he problem, and possible benefit s and risks espe-
cially in cases involving amput at ion or possible dis-
abilit y or disfigurement . Preoperat ive counseling
by t he doct ors, t rained st aff, social workers and
pat ient s who have undergone mut ilat ing surgery
such as mast ect omy or colost omy, will prevent or
reduce depressive effect .
● Prevent ion of respirat ory complicat ions
Cessat ion of smoking
Reducing secret ions
Treat ing bronchospasm
Chest physiot herapy
● Aspirat ion prevent ion
Prevent ion of aspirat ion is t he most import ant
aspect of perioperat ive care St arving t he pat ient
for 6-8 hours prior t o surgery Naso gast ric aspira-
t ion ( Ryle’s t ube ) during surgery I n emergency,
st omach cont ent s t o be empt ied by aspirat ion be-
fore giving anaest hesia
● Preparat ion of bowel
GI T surgery needs complet e evacuat ion and
cleansing of aliment ary t ract . St erilizat ion of t he
bowel by oral ant i microbial agent s should not
be done rout inely. Rout ine nasogast ric t ube as-
pirat ion and st rong purgat ives, enemas are not
indicat ed in elders, since it produces dehydrat ion
and exhaust ion
Ot her s:
● Blood grouping and Rh t yping: Blood grouping
and Rh t yping should be done; reserve necessary
unit s of blood for possible requirement .
● Sleep: Good sleep should be ensured on t he night
before surgery (mild sedat ion)
● Skin preparat ion: Skin preparat ion of local area
viz., haircut , shaving of local part s should be
done, t aking care not t o inj ure t he skin.
● Bat h: Pat ient should be given a good bat h before
surgery and draped in operat ion t heat re clot hing,
cap and overshoes
● Bladder cat het erizat ion: I nsert ion of urinary
cat het er t o prevent Post-operat ive dist ension of
t he bladder and t o measure t he urine out put dur-
ing surgery are import ant in maj or surgeries and
especially in elders.
● Pre-medicat ion: Rout ine pre-medicat ion for an-
aest hesia is best avoided in t he ward and is given
in t he operat ion t heat er under t he direct supervi-
sion of t he anest het ist .
Pr ophyl act i c measur es:
● Ant ibiot ic propylaxis: Prophylact ic ant ibiot ics are
essent ial in elders undergoing valvular surgery
wit h risk of endocardit is, oral, bowel, biliary, pul-
monary and urological procedures.
● I mmunizat ion: Tet anus immunizat ion by t et a-
nus t oxoid inj ect ion may be given during t he
26
first consult at ion t o allow t ime t o develop act ive
immunit y. I t is essent ial t o give inj . Tet anus im-
munoglobulin 500 unit s int ra muscularly before
surgery t o achieve passive immunit y, especially
in t rauma cases, road t raffic accident inj uries and
in emergency surgery.
● Thromboembolism: This complicat ion is very
common among t he elderly especially in cauca-
sians. To prevent t hromboembolism, measures
such as pneumat ic compressive st ockings, exer-
cises, early ambulat ion and ant icoagulant t hera-
py are inst it ut ed.
I mpor t ant Not e
● Writ e preoperat ive orders clearly in t he case
sheet indicat ing t he diagnosis, t he sit e and side
of lesion, blood group, procedure planned and
sign.
● Reconfirm t he correct pat ient , diagnosis, and side
of t he lesion before put t ing t he pat ient on t he op-
erat ion t able and before giving anaest hesia.
● Operat ion will proceed smoot hly if t he prepara-
t ion is good and expect ed findings are present
on t he t able.
Pr eoper at i ve assessment and pr epar at i on
Preoperat ive assessment Preoperat ive preparat ion
Complet e hist ory
chief complaint s h/ o present illness
I nvest igat ion for t he diagnosis and co-morbid condit ions.
assurance, counseling
Past hist ory; Previous medical illness / surgery
DM, HT, I HD, laparot omy, hernia)
Treat ment of co-morbid condit ions. I mprove cardiovascular,
respirat ory funct ions Cont rol diabet es and hypert ension
Medicat ion review non-prescript ion OTC drugs
herbal and nat ive medicines NSAI Ds, aspirin,
OHA, sedat ives H/ o drug allergies.
St op unnecessary OTC drugs, aspirin, and oral hypoglycemic
drugs before surgery.
Personal hist ory habit s, at t it udes, beliefs and
life st yle. H/ o smoking and alcoholism.
St op smoking and alcohol int ake. Exercise and chest
physiot herapy t o improve respirat ory reserve.
Family and caregiver hist ory
Availabilit y of family support and caregivers,
St ress fact ors
Det ailed discussion wit h pat ient and t heir family, (and referring
physician) about t he diseases, procedures planned and it s
complicat ions and expect ed out come. Ascert ain pat ient ’s wishes
and preference (s). Get advance direct ives.
I nformed consent for t he procedure.
Physical and general examinat ion
Lymphadenopat hy, ascit ies, edema CVS, RS,
CNS, abdomen, scrot um and perineum.
Assess general condit ion, operabilit y, fit ness for anaest hesia.
Chest physiot herapy and counseling
Cognit ive and funct ional assessment Baseline assessment of cognit ive funct ion and funct ional level t o
be recorded
Nut rit ional assessment Under nourishment , hypoprot einemia, anaemia, dehydrat ion and
elect rolyt es imbalances t o be correct ed.
Parent eral nut rit ion in condit ions such as gast ric out let
obst ruct ion, pancreat it is.
Surgical risk assessment including anaest het ic
risk
The benefit of surgery t o be weighed against t he possible
out come and complicat ions. Preoperat ive anaest het ic
assessment and correct ion of deficiencies
27
Anaesthesia
One of t he achievement s of modern medicine is
it s abilit y t o keep t he pat ient s free from pain t hrough
newer and more pot ent drugs and newer anaest het ic
t echniques. The pat ient should not only be free from
pain, but also be safe during anaest hesia and surgery.
Good anaest hesia should be safe wit h smoot h induct ion,
maint enance and quick reversal wit hout producing any
CVS, RS, and CNS complicat ions.
The maj or risk fact ors
● Poor general condit ion and co-morbid condit ion
● Maj or / emergency surgery
Choi ce of anaest hesi a depends on
The pat ient ’s general condit ion
● Nat ure of surgical procedure
● The experience of t he anest het ist and familiarit y
wit h t he procedures
Types of anaest hesi a
General anaest hesia
Regional anaest hesia - spinal / epidural / local
Local / regional anaest hesia is given by way of
infilt rat ion, field or nerve blocks, and epidural or
spinal, (safer opt ion in select ed cases.)
Local anaest hesi a
Topi cal and i nf i l t r at i on
● Topical anaest het ic agent s are used on t he skin,
uret hra, nasal mucosa and cornea
● I nfilt rat ion anaest hesia for very small lesions / bi-
opsies 1% lignocaine int o / around t he t issues t o
produce analgesia
● Easily administ ered
● St arvat ion not required
● Test dose should be given before infilt rat ion
● Cont raindicat ed in local infect ion and in coagula-
t ion disorders
Regi onal anaest hesi a
Regional anaest hesia is commonly administ ered
in elect ive surgeries. This involves blockade of
maj or nerve t runks, which innervat es t he sit e of
surgery.
The t wo t ypes of regional anaest hesia are spinal
and epidural,
I n spinal anaest hesia t he drug is inj ect ed int o t he
subarachnoid space (int rat hecal)
I n epidural anaest hesia t he drug is inj ect ed int o
epidural space.
Advant ages
● Advant ageous in debilit at ed pat ient s
● Reduces bleeding, Post-operat ive respirat ory
problems and deep vein t hrombosis
● Diminishes st ress response and CNS complica-
t ions
● Decreases convalescence t ime and facilit at es ear-
ly ambulat ion
● Minimizes requirement s of Post-operat ive analge-
sia
● Reduces mort alit y
Di sadvant ages
● Technically difficult
● Epidural is less reliable
● Supplement al sedat ion (compensat ion for inad-
equat e regional anaest hesia) carries risks eg:
airway obst ruct ion, pulmonary aspirat ion and
agit at ion.
Si ngl e dose anaest hesi a
A single dose epidural or spinal anaest hesia is used
t o provide short period of very effect ive analgesia during
operat ion.
Cont i nuous epi dur al anaest hesi a
A st erile epidural cat het er is insert ed int o t he epidural
space and anaest het ic agent is inj ect ed at regular
int ervals and analgesia provided for many hours or even
days. This is part icularly valuable in pat ient s wit h poor
respirat ory funct ions in abdominal or t horacic surgeries.
Gener al anaest hesi a
GA is fast er and reliable
Difficult y in elders- due t o cervical spine problem
and t racheal narrowing.
Di sadvant ages
● Difficult int ubat ion
● Myocardial depression
28
● CNS complicat ions
Causes
Pot ent ial causes of int raoperat ive inst abilit y
1. Hypot ension,
2. Hypoxia,
3. Hypot hermia,
4. Anaphylaxis
5. Malignant hypert hermia
I mpor t ant Not e
Anaphyl axsi s
● Causat ive agent s: muscle relaxant s, lat ex, induc-
t ion agent s et omidat e, t hiopent one, propofol and
narcot ic agent s
● Manifest at ion: cut aneous erupt ions, hypot en-
sion, cardiovascular collapse, bronchospasm and
deat h
● Treat ment : I n suspect ed cases I nj epinephrine
0. 3 t o0.5ml of 1: 1000 sc
● I n severe anaphylaxis give epinephrine 0.5 ml
I V at 5 -10 minut es int erval/ hist amine blockade
wit h diphenhydramine and hydrocort isone, fluid
boluses, pressors, oro t racheal int ubat ion ,neb-
ulised B2agonist s are given. Post-operat ive moni-
t oring in int ensive care
Mal i gnant hyper t her mi a
Cause: hypermet abolism and muscle inj ury due
t o halogenat ed anaest het ic agent or succinyl
choline
Manifest at ions: I ncreased sympat het ic nervous
syst em act ivit y, muscular rigidit y, high fever, hy-
percar bia, arrhyt hmia, hypoxaemia and rhab-
domyolysis
Treat ment : Discont inue t he inhalat ion drug, ad-
minist er dant rolene sodium 2 - 3 mg/ kg I V.
Common causes of f ai l ur e t o br eat he af t er
gener al anaest hesi a ar e:
● Obst ruct ion of t he airways, hypoxia or hypercar-
bia of any cause
● Cent ral sedat ion from opioid drugs or anaest het ic
agent s
● Persist ent neuromuscular blockade
● Pneumot horax from pleural damage during an-
aest hesia and surgery
● Circulat ory failure leading t o respirat ory arrest .
I nt r a oper at i ve management
Moni t or i ng of vi t al par amet er s
Monit or cont inuously t he vit al paramet ers- pulse,
blood pressure, respirat ory rat e, ECG, oxygen sat urat ion
and urine out put and immediat e int ervent ion done t o
prevent Post-operat ive complicat ions.
Three fact ors such as hypoxia, hypot hermia
and hypot ension are int erlinked t o each ot her and
produce combined ill effect s leading t o life t hreat ening
complicat ions and hence t hey need close monit oring.
The det ails are described below
Hypoxi a
Monit or cont inuously by pulse oximet ry
Treatment
Administ er int raoperat ive oxygen t o prevent hypoxia
during surgery. (PaO2 decreases wit h increasing age
due t o hypovent ilat ion-pulmonary dysfunct ion and
anaest het ic drugs such as opioids, muscle relaxant s and
CNS depressant s).
Hypot her mi a
● Measure core t emperat ure by t rans-esophageal/
rect al t hermomet er.
● Prevent heat loss in t he OT (body t emperat ure
is labile under general anaest hesia, pat ient s are
prone t o hypot hermia during surgery.)
● Cover t he pat ient s wit h sheet s, blanket s and
t hermal pads t o prevent and t reat hypot hermia
as t here is heat loss in t he operat ing room under
general anaest hesia.
Hypot ensi on
● Monit or blood pressure cont inuously
● I nfuse fluids appropriat ely.
● Blood loss, anaest het ic drugs (profound vasodila-
t at ion) and muscle relaxant (fluid shift s t o ext ra
cellular space) leads t o severe hypot ension lead-
ing t o irreversible shock.
Bl ood t r ansf usi ons
● Keep blood loss t o t he minimum
● Avoid unnecessary and single unit t ransfusions
29
● Hypot ension refract ory t o volume replacement
wit h fluids require blood t ransfusion (> 2lit res of
cryst alloid)
● Hypoperfusion is an indicat ion for t ransfusion
even if t here is no hypot ension
● Acut e blood loss, rapid loss of more t han 20% of
blood volume, Hb level of 6gms/ dl or 6-9gms / dl
wit h clinical evidence of hypot ension and shock
require blood
● Problems in blood t ransfusion includes availabil-
it y, short shelf life, t ransmission of diseases and
t ransfusion react ions.
Tr ansf usi on nor ms-
● Check blood grouping and Rh t yping preopera-
t ively and record in t he case sheet
● Ant icipat e blood loss prior t o surgery, and re-
serve/ order required unit s of blood.
● Send blood samples immediat ely on drawing
blood properly labeled wit h all t he necessary par-
t iculars such as name, age, MRD number (hospi-
t al number)and blood group.
● Reconfirm pat ient ’s group on receipt of blood
sample and donor blood and cross mat ch and
confirm compat ibilit y.
● Use t he fresh blood for bet t er result s (avoid blood
st ored for more t han 21 days).
● Recheck t he blood bag received in OT/ ward again
t o reconfirm t he correct ness of blood group and
t he correct pat ient .
● Warm blood t o room t emperat ure before t ransfu-
sion t o prevent hypot hermia.
● Check and record pulse, blood pressure and clini-
cal condit ion and t ime of st art ing blood wit h t he
bag number group et c.
● Observe t he pat ient closely t ill t he t ransfusion is
complet ed.
● St op t ransfusion if t he pat ient complains of
* Dysponea
* Hypot ension
* Severe abdominal pain
* Hemorrhage
* Hemat uria.
● Administ er inj calcium gluconat e t o avoid coagu-
lopat hies in mult iple t ransfusion
● Consider blood component s (FFP, plat elet s, fi-
brinogen concent rat e)
● Wat ch for t ransfusion react ions (immediat e /
lat e).
● Record t he clinical condit ion in t he case record
aft er complet ion.
● Keep t he blood samples of donor and t he recipi-
ent for a minimum of 3 days.
Oper at i on t heat r e di sci pl i ne
1. Maint ain st erilit y of operat ion t heat re at all t imes
by regular and effect ive operat ion t heat re wash-
ing, fumigat ion and aut oclaving of inst rument s so
as t o avoid infect ion.
2. Allow minimum persons int o t he t heat re
3. Prevent ent ry of persons if t hey have infect ion
4. Change complet ely t o t heat re dress
5. Wear cap and mask and OT shoes properly
6. Be clean – cut nails, cut hair and have bat h. Ban-
gles, chains, bindis, rings and flowers should not
be worn
7. Do not t ouch any art icle wit h bare hands – use
Cheat le’s forceps or gloves
8. Avoid unnecessary movement s
9. Avoid t alking or noise
10. Check t he inst rument t able before surgery and
always inform t he requirement of inst rument s t o
t he t heat re st aff nurse in advance
11. Wash up aft er posit ioning t he pat ient and do not
leave it t o your assist ant .
12. Confirm proper posit ioning of t he pat ient , ade-
quat e height of t he t able and proper air condi-
t ioning as well as light ing before surgery
13. Handle diat hermy carefully t o avoid inadvert ent
inj ury t o ot her organs
I mpor t ant Not e
● Assessment and preparat ion of t he pat ient is es-
sent ial before anaest hesia and surgery.
● Enquire about allergy t o drugs, previous illness,
surgery and anaest hesia
● Discuss wit h t he surgeon / pat ient / pat ient ’s
relat ives regarding t he anaest het ic risk and com-
plicat ion and get writ t en consent
● Examine oral cavit y for loose t oot h and dent ures,
30
t racheal posit ion and spine for mobilit y, disc
space reduct ion and kyphoscoliosis.
● Ensure gast ric empt ying before induct ion of GA
t o prevent aspirat ion
● Maint ain cardio respirat ory, renal funct ion and
glycemic cont rol
● Avoid hypoxia, hypot ension and hypot hermia.
● Reduce exposure t o known risk fact ors for acut e
organ failure, especially acut e renal failure.
● I nit iat e invasive monit oring if required
● Ensure quick reversal wit hout CNS complicat ion.
● Convert from spinal anaest hesia t o general if re-
quired
● Cont inue monit oring and vent ilat e elect ively in
Post-operat ive period t o opt imize recovery
Post-operative care
Numerous physiological and pharmacodynamic
changes occur due t o surgical t rauma, anaest hesia
(drugs used for induct ion, sedat ion, reversal and muscle
relaxant s) and in t he immediat e Post-operat ive period.
Management of pat i ent s af t er maj or sur ger y
● Monit or t he cardio-respirat ory funct ion in high
dependency unit (in high risk pat ient s such as
children, elders and following maj or surgeries) in
t he int ra and Post-operat ive periods.
● I nt ervene and adj ust t herapy every few hours
if opt imum cardio-respirat ory funct ion is t o be
maint ained.
● Expect and t reat complicat ions quickly
● Monit or t he respirat ory funct ions cont inuously
and vent ilat e elect ively if required.
Ear l y Post -oper at i ve per i od
Moni t or i ng of vi t al par amet er s i s essent i al
● Blood pressure, t emperat ure, pulse, respirat ory
rat e
● Fluid and elect rolyt es balance urine out put (re-
place volume wit h appropriat e fluids)
● Maint ain glycemic cont rol, liver and renal func-
t ions
● Care wound and drains
● Good nut rit ional int ake and bowel movement
Hypoxi a
Monit or cont inuously by pulse oximet ry and int ervene
t o prevent hypoxia. Abdominal pain and t he effect s of
opioid drugs given t o relieve Post-operat ive pain can
depress respirat ory funct ion.
Treatment
Administ er oxygen t o all elderly pat ient s aft er surgery
t o prevent hypoxia. Post-operat ive hypoxia could persist
for several days, especially aft er abdominal surgery, and
also aft er hip surgery.
Oxygen administ rat ion at 2 lit res / minut e
int ermit t ent ly t hrough t win nasal cat het er is an effect ive
way of prevent ing t his hypoxia and is well t olerat ed by
pat ient s.
Hypot her mi a
There is heat loss in t he operat ing room under
general anaest hesia. The young and t he older pat ient s
are oft en cold aft er lengt hy procedures and rewarming
will t ake a longer t ime.
Treatment
I t is necessary t o cover t he pat ient wit h warm
blanket s. I n t he cold pat ient , t he drugs inj ect ed int o
cold muscles will not be absorbed int o t he circulat ion
unt il t he muscle warms and t he vessels dilat e. Hence
t he first dose of opioid analgesic should always be given
int ravenously and t he int ramuscular rout e reserved for
t he warm pat ient .
Hypot ensi on
Anaest het ic drugs and muscle relaxant s may lead t o
profound vasodilat at ion and lot of fluid is divert ed t o
ext ra cellular space. The fluid loss is poorly t olerat ed in
older pat ient s and appropriat e care and infusion should
be st art ed. Hypot ension causes poor perfusion t hereby
leading t o hypoxia. Cont inuous BP monit oring, pulse
oximet ry and appropriat e fluid infusion (25t o30ml/ kg
body weight ) are essent ial.
Treatment
Plasma volume is maint ained adequat ely wit h
appropriat e int ravenous fluids, blood and it s component s
or plasma expanders. The met abolic response t o surgical
t rauma leads t o sodium and fluid ret ent ion Monit or t o
avoid fluid overloading. Fluid overload is hazardous due
t o poor cardiac funct ion leading t o right heart failure in
t he elderly.
Ur i ne out put
31
● Monit or urine out put aft er maj or surgery
● Maint ain out put by ensuring adequat e fluid vol-
ume init ially
● Measure cent ral venous pressure t o check t he
adequacy of fluid replacement
● Rest rict t he use of indwelling cat het ers
● I nsert bladder cat het er asept ically
● Take necessary precaut ions if kept for prolonged
periods
Or i ent at i on
I mmediat ely aft er surgery, many pat ient s are
confused ( Post-operat ive cognit ive dysfunct ion ). Such
confusion last s longer, if given long-act ing sedat ive
and amnesic drugs.
Post -oper at i ve anal gesi a
● Assess pain- ask t he pat ient frequent ly about
t heir pain level.
● Administ er pain medicat ion on a regular basis
and whenever necessary.
● Cont inuous epidural anaest hesia is valuable in
pat ient s having abdominal or t horacic surgery
wit h poor respirat ory funct ion.
● Aft er minor surgery, oral soluble paracet amol
can be given early for relief of less severe pain.
Opioid drugs for severe Post-operat ive pain are
best given init ially int ravenously in increment al
doses unt il t he desired effect is achieved. Ad-
equat e pain cont rol decreases t he Post-operat ive
morbidit y and reduces t he hospit al st ay.
Car e of dr ai ns and wound
Connect drains t o proper and st erile cont ainers
and measure and record. Aft er maj or surgery, drains
are kept for draining t he collect ed fluid, blood et c., t he
amount of drainage should be carefully monit ored and
appropriat e fluids / blood replaced. I n case of large
quant it ies of drainage in a short t ime, or severe blood
loss, t he wound should be re-explored. Wound should
be dressed properly and kept clean and dry, change of
dressing should be done asept ically if required. Drain
sit es are t o be properly covered wit h adequat e st erile
pads.
Lat e Post -oper at i ve per i od
1. Cont rol of infect ion
* Cont rol infect ion wit h appropriat e ant ibiot ics,
if required assess cult ure and sensit ivit y of
discharge from t he wound; or if respirat ory
or urinary infect ion is suspect ed, sput um and
urine cult ure sensit ivit y.
* Reduce hospit al st ay t o eliminat e t he risk of
opport unist ic infect ion. Reduce Post-operat ive
respirat ory failure in case of upper abdominal
surgeries.
2. Deep vein t hrombosis (DVT) prophylaxis
Deep vein t hrombosis prophylaxis is advocat ed
for maj or surgeries and ort hopaedic surgery. I n-
fusion of low molecular weight heparin has a vit al
role in prevent ion of deep vein t hrombosis. Early
ambulat ion reduces deep vein t hrombosis.
3. Early mobilizat ion
Ambulat e pat ient as early as possible t o prevent
problems like
* At elect asis and pneumonia
* Ort host at ic hypot ension
* Decreased cardiac out put and st roke volume
* Urinary ret ent ion
* Negat ive nit rogen balance
* Depression and sensory deprivat ion
* Decrease t issue sensit ivit y t o insulin
* Deep vein t hrombosis
* Const ipat ion and fecal impact ion
* Loss of muscle st rengt h
* Decubit us ulcerat ion.
Physiot herapy t o improve respirat ory funct ion
and limb exercises t o improve muscle st rengt h
and movement s
4. Prevent ion of pressure ulcers
Prevent ion of pressure ulcers (Decubit us ulcers)
is a crit ical part of Post-operat ive care
* Turn t he pat ient frequent ly in t he bed t o pre-
vent t he pressure ulcers.
* Use of alpha beds and keeping t he back dry
as well as early mobilizat ion prevent s pressure
ulcer.
5. Rehabilit at ion and follow up
* Mobilize t he pat ient early t o prevent compli-
cat ions and educat e pat ient and family mem-
bers in t he import ance of mobilizat ion and
32
physiot herapy.
* Provide psychological support by t rained psy-
chologist , medical social workers and commu-
nit y healt h workers in cases where no family
support is available.
* Encourage t he pat ient t o do his / her own
day-t o-day act ivit ies especially in older people
t o prevent decline in funct ional st at us in t he
Post-operat ive period.
* Refer elders / pat ient s for proper care and fol-
low up aft er discharge. (Some may not have
proper home or care giver or family members
t o t ake care of t hem; social service organiza-
t ions and old age care homes may be ident i-
fied)
Key poi nt s
● Monit or Post-operat ive pat ient s int ensively
● Expect complicat ion and int ervene early
● Prevent hypot ension, hypoxia and infect ion
● Ambulat e early and give physiot herapy
Wound care
“ Skin is t he best dressing”
Care of wound is t he fundament al funct ion of surgical
pract ice from ancient t imes. Wounds occur in many
ways, commonly due t o t rauma or deliberat ely made
by t he surgeons t o gain access t o deeper st ruct ures
(incisions). Wound healing is a nat ural process and all
t ypes of wounds heal and t he repair process is t he same
for different kinds of t issues and wounds.
Wounds are of different t ypes and can be classi-
fied in many ways
● Acut e or chronic, if it persist s over 6 weeks
● Open and closed (skin surface not breeched as in
blunt inj uries)
● Clean or unclean (infect ed), et c
Tr aumat i c wounds ar e f ur t her cl assi f i ed as:
● Abrasion (t angent ial force t o skin, skin surface is
rubbed off )
● Bruise, cont usion, and hemat oma (blunt inj ury,
closed wound)
● Lacerat ion (shearing force as in falls, road acci-
dent s, irregular, ragged edges and inj uries wit h
varying dept h, damage t o deeper st ruct ures de-
pending on t he force)
● Tract ion and avulsions. Degloving inj uries are
caused by shearing forces t hat separat e t issue
planes, skin and subcut aneous layers are sepa-
rat ed from deep fascia in limbs
● Crush inj uries occur due t o severe force applied
t o t he t issues in t he closed space leading t o t is-
sue damage, bleeding exudat es and swelling
● Penet rat ing wounds occur due t o sharp obj ect s
such as knife, size of t he wound may be small
but t he direct ion and dept h of inj ury is import ant ,
requires t horough and careful explorat ion.
Chr oni c wounds
Ul cer s
Def inition
An ulcer is a discont inuit y of an epit helial surface.
Cl assi f i cat i ons:
● Specific ulcers are defined as ulcers due t o spe-
cific diseases such as t uberculosis or syphilis.
● Non-specific ulcers are defined as ulcers due t o
infect ion of wounds, physical or chemical agent s
or due t o local irrit at ion.
● Malignant ulcers are defined as ulcers due t o ma-
lignant changes occurring in t he layers of t he skin
e.g epit helioma and rodent ulcer.
● Art erial ulcers occur due t o occlusion of blood
supply and involve t he deeper st ruct ures, deep
fascia, muscle.
● Venous ulcers due t o st asis of blood in t he veins
involve t he skin, subcut aneous and superficial
t issues. e.g varicose ulcer
Wound heal i ng
● I nflammat ory phase (react ive) limit s t he damage
and furt her inj ury t o t issues.
● Proliferat ive phase (repair/ regenerat ive phase)
mat rix synt hesis, neovascularisat ion and reepi-
t helialisat ion of t he wound.
● Mat urat ion phase (Re-modeling) collagen cross-
linking, shrinking and cross cont ract ion of t he
wound t akes place.
Causes of non-heal i ng of ul cer s
33
● Poor blood supply, oedema, chronic smoking
● Malnut rit ion, diabet es
● I mmunosuppressant s
● Bact erial cont aminat ion
● Non-specific infect ion t urning t o specific infect ion
● Neurological condit ions
● Chronic irrit at ion
● Malignant change
Management Gui del i nes
Acut e wound car e
● Minimize unnecessary blood loss
● Avoid t he format ion of a haemat oma
● Adequat e cleaning, debridement , edema cont rol
● Remove debris and necrot ic t issue, irrigat e gent ly
wit h wat er / normal saline
● Expose viable t issues, excise eschar by sharp me-
chanical debridement
● Use t opical agent s, (Chemical debridement ) an-
t isept ics (chlorhexidine, povidone iodine, alcohol,
hydrogen peroxide, t riclosan) ant ibact erials (sil-
ver sulfadiazine, neomycine, polymyxin, bacit rac-
in, mupirocin) for sit es, cavit ies t hat are difficult
t o access
● Apply dressings aft er complet e debridement
● Maint ain proper wound environment and prevent
ischemia
● Keep t he bact eria count as low as possible
● Facilit at e healing of acut e wound, by closure
● Delay closure for several days t o allow infect ion
t o clear
Post r epai r wound car e
● Apply non adherent dressing for 24 t o 48 hours
t o ensure adequat e epit helializat ion and t o pre-
vent cont aminat ion of t he wound.
● Keep wounds clean and dry.
● Avoid soaking or scrubbing t he wound. Gent le
blot t ing of t he wound wit h a t owel is bet t er t han
repet it ive wiping of t he wound.
● Avoid prophylact ic parent eral ant ibiot ics for rou-
t ine lacerat ion repair.
● Prepare and decont aminat e wound t o prevent in-
fect ion rat her t han using ant ibiot ics.
● Prot ect scars t hat are exposed t o sunlight wit h
sunscreen for at least 6 t o 12 mont hs t o minimize
subsequent hyperpigment at ion.
● Cosmet ic effect (good scar) depends on proper
wound healing
Chr oni c wounds management
I dent ify and t reat t he predisposing fact ors
Causes
Diabet es mellit us
Peripheral art erial or venous disease
Severe anaemia
Prot ein deficiency
Rheumat oid art hrit is
Syst emic vasculit is
Cushing’s syndrome
Syst emic st eroid t herapy.
Treatment
Non-phar macol ogi cal
● Encourage daily bat h; avoid walking bare foot or
using slippers wit h int erdigit al bars.
● Reduce st anding or excessive walking; wear elas-
t ic st ockings. Elevat ion of leg and foot end of t he
bed while sleeping and leg exercises t o act ivat e
t he calf muscle pump in leg ulcers.
Phar macol ogi cal
● I dent ify t he microorganism and t reat accordingly.
● Send pus/ discharge for cult ure and sensit ivit y
(microbiology).
● Exhibit appropriat e ant ibiot ics. Tubercular ulcer is
t reat ed wit h ant it ubercular drug for a minimum
period of 6 mont hs.
Sur gi cal Tr eat ment
● Clean t he wound wit h normal saline or t ap wat er
only (ant isept ics delay wound healing).
● Surgical debridement for ulcers associat ed wit h
necrot ic t issue or slough.
● Daily dressing: commonly used dressings are:
Occlusive(moist ure ret ent ive) dressings
Hydrocolloid gel for clean and shallow ulcers
Calcium alginat e dressing for bleeding wounds
34
and wounds wit h a cavit y
● Apply split skin graft for early closure of wound.
(Chronic ulcers heal by fibrosis and scar forma-
t ion t akes long t ime t o heal)
● Biopsy of t he wound edge for pat hological diag-
nosis, in chronic non healing ulcers
● Refer pat ient s wit h chronic leg ulcer t o vascular
surgeons or general surgeon wit h some experi-
ence in peripheral vascular problems for surgical
t reat ment
Pat i ent Educat i on
● Teach t he care of leg ulcers, wearing socks and
proper foot wear and compression st ocking t o
prevent ulcers in fut ure
● Massage aft er bat h t he healed scar area wit h an
emollient cream such as lanolin or some oil t o
keep t he scar t issue soft and supple t o prevent
furt her breakdown.
● Regular use of calf muscle act ivat ing
● Chemical agent s, enzymes t o digest necrot ic t is-
sues
● Dressings
● Dressings t hat absorb moist ure such as copoly-
mer st arch dressing (alginat e)
● Zinc oxide t o form a moist ure barrier
● Hydro colloid dressing
● Ant ibiot ics aft er cult ure and sensit ivit y, if infec-
t ion is present
● Vacuum-assist ed devices
Sur gi cal management
● Excise dead and devit alized st ruct ures
● Cover wound by local/ myocut aneous/ compos-
it e/ rot at ion flaps adequat ely
Gener al measur es f or pr event i on:
● Avoid prolonged lying down in supine posit ion,
frequent t urning, and use of wat er or alpha bed
● Educat e pat ient s on prevent ion and care of ulcers
I mpor t ant Not e
● Prevent ion is t he best form of management
● Educat e pat ient s / care givers on prevent ive
st rat egies
● Avoid prolonged lying down in t he supine posit ion
● Avoid frict ion and shearing forces while t urning
t he pat ient
● Avoid soiling of bed by urine, mot ion, sweat or
discharges
● Turn pat ient frequent ly t o prevent pressure ef-
fect s
● Care of t he skin, back, perineum and scrot um
● I mplement proper bed making
● Use alpha bed/ wat er bed if necessary
● Provide balanced nut rit ion
● Encourage early ambulat ion
● Exercises and leg elevat ion
● Avoid prolonged period of st anding or sit t ing wit h
legs down.
● Good personal hygiene (daily bat h) and good nu-
t rit ion.
● Cont rol of diabet es is necessary.
Pr essur e ul cer s
Def inition
A pressure ulcer is defined as a lesion occurring over
t he bony prominence or on t he firm surface, caused
by unrelieved pressure, result ing in t he damage of t he
underlying t issue.
Pressure ulcers are t he cost ly complicat ion of
immobilit y and can be easily prevent ed. Healing of
all t hree phases (ext ension, t ransit ion, and repair)
of wound is delayed due t o poor nut rit ional st at us,
presence of neurological condit ions and diabet es. I n t he
very old and bedridden pat ient s t he problem assumes
import ance due t o t he difficult ies encount ered in t he
healing and it s added complicat ions.
Prevent ion is t he best form of t reat ment
Management of pr essur e ul cer s
1. Prevent ion of ulcers
2. Eliminat e ext rinsic fact ors
3. Prevent ion of furt her det eriorat ion and promot ion
of healing of exist ing ulcers
* Creat e and maint ain proper environment
(clean wound, adequat e oxygenat ion)
* Provide nut rit ional support
4. Surgical management
35
* Wound debridement
* Plast ic surgical int ervent ion
5. General t reat ment measure t o promot e healing
* Wound cleaning (washing wit h soap and wa-
t er, normal saline, avoid irrit ant s)
* Debridement (removal of dead t issue, eschar
excision)
* Mechanical removal by wet dressing, hydro-
t herapy
Sutures
Sut ur es
The purpose of sut uring is t o hold t he t issues unit ed
t ill t he nat ural process of repair and firm union bet ween
t he cut edges is complet ed.
Def inition
A ligat ure is a band or t ie used around a duct ular
st ruct ure in order t o const rict it like t ying a blood vessel
using cat gut or silk.
There are different kinds of sut ure mat erials available
and t he surgeon is expect ed t o select t he right kind of
sut ure mat erial for t he different t ypes of t issue closure
for best result s.
An ideal sut ure or ligat ure should have t he fol-
lowing qualit ies-
● Adequat e t ensile st rengt h (t ensile st rengt h means
minimum amount of t ension (by weight ) required
t o disrupt t he sut ure mat erials. The higher t he
st rengt h, t he bet t er is t he mat erial).
● Least t issue react ion
● Non-allergic, non-capillary, non-elect rolyt ic and
non-carcinogenic.
● Should produce a secure knot wit hout cut t ing or
fraying.
● Easy t o st erilize, cheap, comfort able and handy
Cl assi f i cat i on of sut ur es
1. Absorbable sut ure
* Nat ural: Plain and chromic cat gut (prepared
from sheep’s gut ) t ensile st rengt h depends
upon t he size of t he mat erial, plain cat gut
last s upt o 7 - 10 days and absorbed by en-
zymat ic prot eolysis. Bact erial infect ion leads
t o increased prot eolysis and rapid absorpt ion
of sut ures even before t he complet e union of
t issues leading t o wound dehiscence.
* Synt het ic: Polyglycolic Acid (Dexon), Polygla-
ct in (Vicryl), Polydiaxanone (PDS) Approxi-
mat ely 60% remains at 2 weeks and 30% re-
mains at 3 weeks. Degradat ion by hydrolysis
is complet e by around 60-90 days. Vicryl is
an ideal sut ure mat erial for medium t erm and
widely used for bowel anast omosis.
* Advant ages Great t ensile st rengt h and lit t le
t issue react ivit yEasily handled like silk and
knot s well
* Absorbed in 60-90 days
2. Non-Absorbable sut ures
* Nat ural eg: silk, cot t on, linen, met al (st ain-
less st eel)
* Synt het ic eg: dacron, nylon, polypropylene,
proline
Sut ur e needl es
Sut ure needles are of t wo t ypes:
St r ai ght and cur ved needl es
● St raight needles are used usually on t he surface
st ruct ures like skin or in bowel anast omosis
● Curved needles are used when sut uring in t he
dept h, abdominal and t horacic cavit ies and in
vascular or ot her anast omosis. Curved needles
are usually direct ed t owards t he surgeon while
sut uring.
● Cut t ing needle - Triangular in cross sect ion.
Cut t ing needles are mainly used t o sut ure skin,
aponeurosis, t ough deep fascia et c.
● Round needle - Rounded in cross sect ion. Mainly
used in bowel anast omosis.
● At raumat ic sut ures are special t ype of sut ure ma-
t erial in which t he needles do not have t he eye t o
t hread sut ure mat erial and t he sut ure is swaged /
impregnat ed int o t he needle. The diamet er of t he
needle is nearly t he same as t hat of t he sut ure
mat erial t o prevent / minimize needle punct ure
leakages. At raumat ic needles are used for vascu-
lar anast omosis, bowel anast omosis, subcut ane-
ous t issues et c.
Pr i nci pl es of sut ur i ng
● All sut ures act as foreign bodies and increase in-
fect ion
● Use t hin at raumat ic sut ures
36
● Avoid including large chunks of t issues in sut ures
or in t he ligat ures t o prevent avascular necrosis
and infect ion
● Sut ure wit h right degree of t ension
● Prefer monofilament sut ures inst ead of braided
silk
● Met allic sut ures are permanent and st rongest
while nat ural sut ures are t he weakest
● Synt het ic mat erials have int ermediat e posit ion
and hence ideal choice
● Cont inuous sut ures are as good as int errupt ed
ones; breakage is rare if placed properly.
Good sut ur i ng t echni que:
● Keep t he needle t ip perpendicular t o t he skin at
about 0.5 cms from t he cut edge of t he skin and
pierce it t o t he required dept h avoiding pot ent ial
spaces (curved needle direct ed t owards you and
st raight needle away)
● Turn t he needle t o t he ot her side of t he incision
by circular movement of t he wrist and t he needle
t ip should come out perpendicular and equidis-
t ant from t he incision on t he ot her side
● Pull t he needle along t he curvat ure of t he needle
always
● Approximat e t he skin properly wit hout any over-
lapping or in folding
● Place t he knot s on one side of t he sut ure wit h-
out t ension and t he t hread should be cut less
t han t he int er-knot dist ance
Ski n:
● Usually int errupt ed silk sut ures preferred
● Subcut icular st it ch is ideal for skin closure result s
in t hin scar
● Simple or mat t ress sut ures depending on t he
t hickness of t he subcut aneous t issue, sit e and
t he surgeon’s preference
● I n malnourished and cancer pat ient s, when de-
layed healing is expect ed t he sut ures are left
longer, up t o 2 weeks.
● Secondary sut uring ret ained up t o 2 weeks.
● I f t here is swelling, edema, collect ion or infec-
t ions remove t he part icular sut ure immediat ely.
● Tit anium clips can also be applied for skin clo-
sure. painful while removing clips, not very com-
monly used in general surgery.
● St eri-st rips and adhesive glues are also used for
bet t er cosmet ic result s in skin closure.
Face - Monofilament thin non-absorbable
simple sutures.
● Remove sut ures by 4-5 days
● Heal well due t o good blood supply.
● Trunk and Limbs - Preferably monofilament
● Removed around 7 – 10days
● Back- Sut ures removed at around 10 days
Aponeur osi s and l i gment s:
Non-absorbable st rong monofilament like prolene
is used eg: Rect us closure, inguinal hernia repair.
Muscl es:
Muscle t issues are sut ured by chromic cat gut st iches.
The first knot snuggly placed wit hout t ension and t he
second knot only t ight ened t o prevent necrosis of t he
muscle t issue.
Bl ood vessel :
I n blood vessels connect ive t issue response is
limit ed and hence, prolonged sut ure support is
required
Monofilament s of t hin caliber such as 8-0 t o 10-0
can be used depending upon t he vessel
I nt imal sut ure line must be smoot h, t o prevent
clot t ing in t he sut ure line
Knot s must be secure
Needle must pass from wit hin out wards
St omach and i nt est i nes:
I n int est ines healing t akes place in t he serosal layer.
Hence serosa t o serosa closure is essent ial t o prevent
leakage and proper healing. Avoid t aking bigger bit es
of t issues t o prevent valvular effect and st enosis.
I nt errupt ed sut ures prevent t he purse-st ring effect .
Usually small int est ines require double layer closure,
inner chromic cat gut or vicryl, and out er layer of silk
sut ure, single layer closure is adequat e provided t he
correct surgical t echnique is followed.
* St omach and small bowel - Two layer closure
* Large bowel - Single layer closure
Two l ayer ed cl osur e:
37
● I nner (including all layer of bowel)-Cont inuous
2/ 0 or 3/ 0 vicryl or cat gut st iches are locked t o
get perfect hemost asis
● Out er (seromuscular t o ensure serosal opposi-
t ion) I nt errupt ed 2 0 or 3 0 silk
Geni t o-ur i nar y t r act :
Healing is good and t ensile st rengt h recovered wit hin
3 weeks, in genit o-urinary t ract . Hence, absorbable
mat erial (chromic cat gut ) is good enough for sut uring
t he uret hra, bladder and uret er.
Lungs:
Lung t issues are repaired by chromic cat gut / vicryl
mat t ress sut ures
Wound dehiscence
Def inition
Wound dehiscence is defined as t he wound giving
way aft er primary closure following surgery. Dehiscence
of wound is relat ed t o t he rat io of collagen synt hesis t o
lysis. More t he lysis dehiscence will follow as in infect ion
t here is soft ening of t he edge by collagenase act ivit y.
St arvat ion leading t o weight loss (< 20%) impairs
collagen synt hesis St eroid given on long t erm affect s
wound response t o repair
Dehi scence can be pr event ed by
● Well nourished and oxygenat ed t issue (early rap-
id rest orat ion of circulat ing volume)
● Prevent ion of collect ions and infect ion
● Good surgical t echnique
● Properly placed incisions
● Gent le handling of t issues
● Precise select ion of sut ure mat erial
● Closure in layers, wit h drains if required
● Tensionless sut ure t echniques
Treatment
● Re-sut uring of t he wound edge
● Wash wound t horoughly
● Trim wound edges
● Use proper sut ure mat erial, (vicryl, silk)
● Sut ure wit hout t ension
● Keep drains, if t here is oozing or collect ion
● Prevent infect ion- administ er ant ibiot ics.
● Promot e healing (prot eins, vit amins).
I mpor t ant Not e
● Prevent ion is always bet t er t han cure
● Thin serous discharge is t he forerunner of wound
dehiscence.
● Take all necessary st eps t o prevent wound gap-
ing at all cost s I t is alarming and demoralising t o
see t he wound dehiscence in t he post op period
and has depressing effect on t he pat ient .
● I ncreases t he healing t ime and cost .
39
Emergencies
Chapter 2
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
● Anaphylaxis
● Shock
● Cardio Pulmonary Resuscit at ion
● BLS
● ACLS
● Burns
● Fluid and Elect rolyt e I mbalance and Replacement
● St ridor
● Sept icaemia
● Coma
● Poisoning
* Copper Sulphat e Poisoning
* OPC Poisoning
* Pot assium di chromat e Poisoning
* Mozhikizhangu Poisoning
● Emergency Surgical Procedures
41
Anaphylaxis
I t is a generalized hypersensit ivit y react ion
charact erized by hypot ension, Peripheral circulat ory
collapse and respirat ory difficult y in t he from of st ridor
and dyspnoea. Anaphylaxis can occur due t o food,
inhaled/ ingest ed allergens or drugs ( Table 2.4).
sympt oms may occur inst ant aneously or wit hin a few
minut es aft er an int ravenous inj ect ion of t he offending
agent . At t imes t he react ion may develop aft er 1/ 2 - 1
hour of t he exposure. Anaphylaxis t o oral drugs may t ake
1-2 hours, but in many pat ient s it can be inst ant aneous.
commonl y used agent s i mpl i cat ed i n
anaphyl act oi d r eact i ons
1. Ant ibiot ics
* Penicillin and analogues
* Tet racycline
* Sulfonamides
* St rept omycin
2. Local anaest het ics
* I nj . Lidocaine
3. General anaest het ics & muscle relaxant s
* I nj . Thiopent al
* I nj . Tubocurarine
4. Non-st eroidal ant i-inflammat ory agent s
5. Blood product s and vaccines
* Red blood cell, whit e blood
* Tet anus cell& plat elet t ransfusions
* Dipht heria
* Gamma globulin
* Snake and spider ant ivenoms
* Rabies
6. Diagnost ic agent s
* I odinat ed radiocont rast agent s
7. Venoms
* Bees, wasps, spiders, j ellyfish
8. Hormones
* Inj. Insulin � Pituitary extracts
* Inj. Hydrocortisone � Vasopressin
9. Ext ract s of allergens used for desensit izat ion
* Food
* Eggs
* Nut s
* Milk and milk product s
* shellfish
* Legumes (peanut s, soyabeans,
* Kidney beans, chick peas)
* Cit rus fruit s
10. Ot her drugs
* Prot amine
* ACE inhibit ors
* Parent eral iron
* I nj . Dext ran
Treatment
A Severe anaphylact oid react ion is a life-t hreat ening
emergency. Effect ive t reat ment depends on prompt
diagnosis and rapid supplement at ion of appropriat e
t herapy.
1. I nj . Adrenaline 1 : 1000, 0.01 ml/ kg (maximum
0.3 ml in children and 0.5 ml in aduit s) by I M in-
j ect ion. I f necessary, dose can be repeat ed every
15 minut es. I f t he anaphylaxis is t o inj ect ion of
an allergen ext ract or t o a hymenopt era st ing int o
an ext remit y, half t he dose of adrenaline can be
infilt rat ed locally, subcut aneously aft er dilut ion
wit h 2 ml saline. A t ourniquet above t he sit e can
also slow syst emic dist ribut ion of allergen. I t can
be loosened every 3 minut es.
2. For severe anaphylaxis wit h shock as in all medi-
cal emergencies, init ial management should
be direct ed at t he ABC of resuscit at ion, name-
ly maint enance of adequat e airway - suct ion,
breat hing and circulat ion. if working alone, call
for assist ance
3. Est ablish one or preferably t wo, wide bore int ra-
venous lines. Commence rapid fluid resuscit at ion
wit h normal saline.
4. I f t here is severe laryngeal obst ruct ion, bron-
chospasm, circulat ory shock or coma,int ubat e
and commence int ermit t ent posit ive pressure
vent ilat ion.
5. I f t here has been lit t le or no response t o t he ini-
t ial int ramuscular dose of adrenaline, administ er
adrenaline 5 mcg/ kg slowly in t o t he int ravenous
line. Repeat at 5 minut es int ervals depending on
response. I f t he pat ient remains in shock, st art
an adrenaline infusion (preferably via a cent ral
42
venous line), commencing 0.1 mcg/ kg/ min in
children and 0.2 mcg/ kg/ min in adult s,t it rat ion is
required t o rest ore blood pressure. Large doses
of adrenaline may be needed.
6. I f t he only manifest at ion of anaphylaxis is urt i-
caria or angioedema, int ial I M dose of adrenaline
should be given in addit ion t o H ant agonist s. I f
no progression occurs, pat ient can be kept under
observat ion for at least 12 hours and t hen dis-
charged.
Addi t i onal measur es
1. Administ er Salbut amol or Terbut aline by aerosol
or nebulizer.
2. I nj . Diphenhydramine 1 mg/ kg slow int ravenous-
ly.
3. I nj . Ranit idine 1 mg/ kg slow int ravenously.
4. I nj . Hydrocort isone 2-6 mg/ kg or Dexamet ha-
sone 0.1-0.4 mg/ kg I V.
Suppor t i ve t r eat ment
Observe vit al signs frequent ly and if possible, Monit or
elect rocardiogram and pulse oximet ry.
All pat ient s who have suffered a severe anaphylact oid
react ion must be admit t ed t o t he hospit al. Pat ient s who
remain clinically unst able aft er int ial resuscit at ion should
be admit t ed t o an int ensive care unit . I f nat admit t ed
t o hospit al and if t hey respond t o t he int ial t reat ment ,
provide infomat ion t o t hem about possible lat e react ion.
Pat i ent educat i on
To check and look for t he cause (food, drugs et c.)
and t o avoid it in fut ure.
Ref er ences
1. General ASpect s of Treat ment . I n: Text book of
Dermat ology. Champion RH et al (eds), 6t h Edi-
t ion, Blackwell Science Lt d. London. pp-3289.
2. Urt icaria and Angioedema. I n: Dermat ology in
General Medicine. Freedberg I M et al (eds), 5t h
edit ion, The McGraw Hill Company I nc., pp-1409.
3. Anaest hesia at t he Dist rict Hospit al. I n: World
Healt h Organizat ion in collaborat ion wit h t he
World Federat ion of Societ ies of Societ ies of Soci-
et ies of Anaest hesiologist s, Geneva, 2nd Edit ion,
2000 World Healt h Organizat ion.
4. Drugs Used in Anaest hesia. I n: WHO Model Pre-
scribing I nformat ion, 1989, World Healt h Organi-
zat ion.
5. Anaest hesia at t he Dist rict Hospit al. I n: World
Healt h Organzat ion in collaborat ion wit h t he
world Federat ion of Societ ies of Anest hesiolo-
gist s, Geneva, 1988, World Heait h Organizat ion.
Shock
Def i ni tion
Shock is defined as an acut e circulat ory failure leading
t o inadequat e t issue perfusion result ing in generalized
cellular hypoxia and end organ inj ury. Shock is classified
as
● Hypovolemic shock
● Obst ruct ive shock
● Cardiogenic shock
● Dist ribut ive shock
Hypovolemic shock
Reduct ion in t he blood volume
Causes
Hypovolemic shock is due t o inadequat e int ake
of fluids relat ive t o losses (dehydrat ion) or increased
losses due t o
● Bleeding
● Diarrhea
● Diuresis
● Excessive sweat ing or
● Third space loss as in burns, t he crush syndrome,
perforat ing gast roint est inal wounds, et c.,
Symptoms
● Breat hlessness
● Thirst and dry mout h
● Bluish discolorat ion / cyanosis
● Cold and pale skin
● Delayed capillary fill (3 seconds or more)
● Depressed ment al st at us or loss of consciousness
● Decreased or no urinary out put
● Marked t achycardia > 120/ min (for children ac-
cording t o age)
43
● Decreased syst olic blood pressure (Age appropri-
at e for children)
● Narrowed pulse pressure or immeasurable di-
ast olic pressure
● Weak or absent peripheral pulses/ weak cent ral
pulses
I nvesti gati ons
● CBC- decreases in Hb (blood loss)/ increases
in PCV (loss plasma or fluids), Leukocyt osis or
leukopenia ( in sepsis)
● Blood glucose (diabet ic ket oacidosis)
● BUN, creat inine
● Elect rolyt e levels (eg, Na, K, Cl, HCO3)
Signs of Shock
44
● Prot hrombin t ime
● ABG
● Urinalysis- myoglobin or hemoglobinuria (in pa-
t ient s wit h t rauma).
● Blood grouping and Rh typing
Treatment
● Admit t o hospit al
● Supplement wit h high-flow oxygen
● Support wit h vent ilat ion if needed
● St art t wo large bore I V lines
● Resuscit at e wit h fluids
* One t o t wo lit res of isot onic normal saline or
ringerlact at e for an adult
* Also blood, albumin, fresh frozen plasma, hex-
ast arch, pent ast arch, and dext ran 70 are used
* Fluid requirement has t o be calculat ed prop-
erly for children and administ ered carefully.
● Observe for vit al signs
● Cont inue cryst alloid infusion
● Arrange for urgent blood or plasma infusion if
lit t le or no improvement is seen wit h cryst alloid
infusion; consider early blood t ransfusion in sus-
pect ed blood loss as in t rauma.
● Raising t he hypot ensive pat ient ’s legs may be
useful t hough, cont roversial
● Cont rol furt her loss of blood, plasma or fluid by
surgical or pharmacological agent s
Fluid therapy for children
● Rapid I V access; if not possible int ra osseous ac-
cess
● I nit ial fluid bolus for shock
* I nt ravenous fluids ringer lact at e or normal
saline 20ml/ kg rapidly in hypovolemic shock
over 5-20 minut es. Repeat boluses 2-3 t imes
aft er reassessment of cardio-pulmonary st a-
t us at t he end of each bolus
● 2 or 3 fluid boluses will be required in hypovo-
lemic or sept ic shock
● I n case of blood loss, at t empt replacement wit h
blood aft er 2 boluses
● Reassess cardio-pulmonary st at us following each
bolus by pulse volume, heart rat e, skin perfusion,
urine out put , sensorium, blood pressure, liver
size and lung signs.
● Wit hhold furt her boluses if cardiogenic shock oc-
curs (airway inst abilit y, pink frot h, apnea, devel-
opment of grunt , ret ract ions, abdominal respira-
t ions, fresh rales, gallop rhyt hm, enlargement of
liver).
● St art vasopressor agent s (Dopamine or Dob-
ut amine) as int ravenous drip
For Pedi at r i c use
● Dopamine
* St art at 10 mcg/ kg/ min; t it rat e dose by incre-
ment of 2-3 mcg/ kg/ min every 15 minut es
upt o 20 mcg/ kg/ min
* Weight X 6 = mg of dopamine t o be added
t o 100 ml of NS; 1ml/ hr will deliver 1mcg/ kg/
mt ; I ndicat ed in hypot ensive shock only aft er
fluid boluses
● Dobut amine
* I ndicat ed in cardiogenic shock wit h normal or
increased blood pressure
* I not rope of choice
* dose: 10-20 mcg/ kg/ min
* Preparat ion similar t o dopamine.
For adul t s
● Dopamine
* 2-4 mcg/ kg/ min in normal saline as I V drip
and adj ust ed wit h blood pressure and in-
crease at 5 minut es int erval t o appropriat e
hemo- dynamic end point .
● Dobut amine
* 2-20 mcg/ kg/ min, as int ravenous drip similar
t o dopamine.
* Treat t he underlying condit ion
* Treat t he associat ed met abolic dist urbances
Ref er r al
● Hypovolemic shock due t o t he loss of plasma vol-
ume can be managed adequat ely in t he primary
healt h cent ers and peripheral hospit als.
● Hemorrhagic shock and loss of fluid in t he t hird
space may require referral t o higher cent ers.
45
Obstructive shock
Def i ni tion
Obst ruct ive shock is a condit ion where in t here
is an obst ruct ion of t he blood flow t o and from t he
heart , which may be due t o inflow obst ruct ion as in
t he case of pericardial t amponade, acut e pneumot horax
or hemot horax and out flow obst ruct ion as in acut e
pulmonary embolism.
Diagnosis may be made from t he hist ory and clinical
examinat ion.
Symptoms
● Breat hlessness
● I ncrease in JVP and pulsus paradoxus (pericar-
dial effusion)
● Cyanosis and decrease j ugular venous dist ension
(t ension pneumot haorax)
● Unilat eral swelling (DVT which may lead t o pul-
monary embolism)
I nvesti gati ons
● Basic invest igat ions
● X-ray chest
● ECG
● Echocardiogram
● CT scan/ perfusion scan
Treatment
● Admit t o hospit al
● Relieve t he obst ruct ion (life saving procedure)
● Proceed for urgent peri-cardiocent esis for cardiac
t amponade
● I nit iat e needle t horacost omy for t ension pneu-
mot horax
● St art t hrombolysis and proceed for surgical re-
moval if massive pulmonary embolism
Ref er r al
Obst ruct ive shock almost always requires invasive
t reat ment and hence t hese cases require referral
t o higher cent ers aft er providing support ive and
resuscit at ive measures.
Cardiogenic shock
Cardiogenic shock is due t o myocardial dysfunct ion
wit h decreased cardiac out put and evidence of t issue
hypoxia in t he presence of adequat e int ravascular
volume.
● Hypot ension and poor t issue perfusion
● Oliguria
● Clouded sensorium
● Cool, mot t led ext remit ies
● Ot her feat ures of myocardial dysfunct ion such as
* Gallop rhyt hm
Pulmanory embolism ventilation - perfusion scna
46
* Pulmonary oedema and hepat omegaly sec-
ondary t o acut e myocardial infarct ion
* Aort ic or mit ral regurgit at ion or vent ricular
sept al rupt ure (aft er excluding or correct ing
fact ors such as hypovolemia, hypoxia, and
acidosis), myocardit is.
I nvesti gati ons
● Complet e blood count
● Blood glucose
● BUN, creat inine
● Elect rolyt e levels
● ECG
● Chest X-ray
● Urinalysis
● Ot her special invest igat ions ( depending upon
t he cause)
Treatment
● Admit t o hospit al
● Provide oxygen by face mask
● St art venous access
● Relieve t he pain wit h st rong analgesics (narcot ics
analgesics)
● Challenge wit h 250 t o 350 ml of fluid if t here are
no lung crackles (I n children smaller volume. i.e-
5-10 ml/ kg fluid boluses over 20 minut es wit h
careful monit oring)
● St art vasopressor Dopamine drip if SBP remains
less t han 80 mm/ Hg
● Prefer Dobut amine as drip if SBP is more t han 80
mm/ Hg
● Cont inue ot her support ive measures, as required.
Ref er r al
Cardiogenic shock may require invasive t reat ment
depending upon t he cause and hence needs referral t o
higher cent ers.
Distributive shock
Def i ni tion
Dist ribut ive shock is a st at e of low peripheral
vascular resist ance.
● Condit ions t hat come under t his cat egory are
* Allergic shock / Anaphylact ic shock
* Sept ic shock and
* Neurogenic shock
● This condit ion requires large amount of fluid. End
point s of fluid resuscit at ion are t he same as for
hypovolemic shock at t his st age
● I f hypot ension persist s, inot ropes and vasopres-
sors may be necessary.
Anaphylactic shock
Anaphylact ic shock occurs as a result of inj ect ion,
ingest ion, inhalat ion, or skin cont act of an allergen.
I t is an emergency and immediat e management
saves t he lives. I f not t reat ed prompt ly, t he out come is
invariably fat al.( for more informat ion, read t he chapt er
on Anaphylact oid and anaphylact ic react ions).
Symptoms
● Skin erupt ions
● Peri-orbit al fullness
● Sweat ing
● Hypot ension
● Breat hlessness
● Coughing due t o laryngeal edema
Treatment
● Treat ed wit h int ramuscular epinephrine (0.3-
1mg) and volume resuscit at ion.
● I nt ravenous cort icost eroids, and vasopressors
● Ot her agent s preferred are I nj .chlorpheniramine
and H2 recept or blockers
Ref er r al
I n most of t he occasions referral may not be required
if managed properly.
Septic shock
Causes
Sept ic shock result s as a consequence of release of
t oxin by gram negat ive bact eria (E.coli,Prot eus,Klebseilla)
and gram posit ive cocci and fungi.
Symptoms
● Evidence of volume deplet ion such as dry mu-
47
cous membranes, and cool, clammy skin.
● Somet imes pat ient s will be warm along wit h hy-
pot ension.
● Signs and sympt oms pert aining t o pneumonia,
UTI , meningit is. int ravenous cat het er infect ion
or ot hers.
● Signs of possible infect ion include
* Fever
* localized eryt hema or t enderness
* Consolidat ion on chest examinat ion
* Abdominal t enderness
* Meningismus.
● Signs of end-organ hypoperfusion which include
* Tachypnea
* Oliguria
* Cyanosis
* Mot t ling of t he skin
* Digit al ischemia
* Abdominal t enderness
* Alt ered ment al st at us
I nvesti gati ons
● Complet e blood count (CBC)
● Art erial Blood Gas analysis
● Met abolic paramet ers
● Microbiological evaluat ion
● Cult ures from relevark sit es
● Ot her invest igat ions as needed
Treatment
● Volume resuscit at ion wit h fluids, changes t he
clinical pict ure t o hyperdynamic shock, wit h t ach-
ycardia, bounding pulse wit h a widened pulse
pressure, a hyperdynamic precordium and warm
ext remit ies.
● 500 t o 1000 ml fluid over 5 t o 10 minut es t o in-
crease t he mean blood pressure 65 t o 75 mm of
Hg.
● Take care while administ ering fluid in children.
End point s of fluid resuscit at ion are fall in heart
rat e, urine out put > 0.5 ml / kg/ hour, cent ral
venous pressure of 8 – 12 mm Hg, cent ral venous
oxygen sat urat ion > 70%, fall in base deficit ,
and fall in blood lact at e concent rat ion
● Norepinephrine as int ravenous drip is superior
in t he t reat ment of hypot ension of sept ic shock
(0.05-5 µgms/ kg/ min)
● I nj . Hydrocort isone as int ravenous ( usefulness
is cont roversial)
● Ant imicrobial select ion may be based on t he basis
of underlying illness, pat ient s suscept ibilit y and
local resist ance pat t ern
● Target t ed narrow spect rum t reat ment is probably
j ust ified, if st rong clues t o t he sources of infec-
t ion exist . Some examples are
* Pneumonia –second or t hird generat ion ce-
phalosporin or macrolide
* Urinary t ract infect ion – Ampicillin plus Gen-
t amycin
* Meningit is - t hird generat ion Cephalosporin
* I nt ra-abdominal.infect ion - t hird generat ion
Cephalosporin
* Primary bact eremia – Piperacillin and Tazo-
bact um?
● Maint ain normal blood glucose levels
● Avoid int ravenous sodium bicarbonat e
Cour se and out come
● Early diagnosis and prompt t reat ment influence
t he out come. However, t he diagnosis cannot be
made in all cases on t he basis of init ial findings
on hist ory t aking and physical examinat ion
● Wit h effect ive ant ibiot ics, volume replacement
and vasopressors improvement may appear wit h-
in 24 t o 48 hours
● Prognosis in sept ic shock is very grave (mort alit y
roughly 50%)
● Common sequence of organ failure is primarily
heart and circulat ion followed by kidneys, respi-
rat ory syst em and brain, t ert iary involvement will
be liver and hemost at ic syst em.
Ref er r al
Pat ient s not responding need referral t o a higher
cent er.
Cardiopulmonary resuscitation (CPR)
CPR consist s of a series of maneuvers by which
oxygenat ed blood supply t o brain and vit al organs is
48
maint ained during cardiopulmonary arrest (CPA) i.e.,
cessat ion of respirat ion and circulat ion,
I n children,CPA is not sudden but end result of
long period of hypoxaemia secondary t o inadequat e
vent ilat ion, oxygenat ion or circulat ion. Therefore,
prompt management of t hese is essent ial t o prevent
CPA, t he out come of which is poor.
Di agnosi s of car di opul monar y ar r est
Car di ac ar r est
1. Absence of pulse in maj or art eries (carot id or
femoral in older children and femoral or brachial
in infant s as carot id is difficult t o plpat e due t o
short neck).
2. Absence of heart sounds on auscult at ion.
3. Asyst ole / vent ricular fibrillat ion on ECG.
Respi r at or y ar r est
Absence of respirat ion on looking (absent chest
movement s), list ening (absent air flow on bringing
ears in front of mout h) and feeling (absent air flow on
keeping hands in front of mout h or nose).
Level s of CPR .
There are t wo levels of CPR.
1. BLS (basic life support ) The element s of CPR
provided wit hout addit ional equipment , skill and
speed are mose essent ial.
2. ACLS (Advanced cardiac life support ). Use of
equipment and drugs for assist ing vent ilat ion or
circulat ion.
Basic life support
Call for help. Posit ion t he vict im supine on firm flat
surface wit h head level wit h t he heart .
1. Airway
* Clear airway by cleaning blood, secret ions,
foreign part icles(suction if available).
* Prevent post erior displacement of t ongue due
t o muscle relaxat ion during CPA , by head
t ilt and chin or j aw t hrust (may use an air-
way if available). Head t i l t : Put a hand at
forehead and t ilt head back t o sniffing or
neut ral posit ion in an infant and lit t le more
in older children and adult s. (Caut i on: I n
a pat ient wit h suspect ed cervical spine in-
j ury head t ilt shoule be avoided) Chi n l i f t :
Put finger of ot her hand under bony part
Jaw t hr ust : Place 2-3 fingers under each
side of lower j am at it s angle and lift j aw up-
ward wit hthe elbow resting on the surface
on which victim is lying.
2. Breat hing
* Det ermine t he absence of breat hing. Give
mout h t o mout h / nose/ mask/ airway
breat h(may use bag and mask if available).
I nhale and t hen make a seal around t he
mout h and nose t oget her in an infant and seal
mout h only in older children and adult s (nose
pinched wit h t he hand used for head t ilt ) t o
exhale smoot hly. Rat e of breat hs should be
20/ min for infant s; 15/ min in older child and
10-12/ min in adult s.
c. Circulat ion
* Det ermine t he absence of pulse aft er 2 breat hs
(rescue breat hs). Ext ernal cardiac massage if
asyst ole and unresponsive t o rescue breat hs.
I n children, perform cardiac massage if HR
< 60/ min wit h signs of poor perfusion.
* Rescuer should st and or kneel at t he side of
t he pat ient so t hat his hips are on a level
with the victim’s chest.
* I n a newborn 2 t humbs are posit ioned side
by side on st ernum j ust below the nipple
line, with fngers encircling chest and sup-
porting the back and compress sternum by
0.6-1.2cm (120/min).
* I n an infant put index finger at t he int ersec-
t ion of int ermammary line and sternum. Use
2-3 fngers (index, middle and ring) to
compress st ernum by 1.5-2.5 cm(100/ min)
and do not lift t he finger when compression is
released. Two t humb- encircling hands t ech-
nique can also be used.
* I n children(1-8 years) use heel of hand on
lower half st ernum wit h long axis of heel
same as long axis of sternum and com-
press 2.5-3.5cm (100/min)
* I n adult s t he heel of one hand is placed on t he
lower st ernum and t he ot her hand placed on
t op of t he first . The elbows should be locked in
posit ion wit h t he arms st raight and t he shoul-
ders over t he hands. St ernum should depress
by 3.5-5.0 cm and t he rat e of compression
should be 80 t o 100/ min.(CAUTI ON: Do not
exert pressure on t he ribs, cost al cart ilages
49
or xipoid)
Combi nat i on of vent i l at i on and car di ac massage
I f bot h cardiac and respirat ory arrest-Compression:
vent ilat ion= 1.5: 2 in adult s and children> 8 years:
Children and infant s 1-8 years = 5: 1; Neonat es= 3: 1.
Advanced Cardiac Life Support (ACLS)
I f ACLS facilit y is available, shift t he pat ient t o ACLS
as soon as possible. I f t his is not available t hen cont inue
cardiac massage t ill spont aneous HR is more t han 60-
80/ min and cont inue art ificial breat hing t ill adequat e
respirat ory effort s are present (good chest movement ,
no cynaosis or shock). For ALCS proceed in t he folowing
order.
1. ECG monit oring (if available)
* I f vent ricular fibrillat ion, defibrillat ion.
* I n adult s.First shock at 200 Joules; if t he first
is unsuccessful t hen a second shock at 200-
300 Joules. I f bot h fail, addit ional shocks at
300-360 Joules are given.
* I n children. 2 Joules / kg and can be repet-
ed a few t imes (if does not revert t o normal
rhyt hm). Cont inue cardiac massage in t he
mean t ime.
* All pat ient s require oxygen(100%) because
even wit h best CPR only a fract ion of t he
cardiac out put is provided and alo t here are
ot her fact ors causing vent ilat ion perfusion
mismat ch.
* Est ablish I V line as early as possible t o give
drugs and fluids and int ubat ion of t rachea
should be done t o cont inue art ificial vent ila-
t ion.
* Drugs are used in t he following order if indi-
cat ed.
I nj .Adr enal i ne
I ndicat ion: Asyst ole, sympt omat ic bradycardia
unresponsive t o vent ilat ion, I n adult s: 1 mg I V every
3-5 minut s. I n children: 0.1 ml/ kg of 1: 10,000 solut ion
(0.01 mg/ kg ) I V, int ra-osseous or 0.1 ml/ kg of: 1: 1000
solut ion by endot racheal t ube followed by several
posit ive pressure breat hs. Can be repeat ed every 5
min by eit her rout e. I V rout e is preferred and should
be used as soon as I V access is achieved (I nt racardiac
rout e is not desirable).
I nj .Li gnocai ne
I ndicat ion: Vent ricular t achycardia or fibrillat ion non
resposive t o recurs aft er defibrillat ion.I n adult s: I nit ial
bolus dose is 1.5 mg/ kg. Addit ional bolus of 0.5-1.5
mg/ kg can be given 5-10 miut es during CPR up t o a
t ot al dose of 3 mg/ kg.I n children: I nj . 1 mg/ kg I V st at
followed by infusion at 20-50 mcg/ kg/ min.
I nj . Ami odar one
I ndicat ion: Shock refract ory vent ricular fibrillat ion
( as an alt ernat ive t o or aft er failure of lignocaine).I n
adult s: I nit ially 300 mg rapid infusion in 20-30 ml saline
followed by 150 mg over 10 minut es followed by 1 mg/
min for upt o 6 h t o 0.5 mg/ kg/ day.
I nj .At r opi ne
I ndicat ion: Vagally mediat ed bradycardia during
int ubat ion, HR< 80 or asyst ole in an infant and
sympt omat ic bradycardia wit h AV block in any child.
Dose and rout e: 0.02 mg/ kg bolus(not < 0.1 mg or >
0.5 mg for a child and 1.0 mg for an adult ). This dose
may be repeat ed aft er 5 minut es for a maximum t ot al
dose of 1.0 mg for a child and 2.0 mg for an adult .
I nj .Nal oxone
I ndicat ion: Narcot ic overdos or poisoning and
newborn resuscit at ion (if mot her has been given
morphine or pet hidine during labour. Dose and rout e
0.1 mg/ kg I V.
I nj . Sodi um bi car bonat e ( NaHC03)
Not required rout inely as it can cause alkalosis lat er
and worsen respirat ory acidosis by releasing CO2 in
inadequat e vent ilat ion. I ndicat ion: Hyperkalaemia,
significant met abolic acidosis (pH< 7.2) or prolonged
CPR. I n adult s and in children: I nj .Sodium bicarbonat e
1 mEq/ kg st at and 0.5 mEq/ kg every 10 minut es in
prot ract ed resuscit at ion.
I nj .Cal ci um
I ndicat ion: Not used rout inely now a days unless
t here is hyperkalemia, hypocalcaemia or calcium
channel blocker t oxicit y. Dose and rout e: (in children)
0.5 ml/ kg of calcium gluconat e I V . I n adult s 10 ml t o be
given as a slow infusion under ECG monit oring.
I nj .Gl ucose
I ndicat ion - Hypoglycaemia Dose and rout e: - 0.5 -1
g/ kg I V. 5. Try t o get ABG, serum elect rolyt es and blood
sugar (dext rose st ick/ glucomet er) - post resuscit at ion
50
care.
● Maint ain mechnical vent ilat ion for several hours
t o ensure adequat e oxygnat ion and vent ilat ion.
● Look for and t reat seizures.
● I nj .mannit ol 0.5-1 g/ kg I V if raised int racranial
t ension.
● Maint ain t emperat ure, fluid and elect rolyt e bal-
ance and ABG.
● Treat shock wit h fluids, dopamine, dobut amine
and adrenaline infusion as required.
● Treat t he underlying pat hology causing CPA.
Moni t or i ng
Pulse should be palpable and chest expansion should
be seen during effect ive CPR, Blood pressure, Sp02, ET
CO2 ( I n int ubat ed pat ient and if facilit y available) , ABG
should be monit ored during and soon aft er CPR.
Ter mi nat i on of CPR
I f asyst ole persist s for > 10 minut es aft er CPR has
been performed, vent ricular fibrillat ion eliminat ed,
successful endot racheal int ubat ion accomplished
and confirmed, adequat e vent ilat ion provided and
appropriat e medicat ions given.
Pat i ent educat i on
● Explain t o parent s t hat many causes of CPA are
prevent able e.g., injuries (by providing safe
environment), poisoning (by keeping drugs
out of reach of children), foreign bodies (safe
t oys and avoid beads, balloons et c., and avoid
eat ables like peanut s in infant s). Young children
should be closely supervised.
● Generlal public should be t rained in BLS.
● Healt h care workers should be able t o recognize
and refer emergencies in t ime, and also know
about BLS.
Ref er ences
1. Management of Caradic and Respirat ory Arrest .
I n: Davidson’s A pract ice of Anaet hesia, 6t h Edi-
t ion, Wylie and Churchill, 1995. pp1409-1425.
2. New Guidelines for Cardiopulmonory Resucit a-
t ion and Emergency Cardiac Care - Changes
in t he Management of Cardiac Arrest . JAMA
2001; 285(10) 1267.
3. Cardiopulmonory Resuscit at ion in infant s and
children. I n: principles of Crit ical Care Ed.Udwadia
FE,1995, Oxford Universit y press Delhi.
4. Cardiopulmonory Resuscit at ion (CPR) I n: Har-
rison’s principles of I nt ernal Medicine. Kasper
Dt .Braunwald E,Fauci As et al (eds) 16t h Edit ion
2005, MeGraw Hill Company I nc, New York, pp
1608- 1624.
BURNS
Burns are a moj or prevent able cause of morbidit y
and mort alit y. These can be heat or space heat ing,
moist heat - scalds and fat burns, ionizing radiat ion,
elect ric burns, frict ion, chemicals and cold - frost bit e.
SALI ENT FEATURES
● Burns, pain, anxiet y fluid loss and dehydrat ion,
local t issue oedema and infect ion.
● Early complicat ions include shock, t oxaemia,
sloughing of mucous membranes-gast roint est inal
t ract and respirat ory t ract , inhalat ion inj uries,
acut e renal failure, and haemat emessis ( Cur l i ng
ul cer ) .
● Lat e complicat ions include, prot ein losing en-
t erpat hy, secondary haemorrhage, hypert rophic
scar/ keloid and cont ract ure.
Treatment
I mmedi at e r esusci t at i on and car e
● Clear airway, suspect inhalat ion inj ury if hist ory of
being t rapped in close space, facial burns, st ing-
ing of eyebrows/ nasal hairs, respirat ory dist ress,
hoarseness of voice or st ridor, alt ered conscious-
ness and soot in sput um.
● Check for breat hing and circulat ion and provide
support .
● Rule out ot her associat ed inj uries.
● I nsert nasogast ric t ube in all maj or burns.
Assess t he sever i t y of bur ns
Assssment includes calculat ion of surface area of
burns: Rule of nine/ chart s, dept h of burns, locat ion of
burns, pat ient ; s age and presence of associat ed inj ury
or disease. Cr i t er i a f or admi ssi on or t r ansf er t o a
bur ns cent er
51
● Burns of more t han 20% body surface in an
adult .
● Burns of more t han 10% body surface area in a
child under 10 or adult over 50 years,
● Burns of more t han 5% body surface area in
an infant .
● Burns of head, face, neck or perineum.
● Respirat ory burns or inhalat ion inj ury.
● Circumferent ial burns.
Transfer should be done in a fully equipped
ambulance wit h secured airway and circulat ory support .
Fluid and electrolyte imbalance
and replacement ( In Adults)
Dist urbances in fluid and elect rolyt e balance occur
in a wide spect rum of diseases, are not confined t o any
part icular field of medicine and are common following
burns, t rauma and maj or surgery.
The convent ional and easy met hod of evaluat ing
dist urbances in fluid and elect rolyt e balane is t he
frequent measurement of t he concent rat ion of serum
elect rolyt es. I t is crucial t o remember t hat int racellular
and ext racellular elect rolyt es are normally const ant , and
t hat maj or shift s in and out of ‘compart ment s’ can occur
in disease wit h minimal changes in serum elect rolyt e.
Composit ional changes also involve dist urbances in
acid-base balance.
Vol um changes: vol ume def i ci t
1. Obvious causes
* Vomit ing diarrhoeas, int est inal fist ulae, na-
sogast ric suct ion, fluid loss following burns,
sequest rat ion of fluid in soft t issue inj uries
and infect ions, diuret ics, renal disease/ ader-
nal insufficiency.
2. Less obvious causes
* unsuspect ed inadequat e fluid int ake, fluid
loss t hrough excessive sweat ing as in high
fever, hot humid t emperat ure, haemodialysis,
haemofilt rat ion from surgical incisions and in
diseases like t et anus.
Management
The first principle is t o rest ore circulat ing volume
t hrough infusion of int ravenous fluids. Once t his is
sat isfact orily achieved, dist ubances in elect rolyt es and
acid-base balance if present need t o be rect ified. Various
fluids used for volume replacement are given below:
Repl acement f l ui ds
1. Replacement fluids are used t o replace abnormal
loss of blood, plasma or ot her ext racellular fluids
as first line t reat ment for hypovolaemia in.
* Treat ment of pat ient s wit h est ablised hypovol-
aemia e.g. haemorrgagic shock.
* Maint enance of normovolaemia in pat ient s
wit h ongoing fluid lossing e.g. surgical blood
loss.
2. I nt ravenous replacement fluids are t he first line
of t reat ment for hypovolaemia. I nit ial t reat ment
wit h t hese fluids may be lifesaving and provide
some t ime t o cont rol bleedig and obt ain blood for
t ransfusion if it becomes necessary.
3. Cryst alloid maint enance fluids, which cont ain
dext rose, are not suit able for use as replacement
fluids. Only cryst alloid solut ions wit h a somilar
concent rat ion of sodium t o plasma (normal sa-
line or balanced salt ) solut ions (Ringer’s lact at e
or Hart mann’s solut ions) are effect ive as replace-
ment fluids.These should be available in all hos-
pit als where int ravenous replacement fluids are
used. Fluids and elect rolyt e requirement in adult s
and children are shown in Table 2.3.
4. Cryst alloids should be infused in a volume at
least t hree t imes t he volume lost in oeder t o cor-
rect hypovolaemia.
5. All colloid solut ion (albumins, dext ran, gelat ins
and hydroxyet hyl st arch solut ions) are replace-
ment fluids. However, t hey have not been shown
t o be superior t o cryst alloids in resuscit at ion.
6. Colloid solut ions should be infused in a volume
equal t o t he blood volume deficit .
7. Plasma should never used as a replacement fluid.
8. Plain wat er should never be infused int ravenous-
ly. I t will cause haemolysis and will probably be
fat al.
9. I n addit ion t o t he int ravenous rout e, t he int raos-
seous, oral, rect al or subcut aneous rout as can be
used for t he administ rat ion of fluids, blood and
cert ain drugs. However, wit h t he except ion of in-
t raosseous rout e, ot her rout es are generally un-
suit able in severely hypovolaemic pat ient s.
10. Rect al fluids are administ ered t hrough a plast ic or
52
rubber enema t ube which is insert ed int o rect um
and connect ed t o a bag or bot t le of fluid. The
fluid rat e can be cont rolled by using a drip giv-
ing-set , if necessary. The fluids used need not be
st erile. A safe and effect ive solut ion for a rect al
rehydrat ion is 1 lit er of clean drinking wat er wit h
t easpoon of t able salt .
11. Subcut aneous fluids: Occasionally, when ot her
rout es of administ rat ion of fluids are unavailable
a subcut aneous infusion can be used. A cannula
or needle is insert ed int o t he subcut aneous t issue
(t he abdominal wall is a preferred sit e) and st erile
fluids are administ ered in a convent ional manner.
Do not give dext rose-cont aining solut ions subcu-
t aneously as t hey can cause sloughing of t issues.
12. Oral and nasogast ric fluids: Oral rehydrat ion can
oft en be used in mildly hypovolaemic pat ient s if
t he oral rout e is not cont raindicat ed. Do not use
if:
* The pat ient is unconscious.
* The pat ient has gast roint est inal lesions or re-
duced gut mot ilit y e.g. obst rut ion.
* General anaest hesia and surgery is planned
imminent ly.
WHO/ UNI CEF f or mul a f or or al r ehydr at i on f l ui d:
Dissolve in one lit re of drinkable wat er
Sodium chloride 2.6 g/ L
Trisodium cit rat e /
dihydrat e
2.9 g/ L
Pot assium chloride 1.5 g/ L
Glucose anhydrous 13.5 g/ L
Result ing concent rat ions
Na+ 75 mmol/ L, C1- 65 mmo1/ L, K+ 20 mmo1/ L,
Glucose anhydrousv 75 mmo1/ L, Cit rat e 10
mmo1/ L,
Tot al osmolarit y 245 mmo1/ L.
Mai nt enance f l ui ds
Maint enance fluids are fluids used t o replace t he
normal physiological loss t hat occurs in a pat ient t hrough
skin, lung, faeces and urine. Since a considerable
proport ion of t he loss is wat er, maint enance fluids are
mainly composed of wat er in t he form of a dext rose
solut ion. Some elect rolyt es may also be included in
t hese solut ions.
All maint enance solut ions are cryst alloid solut ions.
Some examples of cryst alloids t hat are suit able t hat are
suit able as maint enance fluids are: 50% dext rose and
4% dext rose in sodium chloride 0.18%
Fl ui d and el ect r ol yt e f or adul t and chi l dr en
under n0r mol ci r cumst ances
Weight Fluid ml/
kg/24 H
Sodium
mmol/
kg/24 H
Potassium
mmol/
kg/24 H
Children
First 10 kg 100 (4*) 3 2
Second 10
kg
50 (2*) 1.5 1
Subsequent
kg
20 (1*) 0.75 0.5
Adults
All weights
(kg)
35 (1.5*) 1 0.75
* These figures represent t he fluid requirement s in
m1/ kg/ hour.
Saf et y
Before giving any int ravenous infusion:
1. Check t hat t he seal of t he infusion fluid bot t le or
bag is not broken.
2. Check t he expiry dat e.
3. Check t hat t he solut ion is clear and free from vis-
ible part icles.
Stridor
Causes
Common causes of st ridor in children ara (i)
congenit al laryngomalacia, (ii) croup (acut e laryngit is,
laryngot racheobronchit is, epiglot t it is); I n adult s, are (i)
croup, (ii) allergies and (iii) t umours, Sudden onset of
st ridor may be caused by aspirat ion of a foreign boby.
Ot her causes include perit onsillar, ret ropharyngeal
abscesses, angioedema and hypocalcaemic t et any.
Sal i ent f eat ur es
● Noisy respirat ion primarily during inspirat ion pro-
duced by t urbulent airflow t hrough narrowed air
passages.
● Respirat ot y dist ress, rest lessness and cyanosis
are feat ures of severe airway abst ruct ion.
53
Treatment
Treat ment of common causes of st ridor is discussed
below in four sect ions
A. Acut e laryngit is/ laryngot racheobron-
chit is
B. Spasmodic croup
C. Epiglot it t is
D. Dipht heria
Acut e l ar yngi t i s, l ar yngot r acheobr onchi t i s
( cr oup)
I t is an acut e infect ion of t he larynx and is usually
caused by viruses. I n children, may lead t o respirat ory
obst rut ion.
Nonphar macol ogi cal
● Maint ain airway by posit ioning t he pat ient in lat-
eral posit ion wit h neck slight ly.ext ended.
● Gent le suct ion of secret ions, if required.
● Oxygen by vent imask/ hood at t he of 4-6 L/ min.
● Wit h t he support ive and specific t herapy, need
for endot racheal int ubat ion/ t racheost omy may
arise rarely. I n case, t he pat ient is det driorat-
ing st eadily despit e t herapy, elect ive int ubat ion/
t racheost omy should be done t o prevent respira-
t ory failure.
Phar macol ogi cal
Mild cases with minimal stridor (on exertion/
crying) do not require any treatment and may
need rest only. Moderate (stridor at rest) and
severe cases (to be hospitalized immediately) need
specifc therapy in the form of:
1. I nj . Dexamet hasone 0.4 mg/ kg I M st at and fol-
lowed by
2. I nhaled Adrenaline 0.01 - 0.05 mg/ kg/ dose
t o be dilut ed in 3 ml saline every 1-2 hours. A
few doses can be administ ered unt il side effect s
viz. t achycardia, t remors et c. apper. or I nhaled
Budesonide 500-1000 mcg/ dose 12 hourly t ill re-
sponse is seen.
3. I nt ravenous fluids maint enance dose (see re-
spect ive sect ion on fluids and elect rolyt es in
adult s and children).
Spasmodi c cr oup
I t occurs most commonly in children 1-3 years of
age. I t is possibly allergic and recurrent and occurs more
oft en in t he evening or night t ime. I t has sudden onset ,
preceded by mild coryza and hoarseness. Sympt oms
usually diminish wit h in few hours.
Taking out t he child wit h spasmodic croup in fresh
air may decrease t he airway obst ruct ions.
Epi gl ot t i t i s
I t is usually caused by H. influenzae and is a
pot ent ially life-t hreat ening condit ion. Lat eral X-ray of
soft t issue neck may show swollen epiglot t is ( t humb
si gn) . I t is a medical emergency; airway and specific
t herapy must be int roduced aggressively.
Treatment
1. Nonpharmacological t reat ment as above in acut e
laryngit is.
2. I nj . Cefot axime 100 mg/ kg/ day divided int o 3
does.(or) I nj . Ceft riaxone 100 mg/ kg/ day (maxi-
mum dose 4 g/ day) in 2 divided doses. I f cepha-
losporins not available Tab. Chloramphenicol 500
mg 6 hourly. I n Children 100 mg/ kg/ day divided
int o 6 hourly doses.
Di pht her i a
I t is usually seen in non-immunized children.
Sal i ent f eat ur es
● Present s as st ridor but laryngeal examinat ion may
show a membrane like st ruct ure (pseudomem-
brane), removal of which leads t o bleeding.
● Large cervical lymph nodes (Bull neck appear-
ance) and hoarseness.
● Common complicat ions are palat al palsy, I I I
nerve palsy, polyneurit is and myocardit is.
Treatment
1. Support ive t reat ment as above in acut e laryngi-
t is.
2. I mmediat ely refer t he child t o I nfect ious Diseases
Hospit al under supervision and oxygen t herapy.
I n case t he child cannot be t ransferred isolat ion
should be done and following measures should
be t aken immediat ely:
3. I nj . Dipht heria ant it oxin 20,000 - 40,000 I U, I V
or I M for pharyngeal and laryngeal involvement s
54
wit h disease present for < 48 hours; 40,000 t o
60,000 I U for nasopharyngeal infect ions; 80,000
t o 100,000 I U for diffuse involvement t hat has
been present for > 3 days.
4. I nj . Cryst alline penicillin 25,000 - 50,000 unit s/
kg/ day divided int o a doses for 14 days. (or) I nj .
Procaine Penicillin 1 Lac - 25,000 - 50,000 unit s/
kg/ day in 2 divided doses for 14 days. (or) Syr.
Eryt homycin 40-50 mg/ kg/ day divided int o 4 dos-
es for 14 days.
5. I V saline infusion over 60 min.
Moni t or i ng and f ol l ow up
1. Wat ch t he child for alt ered sensorium, degree of
st ridor, pulse rat e, respirat ory rat e and for ot her
feat ures of respirat ory dist ress like int ercost al re-
cession et c.
2. Larryseal examinat ion should not be done unt il
facilit ies for int ubat ion are available because it
might lead t o sudden respirat ory arrest .
3. I f child develops st ridor at rest , hospit alize im-
mediat ely.
4. I ncreasing respirat ory dist ress wit h alt erat ion of
sensorium or cyanosis may be an indicat ion for
int ubat ion.
Pat i ent educat i on
● Avoid overuse and misuse of voice.
● I f st ridor worsens or is not iced at rest , t he pat ient
should immediat ely report t o t he nearest healt h
facilit y.
● Children wit h Dipht heria should be complet ely
immunized aft er recovery of t he current episode
and cont act t o be immunized immediat ely (See
sect ion on immunizat ion).
Ref er ences
1. St ridor in: Scot t Brown’s Ot olaryngology: 5t h Edi-
t ion, Volume 5, 1987 pp. 420-427.
2. congenit al Anomalies of t he Larynx. I n: Nelson’s
Text book of Paediat rics. Behrman RE, Kleigman
RM, Jenson HB (eds). 17t h Edit ion, 2003, pp
1409-1410
Septicaemia
Sept icaemia is a clinical condit ion condit ion associat ed
wit h invasion of blood st ream by microorganisms
giving rise t o feat ures of syst emi c i nf l ammat or y
r esponse syndr ome (SI RS) i.e. presence of any
t wo of t he following: fever/ hypot hermia, t achypnoea,
t achycardia, leucocyt osis/ leucopenia. I t may be
associat ed wit h infect ion at specific sit es (e.g. lungs,
urinary t ract ,gast roint est inal t ract ) or t here may be
no clear originat ing focus. Sept icaemia occurs more
commonly in pat ient s wit h defect ive baby defenses.
I n previously healt hy persons, St aphylococcus aureus,
St rept ococcus pneumoniae and Escherichia coli are
t he most frequent organisms, while in pat ient s wit h
defect ive immune syst ems, Gram-negat ive bact eria
including Pseudomonas aeruginosa may be responsible.
Ot her febrile illnesses due t o ent eric fever and malaria
may be difficult t o different iat e from t hese pat hogens
clinically. Sept icaemia when persist s can result in mult i-
organ dysfunct ion syndrome requiring immediat e t o
maint ain haemost asis.
Sal i ent f eat ur es
● Sick look, feat ures of SI RS, sympt oms of local
sit e of infect ion of respirat ory/ gast roint est inal
syst em et c and sympt oms due t o decreased per-
fusion of various organs e.g. confusion, disorien-
t at ion, decreased urinary out put ,ict erus, bleeding
diat hesis (DI C) and haemodynamic inst abilit y like
hypot ension.
Treatment
Nonphar macol ogi cal
1. Care of airway and breat hing as given in sect ion
on CPR.
2. Removal or drainage of a focal source of infec-
t ion. I ndwelling int ravenous cat het er, Foley’s
cat her et c should be replaced if considered as a
source.
3. General care of skin, orodent al hygiene and nut ri-
t ion supplement at ion should be t aken care of in
prolonged severe seosis.
Phar macol ogi cal
1. Oxygen t herapy - 2-4 lit ers/ min wit h cat het er/
mask (t o keep SPO2 > 95%).
2. I nt ravenous fluids - t o be guided by haemody-
namic st at us. I f in shock, aggressive fluid t herapy
and ment ioned in sect ion on shock t o maint ain
urinary out put at more t han 1 ml/ kg/ hour.
55
3. Ant imicrobial agent s - Ant imicrobial t herapy
should be init iat ed as soon as samples for cul-
t ure are wit hdrawn from blood and ot her relevant
sist es. Choice of ant ibiot ics depends on suspect-
ed organism.
I mmunocompet ent host
1. I nj . Cefot axime 150-200 mg/ kg/ day in 3 divided
doses.(or) I nj . Ceft riaxone 100 mg/ kg/ day (max-
imum dose 4g/ day) in 2 dided doses.
2. I nj . Gent amicin 7.5 mg/ kg/ day in 2-3 divided
doses. (or) I nj . Amikacin 15 mg/ kg/ day in 2-3
divided doses.
3. Add Penicillin/ Vancomycin if St rept ococus/ St a-
phylococus organisms are suspect ed. I nj . Peno-
cillin G aqueous 200,000-300,000 unit s/ kg I V 4
hourly. (or)I nj . Vancomycin 15 mg/ kg/ day in 2
divided doses
I mmunocompr omi sed host
1. I nj . Ceft azidime I V 150 mg/ kg/ day in 3 divided
doses.
2. I nj . Vancomycin 15 mg/ kg/ day in 2 divided doses.
Fol l ow up and moni t or i ng
● Cont inuous monit oring of pulse, respirat ory
rat e,blood pressure, capillary filoling t ime, uri-
nary out put and neurological st at us should be
done for early det ect ion of sept ic shock or mult i-
organ failure.
● Pat ient should be referred t o t ert iary level cent re
if very sick or shows no signs of improvement
aft er init ial t herapy.
Pat i ent / par ent educat i on
● I mmunocompromised pat ient s should be in-
formed about feat ures of early sepsis. Fever in
any child wit h congenit al or acquired immunode-
ficiency st st e should be t aken very seriously.
Ref er ences
1. Sepsis and Sept ic Shock. I n: Harrison’s Principles
of I nt ernal Medicine. Kasper DL, Braunwald E,
Fauci AS et al (eds), 16t h Edit ion, 2005, McGraw
Hill Company I nc., New York, pp 1606-1612.
2. Sepsis and Shock. I .: Nelson’s Text book of Pae-
diat rics. Behrman RE, Kleigman RM, Jenson HB
(eds), 17t h edit ion 2004, WB Saunders, pp 846-
850.
COMA
Coma is defined as a prolonged period of
uncondciousness and lack of react ion t o st imulus.
Pat ient s in coma can not be aroused.
Sal i ent f eat ur es
Following causes affect t he funct ions of ret icular -
act ivat ing syst em and it s connect ions wit h cerebrrum.
● St ruct ural damage t o brain (haemorrhage, t u-
mors, t rauma, localized infect ions, meningit is,
st roke).
● Met abolic dist urbances (ischaemia, anoxia, urae-
mia, diabet es), respirat opry/ hepat ic/ renal failure,
dyselect rolyt aemia, endocrinopat hies, drugs like
opiat es, barbit urat es, benzodiazepines, ant i-de-
pressant s and cyanide.
● Abnormal elecrical act ivit y - periodic lat eralized
epilept iform discharge (PLED).
Treatment
Nonphar macol ogi cal
● The immediat e goal in acut e coma is t he preven-
t ion of furt her nervous syst em damage.
● Hypot ension, hypoglycaemia, hypercalcemia, hy-
poxia, hypercapnia and hypert hermia should br
correct ed rapidly and assiduously.
● An oropharyngeal airway is adequat e t o keep t he
pharynx open in drowsy pat ient s who are breat h-
ing normally.
● Tracheal int ubat ion is indicat ed if t here is apnoea,
upper airway obt ruct ion, hypovent ilat ion or em-
esis, or if t he pat ient is liable t o aspirat e because
of coma.
● Mechanical vent ilat ion is required if t here is hy-
povent ilat ion or if t here is an int racranial mass
and a need t o induce hypocapnia in order t o law-
er int racranial pressure.
● Est ablish int ravenous access.
Phar macol ogi cal
1. I nj . Glucose (25 or 50%) 50 g I V.
2. I nj . Thiamine 100 mg I V.
3. I f opiat e overdose is suspect ed, give I nj . Naloxone
0.8 mg I V. Response is inadequat e, double t he
dose every 15 minut es (for det ails see sect ion on
56
opioid int oxicat ion).
4. I f benzodiazepine overdose is suspect ed give I nj .
Flumazenil 200 mcg I V slowly. I f no response re-
peat 100-200 mcg aft er 1 minut e. I f required give
maximum does of 1 mg or give as I V infusion of
100-400 mcg/ h if drowsiness recurs.
5. I f focal neurological deficit or signs of herniat ion/
decerebrat ion/ decort icat ion occurs, CT scan, EEG
and neurologic consult at ion is required.
6. I f no clear aet iology and no herniat ion - CSF ex-
eminat ion should be done.
7. I f signs of raised int racranial t ension (papilloede-
ma, convulsions, decerebrat e post ure indicat ing
herniat ion) occurs:
* Avoid giving free fluid (glucose solut ion) in-
t ravenously.
* I nj . Frusemide 40 mg I V t o maint ain adequat e
urine out put of 30-50 ml/ h.
* I nj . Mannit ol 1.0 g/ kg I V over 10 minut es.
* Hypervent ilat e t o bring down PCO2 t o 25
mmHg.
* I nj . Dexamet hasone 20 mg I V st at and 6 mg
4 hourly.
Children and young adult s may have ominous early
clinical findings such as abnormal brainst em reflexes
and yet recover. Met abolic comas have a far bet t er
prognosis t han t raumat ic comas. Glasgow coma scale
empirically has predict ive value in case of brain t rauma
( Table 2.5). For anoxic and met abolic coma, clinical
signs such as papillary and mot or responses aft er 1 day,
3 days and 1 week have been shown t o have predict ive
value. Absence of cort ical waves of t he somat osensory
evoked pot ent ials has also proved a st rong indicat or of
poor out come in coma from any cause.
Gr adi ng of coma
Glasgow coma scale for head inj ury ( Table 2-5)
Glasgow coma scale
Eye opening (E) Coma score
Spont aneous 4
To loud voice 3
To pain 2
Nil 1
Best mot or response (M)
Obeys 6
Localizes 5
Wit hdraws (flexion) 4
Abnormal flexion post uring 3
Ext ension post uring 2
Nil 1
Verbal response (V)
Orient ed 5
Confused, disorient ed 4
I nappropriat e words 3
I ncomprehensible sounds 2
Nil 1
Not e: Coma score= E+ M+ V. Pat ient s scoring 3 or 4
have an 85% chance of dying or remaining veget at ive,
while scores above 11 indicat ive only a 5 t o 10%
likelihood of deat h or veget at ive st at e and 85% chance
of moderat e disabilit y or good recovery. I nt ermediat e
scores correlat e wit h proport ional chances of recovery.
Ref er ence
1. Coma. I n: Harrison’s Principles of I nt ernal Medi-
cine. Kasper DL, Braunwald E, Fauci AS et at
(eds), 16t h Edit ion 2005, McGraw Hill Company
I nc., New York, pp 1624-1631.
2. Head I nj ury. I n: Harrison’s Principles of I nt ernal
Medicine. Kasper DL, Braunwald E, Fauci AS et al
(eds), 16t h Edit ion 2005, McGraw Hill Company
I nc., New York, pp 2447-2452.
57
Poisoning
Gener al consi der at i ons
I ncreasing incidence of poisoning is at t ribut able
t o rapid development of newer compounds in t rade,
indust ry and medicine and easy access t o t hem. A
st epwise care approach t o a pat ient of poisoning is
helpful in successful management
St epwi se car e appr oach
● Diagnosis - Suspect and ident ify poison, if pos-
sible.
● Treat ment includes basic principles, ant idot es,
sympt omat ic and support ive.
● Ant icipat e coomplicat ions, preserve evidence and
prevent sequelae as well as recurrence.
Di agnosi s
1. Suspicion of poisoning should be aroused by sud-
den onset of sympt oms, uniform and increasing
severit y of sympt oms in a group e.g. food poison-
ing or indust rial poisoning. Unexplained nausea,
vomit ing, diarrhoea, drowsiness or coma, eupho-
ria, increased psychomot or act ivit y, convulsions,
delirium and unusual breat h smell are sympt oms
which in t he absence of disease need careful
evaluat ion for suspect ed poisoning. Signs and
sympt oms helpful in diagnosis of poisoning are
shown
2. I dent ificat ion of t he subst ance should not t ake
precedence over t he first st ep, since t he process
is slow and unreliable or lack of proper hist ory
might cause confusion. Act ion of poisons is modi-
fied by physical fact ors like quant it y, form, chemi-
cal combinat ion, diluion, rout e of administ rat ion
and host fact ors like age, idiosyncrasy, sleep,
food and use (abuse) of mult iple subst ances.
Copper sulphate poisoning
I nt r oduct i on
Copper sulphat e is blue in colour and used as an
ant isept ic, fungicide, herbicide and in cryst al growing
set s. Copper sulphat e is a powerful oxidizing agent and
corrosive t o mucous membranes. Absorpt ion of copper
Signs and symptomatology of Poisoning
58
sulphat e ranges from 40 t o 60% following ingest ion.
Copper is t ransport ed across t he int est inal mucosa
which is facilit at ed by met allot hionein. Highest
concent rat ion of copper is seen in t he liver, brain,
heart , kidneys and muscles. Ceruloplasmin renders free
copper innocuous wit h subsequent biliary excret ion.
Renal clearance is very low.
Symptoms
● Hypersalivat ion
● Abdominal pain
● Vomit ing
● Hemat emesis and melaena may be fat al
● Shock due t o reduct ion in t he int ravascular vol-
ume
● Jaundice due t o hepat ic cell necrosis and haemo-
lysis
● Oliguria, anuria are due t o acut e t ubular inj ury
● Kidney and liver effect s develop 3 t o 4 days aft er
ingest ion
I nvesti gati ons
● Urine analysis
● Complet e blood count
● Liver funct ion t est s
● Blood urea nit rogen (BUN)
● Creat inine
● Blood grouping and Rh typing
Speci al i nvest i gat i ons
● For Hemoglobinuria
● Serum copper and ceruloplasmin
● Met hemoglobin
● Creat inine kinase
Treatment
● Admission
● Gast ric lavage is absolut ely cont raindicat ed
● Egg albumin (5-6 eggs) is used as demulcent
(early oral administ rat ion has brought down mor-
bidit y and mort alit y).
● H2 recept or ant agonist or Prot on pump inhibit or
as slow I V or orally
● D-Pencillamine 250 mg qid orally
● I nj . Vit amin C 500mgs 8t h hourly in int ravenous
fluid as drip
● Fluid and elect rolyt e balance
● Support ive management - cardiovascular support
● Monit oring - renal and hepat ic funct ion
● Blood t ransfusion in select ed cases
Ref er r al
Referral t o higher cent re for support ive care
and monit oring of cardiovascular, renal, liver and
hemat ological syst ems.
Pr ognosi s
Prognosis depends upon early diagnosis and
appropriat e management .
Pat i ent educat i on
● Oral dilut ion wit h milk or wat er (if performed im-
mediat ely) may be helpful
● Egg albumin (5-6 eggs) is used as demulcent
(earlier oral administ rat ion reduces complica-
t ions)
Organophosphorous, Carbamate and
Rodenticide Poisoning in Children
I nt r oduct i on
Poisoning is common among children and t akes
hundreds of innocent lives every year. Unfort unat ely,
most of t hese are accident al. Alt hough in I ndia
poisoning due t o pest icides and rodent icides are less
in comparison t o kerosene and drug over dosage, t he
pract it ioners and pediat ricians should be aware of t hese
due t o t heir easy availabilit y and accessibilit y. There is
a need t o st rengt hen t he capacit y t o diagnose and t reat
such emergencies.
Epi demi ol ogy
I n t he absence of nat ional regist ers or reliable
hospit al-based dat a, one looks forward t o t ert iary
hospit al dat a. Accordingly, organophosphorous (OP)
and carbamat e poisonings comprise less t han one
percent of t ot al poisonings. Rodent icide poisoning is far
less t han t hat of pest icides.
Causes
● The incidence of pest icide poisoning t ends t o be
59
higher among children from lower socio-econom-
ic classes of societ y due t o poor st orage facilit ies
and parent al negligence.
● I nexperience, lack of mat urit y, illit eracy and in-
abilit y t o assess t he risk make t hem ingest poison
accident ally.
● Older children and adolescent s may be direct ly
exposed as field workers, while younger children
may be brought int o t reat ed fields t o accompany
t heir parent s.
● Work clot hes oft en carry pest icide residues, ex-
posing bot h workers and family members t o
harm.
● St ress fact ors for poisoning are grouped as
* Family st ress
* Deat h of a parent
* Ment al illness in a parent
* Financial problems
* I nt erpersonal conflict s among parent s
* Parent al alcoholism
* Divorce, separat ion
● Parent al st ress
* Punit ive parent
* Conflict wit h parent s
● School st ress
* Poor academic achievement
* Examinat ion failure
* change of school
* Teacher st ress
Pat hophysi ol ogy
● Organophosphorous compounds and carbamat es
bind t o one of t he act ive sit es of acet ylcholinest e-
rase (AChE)1 and inhibit t he funct ionalit y of t his
enzyme by means of st eric inhibit ion
● Carbamylat ion of est ers are more quickly revers-
ible t han phosphorylat ion of t he est ers
● Phosphorylat ion of t he est ers in AchE will under-
go “ aging” process
● Aging means loss of one alkyl or alkoxy group
leading t o st able mono alkyl or mono alkoxy
phosphoryl AchE.
● The main purpose of AChE is t o hydrolyze acet yl-
choline (ACh) t o choline and acet ic acid. There-
fore, t he inhibit ion of AChE causes an excess of
ACh in synapses and neuromuscular j unct ions,
result ing in muscarinic and nicot inic sympt oms
and signs.
● The pat hophysiology of int ermediat e syndrome is
not well defined and various st udies are going on.
● I n some individuals, neuropat hy t arget est erase
(NTE) is t arget ed t o cause Organophosphorous
compounds-induced delayed polyneuropat hy.
Poi soni ng dosage
● Children may die of Organophosphorous com-
pounds wit h very minimal dose of 2mg.(0.1mg/
kg)
● St udies showed t hat young animals were more
suscept ible t han adult s of t he same species, and
t hat may be applicable t o human beings as well.
● The poisoning dose varies from compound t o
compound. Therefore what ever be t he sit uat ion,
t he vict ims should be observed for at least 48 t o
72 hours.
Symptoms
● Children are more vulnerable t han adult s due t o
various risk fact ors such as
* Smaller size
* Differing met abolism and
* Rapidly growing and developing organ sys-
t ems.
* Pediat ric pat ient s had predominat ely CNS de-
pression and severe hypot onia, whereas mus-
carinic sympt oms were infrequent .
● Pest icides can rapidly be absorbed t hrough t he
skin, lungs, gast roint est inal t ract , and mucous
membranes
● The rat e of absorpt ion depends on t he rout e of
administ rat ion and t he t ype of organophospho-
rous or carbamat e
● Sympt oms usually occur wit hin a few hours aft er
GI ingest ion and appear almost immediat ely aft er
inhalat ion exposure
● Pat ient s oft en present wit h evidence of a cholin-
ergic t oxic syndrome, or t oxidrome. I t is useful
t o remember t he t oxidrome in t erms of t he t hree
clinical effect s on nerve endings and t hey are
60
* Nicot inic effect s at neuromuscular j unct ions
and aut onomic ganglia
* CNS effect s and
* Muscarinic effect s SLUDGE/ BBB and DUMB-
ELS
● Nicot inic signs and sympt oms include
* Weakness
* Fasciculat ion and paralysis
● CNS effect s may lead t o
* Seizures and
* CNS depression
● Carbamat es have less CNS t oxicit y
● Respirat ory failure
* There seem t o be t wo underlying mechanisms
for respirat ory failure and t hey are an early
acut e mixed cent ral and peripheral respirat ory
failure, and a lat e peripheral failure rat her
t han t wo dist inct clinical syndromes.
Potassium dichromate poisoning
I nt r oduct i on
I n t he indust ry chromium salt s are used in safet y
mat ches, paint pigment s (chromium compounds
can be red, yellow, orange, and green), leat her
t anning, chrome plat ing, and copy machine t oner.
Also, t hese are used as corrosion inhibit ors, pho-
t ographic chemicals, and in magnet ic t apes. Sal t
of hexaval ent chr omi um [ Cr ( VI ) ] i s t oxi c.
Causes
Poisoning happens due t o pot assium dichromat e
salt s usually as accident al or suicidal, and is rarely
occupat ional or environment al.
● Chromium compounds can be sensit izers as well
as irrit ant s
● Cr (VI ) is a powerful oxidizing agent
● Exposure can cause irrit at ion and corrosion. Cr
(VI ) is absorbed from t he lungs, gut , and skin.
Aft er absorpt ion, Cr (VI ) is reduced t o Cr (I I I )
which forms prot ein complexes
● These complexes are t aken up by bone marrow,
lungs, lymph nodes, spleen, kidney, and liver.
60% of absorbed Cr (VI ) is excret ed by t he kid-
neys and approximat ely 10% is eliminat ed by bil-
iary excret ion.
Symptoms
Acut e Cr (VI ) ingest ion Chronic Exposure
● Abdominal pain,
vomit ing, t hirst and
hemat emesis, and
malena
● Feat ures of shock
due t o reduct ion in
t he int ravascular
volume
● Vert igo, convul-
sions, coma
● Effect s on kidney
and liver develop
one t o four days af-
t er ingest ion
● Jaundice due t o he-
pat ic cell necrosis
● Coagulopat hy occa-
sionally
● Oliguria, anuria due
t o acut e t ubular
necrosis
● Syst emic manifes-
t at ions may develop
wit h dermal cont act
wit h Cr (VI ) com-
pounds.
● Eczemat ous der-
mat it is wit h ede-
ma
● I rrit at ion of t he
conj unct iva and
mucous mem-
branes
● Nasal ulcers and
perforat ions, kera-
t it is, gingivit is, and
periodont it is.
● Acut e hepat it is
wit h j aundice
● Lung cancer is t he
most serious long-
t erm effect
I nvesti gati ons
● Urine analysis
● Complet e blood count
● Liver funct ion t est s
● Blood urea nit rogen (BUN) and creat inine
Speci al i nvest i gat i on
● Urine chromium levels
● Bet a-2 microglobulin
Treatment
● Hospit alizat ion
● I nduct ion of vomit ing is cont raindicat ed
● Gast ric lavage wit h magnesium hydroxide or an-
ot her ant acid
● Fluid and elect rolyt e balance
61
● Support ive management- cardiovascular support
and vent ilat or support
● Monit oring - renal and hepat ic funct ion
Ref er r al
Referral t o higher cent re for support ive care
and monit oring of cardiovascular, renal, liver and
hemat ological syst ems.
Pr ognosi s
Acut e chromium poisonings are oft en fat al despit e
t reat ment and prognosis is variable.
Mozhikizhangu poisoning
I nt r oduct i on
The scient ific name of Mozhikizhangu is Gl or i osa
Super ba. I t belongs t o t he family Colchiaceae.
● I t is also known as kalappat hat t ai kizhangu and
nabhikodi
● Ent ire plant , especially t ubers are ext remely poi-
sonous
● Poisoning due t o t his plant is report ed more fre-
quent ly in cert ain part s of Tamilnadu
● I t is cult ivat ed in Sout h I ndia (e.g. Karur, Mula-
nur) and t hen sold in t he market for pharmaceu-
t ical purposes for t he preparat ion of ant i-cancer
agent s
● I t is also grown as an ornament al plant . Toxic
propert ies of t he plant are essent ially due t o ac-
t ive alkaloid colchicine and ot her derivat ives.
● The chemical const it uent s are absorbed from t he
gast ro int est inal t ract and t aken up int ra-cellular-
ly. 50% is bound t o plasma prot eins.
Symptoms
● Sympt oms appear wit hin 2 t o 6 hours aft er in-
gest ion.
● Numbness and t ingling around t he mout h.
● Burning and rawness of t he t hroat .
● Nausea, int ense vomit ing and abdominal pain.
● Bloody diarrhea leading t o dehydrat ion.
● Respirat ory depression
● Dyspnoea
● Shock
● Hypot ension.
● Marked leucopenia, t hrombocyt openia, coagula-
t ion disorders.
● Oliguria
● Hemat uria
● Confusion, seizures, coma and ascending
polyneuropat hy.
● Alopecia/ dermat it is are lat e manifest at ions.
(develop about 1 t o 2 weeks aft er poisoning )
I nvesti gati ons
● Daily full blood count s, coagulat ion t est s
● Serum elect rolyt e levels and urinalysis
● Liver and renal funct ion t est s
● Blood collect ion for colchicine levels. (Collect ed
and kept in t he dark wit h ant icoagulant ).
Treatment
● Admission
● I nduce vomit ing, if pat ient is conscious and alert
● Carry out st omach wash
● Decont aminat ion of digest ive syst em
Tr eat ment gui del i nes
● Monit or respirat ion
● Adequat e airway
● I mmediat e gast ric lavage
● Ant icipat e and t reat hypot ension wit h adquat e
int ravenous fluids and vasopressors
● Transfuse compat ible blood if required.
● Correct dehydrat ion and elect rolyt e imbalance
● Provide cont inuous cardiac monit oring
● Monit or renal funct ion
● I nit iat e forced alkaline diuresis once shock and
dehydrat ion are correct ed (ant i-colchicines ant i-
bodies have been t ried).
Emergency surgical procedures
Venous cut down
Anat omical considerat ions for venous access The
primary sit e for a peripheral venous cut down is t he
great er saphenous vein at t he ankle, which is locat ed at
a point approximat ely 2 cm ant erior and proximal t o t he
middle of t he medial malleolus
A secondary sit e is t he ant ecubit al vein , locat ed 2.5
62
Cm lat eral t o t he medial epicondyle of t he humerus at
t he flexion of t he elbow
Saphenous vei n cut down:
● Prepare t he skin of t he ankle wit h an ant isept ic
solut ion and drape t he area
● I nfilt rat e t he skin over t he vein wit h 0.25% ligno-
caine if t he pat ient is conscious
● A full t hickness t ransverse skin incision is made
t hrough t he area of anest hesia t o a lengt h of 2.5
cm
● By blunt dissect ion , using a curved forceps , t he
vein is ident ified and dissect ed free of any ac-
companying st ruct ures
● Elevat e and dissect t he vein for a dist ance of ap-
proximat ely 2 cm t o free it from it s bed
● Ligat e t he dist al mobilized vein, leaving a sut ure
in place for t ract ion
● Passat ie around t he vein, cephalad
● Make a small t ransverse venot omy and gent ly di-
lat e t he venot omy wit h t he t ip of a closed art ery
forceps
● I nt roduce a large plast ic canula t hrough t he ven-
ot omy and secure it in place by t ying t he upper
ligat ure around t he vein and t he canula
● Use dist al sut ure t o furt her secure t he canula and
t he t ubing
● At t ach t he int ravenous t ubing t o t he canula and
close t he incision wit h int errupt ed sut ures
● Apply a st erile dressing
Compl i cat i ons of per i pher al venous access:
● Perforat ion of t he post erior wall of t he vein
● Dissect ion of t he vein
● Hemat oma
● Phlebit is
● Cellulit is
● Venous t hrombosis
● Art erial t ransect ion
Or ot r acheal i nt ubat i on Pr ocedur e:
● Ensure t hat adequat e vent ilat ion and oxygena-
t ion are in progress, and t hat suct ion, a range of
endot racheal t ubes and laryngoscopes are avail-
able, t oget her wit h int roducer, boogie and magill
forceps
● Connect laryngoscopic blade and handle, check
t he bulb for bright ness
● Have an assist ant manually immobilize t he head
and neck and a second apply cricoid pressure.
The person must maint ain cricoid pressure irre-
spect ive of all ot her event s unt il direct er t o dis-
cont inue by t he int ubat ing doct or
● Use a rapid sequence induct ion unless pat ient is
unresponsive and flaccid
● Hold t he laryngoscope in t he left hand
● I nsert t he laryngoscope int o t he right side of t he
pat ient ’s mout h displacing t he t ongue t o t he left
● Visually examine t he epiglot t is and t he vocal
cords
● gent ly insert t he endot racheal t ube int o t he t ra-
chea wit hout applying pressure on t he t eet h or
t he oral t issues inflat e t he cuff wit h enough air t o
provide adequat e seal
● Check t he placement by bag- valve - t o t ube ven-
t ilat ion
● Visually observe t he lung expansion wit h vent ila-
t ion
● Auscult at e t he chest and abdomen wit h a st et ho-
scope t o ascert ain posit ion
● Release cricoid pressure only when t he t ube is in
sat isfact ory posit ion and t he cuff inflat ed
● I f t he endot racheal int ubat ion is not est ablished
wit hin 30 seconds, discont inue at t empt s, vent i-
lat e t he pat ient and t ry again
Compl i cat i ons:
● Esophageal int ubat ion, leading t o hypoxia and
deat h
● Right main bronchus int ubat ion, result ing in col-
lapse of t he left lung and hypoxia
● I nduct ion of vomit ing, aspirat ion and deat h
● Dislocat ion of t he mandible
● I nabilit y t o int ubat e
● Airway hemorrhage due t o t rauma
● Chipping or looseniong of t eet h
● Dislocat ion of cervical spine during hyper ext en-
sion or hyperflexion
63
Tr acheost omy
Pr ocedur e:
● Assemble t he necessary equipment ( t racheos-
t omt y t ray, t ube, sut ure- cuffed disposable t ra-
cheost omy t ubes are now available)
● Place t he pat ient supine wit h t he neck ext ended
● Surgically prepare and anest het ize t he area lo-
cally
● Make a t ransverse skin incision over t he lower
neck over t he t rachea - preferably below t he 2nd
t racheal ring
● I ncise t he deep cervical fascia, ret ract t he st rap
muscles lat erally
● Expose t he t rachea beware of t he t hyroid ist h-
mus, ret ract it superiorly, ligat e any vessels care-
fully
● I ncise t he t racheal cart ilage aft er confirming by
aspuirat ion of air, removing a cuff of t hr t rachea
● I nsert a cuffed t racheost omy t ube
● I nflat e t he cuff and vent ilat e t he pat ient
● Close t he incision
● Secure t he t ube t o prevent dislodgement
Compl i cat i ons:
● Asphyxia
● Aspirat ion
● Cellulit is
● Creat ion of false passage in t he t issues
● Tracheal st enosis
● Hemorrhage or hemat oma format ion
● Lacerat ion of t he esophagus
● Mediast inal emphysema
● Vocal cord paralysis, hoarseness
I nt er cost al chest dr ai n
Pr ocedur e:
● Ensure fluid resuscit at ion via at least one large ca-
liber iv line and high flow oxygen by mask
● Assemble t he necessary equipment , scrub, don
gown and gloves
● Det ermine t he insert ion sit e; usually at t he nip-
ple level ( 5t h int ercost al space) ant erior t o t ghe
midaxillary line on t he affect ed side
● Use a 36fr t ube in males, 32fr t ube in females
● Prepare and drape t he chest at t he sit e of t ube
insert ion
● Locally anest het ize t he skin and rib periost eum
and int ercost al muscles. Use 30- 40ml of 0.5%
lignocaine in t he adult and infilt rat e ext ensively
● Make a 2 -3 cm t ransverse incision in t he line of
t he int ercost al space at t he predet ermined sit e
and blunt ly dissect t hrough t he subcut aneous t is-
sues, j ust over t he upper border of t he lower rib
● Punct ure t he pariet al pleura wit h t he t ip of t he
clamp, st ret ching up t he opening and put a
gloved finger int o t he incision t o avoid inj ury t o
ot her organs
● Mount t he t ip of t he t ube in t he j aws of t he for-
ceps and advance int o t he pleural space
● Look for fogging of t he t ube wit h expirat ion and
movement of t he wat er column
● Apply an airt ight dressing and t ape t he t ube t o
t he chest
● Obt ain a chest x-ray
● Obt ain art erial blood gases if necessary
● Keep t he chest drain bot t les empt ied regularly
Compl i cat i ons:
● Tube dislodgemnt
● Chest bot t le elevat ion wit h fluid flowing int o t he
chest cavit y
● Damage t o int ercost al nerve, art ery or vein
● Damage t o int ernal mammary art ery if punct ure
is t oo medial
● I nt ercost al myalgia
● I nt roduct ion of pleural infect ion
● Lacerat ion or punct ure of int ra t horacic or int ra
abdominal organs
● Local cellulit is
● Local hemat oma
● Mediast inal emphysema
● Subcut aneous emphysema
Gast r ost omy:
● Assemble necessary equipment ( laparot omy
t ray, t ube, sut ure)
● Place t he pat ient in supine posit ion
● Done under GA or regional anaest hesia
64
Pr ocedur e
● Small incision made in t he ant erior abdominal
wall , usually in t he midline
● Small incision made in t he ant erior st omach wall
inside a pursest ring
● The cat het er (malecot / foley) is int roduced and
t he sut ure snugged around t he cat het er
● The ant erior wall of t he st omach should t hen be
fixed t o t he ant erior abdominal wall t o prevent
dragging
● Laparot omy wound is closed and t he cat het er
fixed t o t he skin
Compl i cat i ons:
● Tube dislodgement
● Leak
● Hemat oma
● Twist of bowel around any int ra perit oneal t ube
wit h obst ruct ion
65
Cardiology
Chapter 3
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
● Rheumat ic Fever
● I nfect ive Endocardit is
● Acut e Pericardit is
● Cardiomyopat hy
● Hypert ension
● Angina Pect oris
● Myocardial I nfarct ion
● Congest ive Heart Failure
● Pulmonary Embolism
● Arrhyt hmias
67
Rheumatic fever
Rheumat ic fever is due t o an aut oimmune react ion
t o group A st rept ococci and involves many organs,
primarily t he heart , j oint s and t he cent ral nervous
syst em.
Causes
Acut e Rheumat ic fever usually occurs about t hree t o
four weeks (range bet ween 1-5 weeks) aft er an at t ack
of group A st rept ococcal t hroat infect ion. Ant igenic
“ mimicry” bet ween st rept ococcal M prot ein and
myocardial cells is t hought t o be t he cause. Poor socio-
economic condit ions predisposes t o Rheumat ic fever
I mpor t ant not e
Children 5 – 15 years, most commonly affect ed
Updated Jones Criteria 1992 – AHA
Maj or
Migrat ory Polyart hrit is
Cardit is
Sydenham’s chorea
ESR / CRP
Eryt hema Marginat um
Mi nor
Fever
Art hralgia
Elevat ed acut e phase react ant s
Subcut aneous nodules
Prolonged PR int erval
Pl us
Support ing evidence of a recent group A
st rept ococcal infect ion (e.g. posit ive t hroat cult ure
or rapid ant igen det ect ion t est ; or elevat ed or rising
st rept ococcal ant ibody t est ).
Diagnosis – One maj or and t wo minor or t wo maj or
crit eria
Treatment
● Primary Ant ibiot ic t reat ment
* Oral Penicillin V-500 mg bd -10 days (or)
* I nj . Benzat hine Penicillin G – 1.2 million unit s
in single dose (or)
* Eryt hromycin – 250 mg qid – 10 days – I f pa-
t ient is allergic t o Penicillin
● Secondary prophylaxis
* I nj . Benzat hine Penicillin – 1.2 million unit s in
every 3 weeks (or)
* Oral Penicillin V – 250 mg bd – daily (or)
* Oral Sulfadiazine
* Eryt hromycin 250 mg t wice daily
Dur at i on
● Cat egory of pat ient
* Pat ient wit hout proven cardit is
* Pat ient wit h cardit is (mild mit ral regurgit at ion
or healed cardit is)
* More severe valvular disease
* Valvular surgery
● Durat ion of prophylaxis
* For 5 years aft er last at t ack or t ill 18 years of
age whichever is longer
* For 10 years aft er last at t ack or 25 years of
age whichever is longer
* Lifelong
Ar t hr i t i s
● Salicylat es
* Doses upt o 2 gram qid in adult s and 80-100
mg/ kg/ day in children t ill sympt oms persist .
● Naproxen
* Dose 10-20 mg/ kg/ day can also be used.
Car di t i s
Prednisolone 1-2 mg / kg/ day can be used for short
periods or upt o a maximum of 3 weeks
Chor ea
Carbamazepine or Sodium valproat e are preferred
t o Haloperidol t o reduce t he abnormal movement s but
response may t ake upt o 2 weeks.Treat ment should
cont inue upt o 1-2 weeks aft er sympt oms subside.
Ref er ences
● Harrison’s principles of int ernal medicine, 16t h
edit ion, pg. 1977 – 1979
● Braunwald’s heart disease, 7t h edit ion, Pg. 2093
– 2098
68
Infective endocarditis
Causes
I nfect ive endocardit is is due t o t he proliferat ion of
micro-organisms in t he endocardium.
Sal i ent f eat ur es
● Acut e and subacut e endocardit is
● Organisms – Nat ive valve
* Viridians st rept ococci
* St aphylococci
* HACEK
* Ent erococci
* St rept ococcus bovis
● Nosocomial
* St aphylococcus aureus
* Gram negat ive organisms
● Prost het ic valve
* St aphylococcus aureus
* Coagulase negat ive st aphylococci
* Facult at ive gram negat ive bacilli
* Dipht heroids and fungi
● I nj ect ion Drug abusers
* Right heart – St aphyloccocus aureus
* Left heart – St aphyloccocus aureus
* Pseudomonas
* Candida
* Lact obacillus
* Corynebact erium
● Polymicrobial endocardit is
Def i ni tion
Duke’s cr i t er i a
2 Maj or (or) 1 Maj or and 3 Minor (or) 5 Minor crit eria
Maj or
● Posit ive Blood cult ure - Typical organism for in-
fect ive endocardit is from 2 blood cult ures or
organism consist ent wit h infect ive endocardit is
on 2 cult ures, drawn 12 hours apart or all of 3
or 3/ 4 blood cult ures, t he first and last drawn
1 hour apart or single posit ive blood cult ure
Pathogenesis of Rheumatic fever
69
for Coxiella burnet t i or phase1 I gG ant ibody for
C.burnet t i> 1: 800.
● Evidence of endocardial involvement by ECHO
* Veget at ions
* Abscess
* Part ial dehiscence of prost het ic valve
● New valvular regurgit at ion.
Mi nor
● Predisposing fact or : Heart Lesion/ drug abuse
● Fever > 38°C
● Haemat ologic causes
* Art erial emboli
* Pulmonary infarct
* Mycot ic aneurysms
* I nt racranial haemorrhage
* Conj unct ival haemorrhage
* Janeway lesions.
● I mmunologic
* Glomerulonephrit is
* Osler’s nodes
* Rot h spot s, RF
● Microbiologic evidence
* Posit ive blood cult ure but not meet ing maj or
crit eria or Serologic evidence of infect ion
Treatment
● Ant ibiot ics based on Blood cult ure and sensit ivit y:
● St rept ococci / Ent erococci –
Penicillin G: 2 – 3 million unit s I .V. 4t h hourly
along wit h Gent amycin 1 mg/ kg I .V. 8t h hourly
for 2 weeks
● Ent erococci: 4 t o 6 weeks.
● St aphylococci: Oxacillin 2 g i.v. 4t h hourly for 4
– 6 weeks
● I f Met hicillin resist ant : Vancomycin 15 mg/ kg I .V.
12 hourly for 4 t o 6 weeks
● HACEK – Ceft riaxone 2 g/ d I .V. for 4 weeks
Pr ophyl axi s
Dent al procedures wherein t here is manipulat ion
of gingival t issue or periapical regions of t he t eet h or
perforat ion of t he oral mucosa (including surgery on t he
respirat ory t ract )
Condi t i ons f or whi ch pr ophyl axi s i s advi sed
● Prost het ic heart valves
● Prior endocardit is
● Unrepaired cyanot ic congenit al heart disease, in-
cluding palliat ive shunt s or conduit s
● Complet ely repaired congenit al heart defect s
during t he 6 mont hs aft er repair
● I ncomplet ely repaired congenit al heart disease
wit h residual defect s adj acent t o prost het ic ma-
t erial
● Valvulopat hy developing aft er heart t ransplant
Ant i bi ot i c r egi mens f or pr ophyl axi s
● St andard oral regimen
* Amoxycillin 2 gm 1 hour before procedure
● I nabilit y t o t ake oral medicat ion,
* I nj . Ampicillin 2gm I V/ I M 1 hour before pro-
cedure
● Penicillin allergy
* Clarit hromycin or Azit hromycin 500 mg 1 hour
before procedure
* Cephalexin 2 gm, 1 hour before procedure
* Clindamycin 600mg, 1 hour before procedure
● Penicillin allergy, inabilit y t o t olerat e oral medica-
t ion
* Cefazolin or Ceft riaxone 1 gm I V/ I M, 30 min
before procedure
* Clindamycin 600 mg I V/ I M, 1 hour before pro-
cedure
Acute Pericarditis
Def i ni tion
I nflammat ion of Pericardium
Cl assi f i cat i on
● Acut e pericardit is - < 6 weeks
● Subacut e pericardit is - 6 weeks t o 6 mont hs
● Chronic pericardit is - > 6 mont hs
70
Causes
I nf ect i ons
● Viral
* Coxsackievirus A and B
* Mumps
* ECHO virus
* Adenovirus et c.,
● Pyogenic
* St rept ococcus
* Pneumococcus
* St aphylococcus
* Tuberculosis
● Fungal
* Hist oplasmosis
* Coccidiodomycosis
* Candida albicans
Non - I nf ect i ous:
* Acut e myocardial infarct ion
* Post myocardial infarct ion (Dressler’s syndro-
me)
* Uremia
* Neoplasia
* Myxoedema
* Aort ic dissect ion
* Rheumat ic fever
* Collagen vascular diseases
* Post radiat ion
* Trauma
* Drug induced
» Procainamide
» Hydralazine
» Phenyt oin
» I sonicot inic acid hydrazide
» Minoxidil
Symptoms
● Chest pain
* Ret rost ernal or left sided relieved by sit t ing up
and leaning forward and int ensified by lying
supine.
● Pericardial frict ion rub
* High pit ched, scrat ching.
● ECG
* Widespread ST–elevat ion wit h upward con-
cavit y.
● Echocardiography
● Most effect ive t echnique available.
Treatment
Usually wit h ant ibiot ics pat ient s have t o be carefully
observed as t hey may develop Pericardial effusion. I f
cardiac t amponade develops, Peri-cardiocent esis must
be carried out at once.
Cardiomyopathy
Def i ni tion
The cardiomyopat hies are a group of diseases t hat
affect t he heart muscle it self and are not t he result of
hypert ension, congenit al or acquired valvular, coronary
or pericardial abnormalit ies.
Types
● Dilat ed cardiomyopat hy
● Rest rict ive cardiomyopat hy
● Hypert rophic obst ruct ive cardiomyopat hy (HOCM)
Acute Pericarditis
71
Causes
● I diopat hic
● Familial
● I nfect ive – most ly viral, bact erial
● Met abolic causes
● St orage disorders – Glycogen st orage disorder.
● Deficiency – Elect rolyt es, Nut rit ional
● Connect ive t issue disorders – SLE, RA
● Neuro muscular – Muscular dyst rophy, Myot onic
dyst rophy
● Toxic
* Alcohol
* Radiat ion
* Drugs
● Peripart um heart disease
Di l at ed
● Left and right vent ricular enlargement
● I mpaired syst olic funct ion
● Congest ive HF, arrhyt hmias, emboli.
Rest r i ct i ve
● Endomyocardial scarring
● Myocardial infilt rat ion result ing in rest rict ion t o
left and or right vent ricular filling.
Hyper t r ophi c
● Disproport ionat e left vent ricular hypert rophy,
t ypically involving sept um more t han free wall,
wit h or wit hout an int ravent ricular syst olic pres-
sure gradient , usually of a non-dilat ed left ven-
t ricular cavit y.
Not e
● Sudden cardiac deat h can occur.
● Double or t riple apical impulse
Symptoms
As in Congest ive Heart Failure (CHF)
Treatment
● Usual t reat ment as in CHF
● β-blockers are useful
● Spironolact one can be added
Constrictive Pericarditis
72
● Chronic ant icoagulat ion can be done
Dr ugs t o be avoi ded
● Calcium Channel blockers and NSAI DS – in di-
lat ed cardiomyopat hy
● Digitalis, Nitrates, Vasodilators, β-agonists –
(best avoided in HOCM - Hypert rophic obst ruct ive
cardiomyopat hy)
Hypertension
Def i ni tion
● Defined as blood pressure elevat ion t o a level
t hat places t he pat ient at an increased risk for
t arget organ damage
● Blood pressure is considered normal, if blood
pressure is less t han 120/ 80 mm Hg.
● High blood pressure may be due t o syst olic or
diast olic or bot h. Pre-hypert ensive 120-139 / 80-
89 mm.Hg.
● High Blood Pressure may be of
* St age I : 140-159/ 90-99mm Hg
* Stage II : ≥ 160 / ≥ 100 mm Hg.
● High blood pressure may produce a hypert ensive
crisis which includes hypert ensive emergencies
or urgencies.
● I f diast olic blood pressure is 120 t o 130 mm.Hg,
wit h no t arget organ damage it is a hyper t en-
si ve ur gency.
● I f diast olic blood pressure > 130 mmHg and
syst olic blood pressure > 210 mmHg wit h evi-
dence of t arget organ damage, it is a hyper -
t ensi ve emer gency which requires immediat e
blood pressure reduct ion..
● Somet imes only syst olic blood pressure may be
very high (> _140 mm Hg) and t his is called iso-
lat ed syst olic hypert ension.
● When t here is no causat ive fact or it is called Es-
sent i al hypert ension. Hypert ension may be la-
bile or st able.
● I f Hypert ension is due t o cert ain syst emic diseas-
es it is called secondar y hyper t ensi on which
includes renal disease, endocrine disease, vascu-
lar disease, et c.,
Symptoms
● Blood pressure elevat ion is usually discovered in
asympt omat ic period during rout ine screening or
during cert ain associat ed condit ions
● Blood pressure recording should be done wit h
a properly calibrat ed blood pressure apparat us
wit h sit t ing, supine and st anding posit ions under
a non-st ressful sit uat ion. Minimum t wo records
and bot h upper limbs or one lower limb record is
also necessary.
● Before diagnosis, recording t he hist ory is
very import ant which includes family hist ory,
drugs,diabet es, durat ion of hypert ension, age at
which blood pressure is first det ect ed and ot her
sympt oms.
● The physician should carefully look for physical
signs such as evidence of t arget organ damage,
carot id bruit , abdominal bruit s, pulse deficit , S3 /
S4 gallop, cardiac murmurs, JVP, rales, enlarged
kidney, peripheral pulses, flushing, markers of
hyperlipidemia, obesit y, cushingoid feat ures, ves-
sel wall t hickening, et c.
I nvesti gati ons
All hypert ensive pat ient s should undergo t he
following laborat ory t est s t o ident ify t arget organ
damage or t o assess t he adverse effect of drug t herapy.
Test s include
* Urine analysis
* Hemat ocrit
* Plasma glucose
* Serum pot assium and sodium
* Blood urea and creat inine
* X-ray chest
* Elect rocardiography and
* Lipid profile.
● I f secondary hypert ension is suspect ed cert ain
ext ra invest igat ions are mandat ory which include
* Serum calcium, phosphorus
* TSH
* 24 hour urine met a nephrines or VMA, plasma
free met a nephrines
* USG Abdomen wit h renal art ery Doppler.
● The following different ial diagnosis must be ruled
out before est ablishing t he diagnosis of hyper-
73
t ension.
* Drug wit hdrawal,
* Acut e st ress
* Whit e coat hypert ension
* Drug-induced hypert ension
» St eroid
» NSAI DS,
» Cocaine
» Opioid drugs.
● Sudden wit hdrawal of ant i-hypert ensive drugs
also will lead t o rebound hypert ension.
● Any chronic hypert ensive pat ient is examined for
clinical evidence of cardiac failure, renal failure,
coronary art ery disease, cerebro vascular dis-
ease.
Treatment
Once blood pressure is confirmed, lifest yle
modificat ions (LSM) need t o be out lined t o all
hypert ensive pat ient s whet her t hey need medicat ion or
not which includes smoking cessat ion, st ress reduct ion,
j udicious use of alcohol, body weight reduct ion, regular
exercise and adequat e int ake of minerals and vit amins.
● I f cause for hypert ension is det ect ed eg., renal,
endocrine, drug, et c., it is t o be t reat ed appro-
priat ely.
● Pre-hypert ension behavioral modificat ion follow
up
* St age I - Thiazide diuret ics and calcium
channel blockers (or) Bet a blockers + ACEI
* St age I I - Thiazide + ACEI + CCB + bet a
blockers(Dosages t o be adj ust ed according t o
blood pressure response)
● Drugs also t o be added depending upon coex-
ist ing fact ors such as angina, t achycardia, bron-
chospasm, renal insufficiency, obesit y, LVF, hyper
lipidemia, hyper urecemia, diabet es, cost and
drug int eract ion; poor compliance also t o be t ak-
en int o considerat ion.
● Ant i-hypert ensive t reat ment is called for in cer-
t ain special sit uat ions such as hypert ensive emer-
gency and urgency
● I nt ravenous ant i-hypert ensive drugs such as
sodium nit ropruside, Nit roglycerine, Labet alol,
Esmolol, et c., should be given carefully wit h cor-
rect calculat ed dose.
● Special care should be given when pat ient
present s wit h renal failure, st roke, rebound hy-
pert ension, pregnancy, aort ic dissect ion, or acut e
myocardial infarct ion
● The public healt h problem of hypert ension is
enormous and pat ient educat ion is essent ial
● Proper t reat ment is mandat ory and will definit ely
reduce morbidit y and mort alit y.
Angina pectoris
Ri sk f act or s f or Cor onar y Ar t er y Di sease
● Non-modifiable (fixed)
* Age
* Male preponderance
* Family Hist ory
● Modifiable
* Smoking
* Hypert ension
* Lipid disorders
* Diabet es mellit us
* Haemost at ic variables
* Sedent ary life st yle
* St ress
* Obesit y / Over weight
* Diet ary deficiencies of ant ioxidant vit amins
and Polyunsat urat ed fat t y acids.
74
Management of stable angina on effort
Stable Angina on Effort
Review diagnosis
Medical therapy
Exercise tolerance test
Ischaemia at high work
load
Review lifestyle and
control of symptoms
Single or two vessel
disease
Medical therapy
PTCA
CABG
To achieve optimal con-
trol of symptoms
Ischaemia at low work
load
LV and coronary angiog-
raphy
Left main or severe three
vessel disease
CABG for prognostic and
symptomatic reasons
Intercurrent illness or
unsuitable for
revascularisation
-ve
No
yes
+ve
Medical therapy may be the only option if there is very poor LV function or diffuse disease
PTCA: Percutaneous Transluminal Coronary Angioplasty
CABG: Coronary Artery Bypass Grafting
75
Health promotion in Coronary
artery disease
● Avoid smoking
● Regular exercise
● Maint ain ‘ideal’ body weight
● Eat a mixed diet rich in fresh fruit and veget ables
● Aim t o get no more t han 30% of energy int ake
from fat
Myocardial infarction (MI)
Def i ni tion
Myocardial I nfarct ion is due t o t he format ion
of occlusive t hrombus at t he sit e of rupt ure of an
at heromat ous plaque in a coronary art ery.
Symptoms
● Chest Pain – Ret rost ernal / Subst ernal / Epigas-
t ric region
● Prolonged Cardiac Pain – referred t o chest , t hroat ,
j aws, arms, epigast rium or back associat ed wit h
sweat ing, pain on exert ion and relieved by rest
● Anxiet y, Angor animi (fear of impending deat h)
● Nausea and vomit ing
● Breat hlessness
● Collapse / syncope
Physi cal Si gns
● Signs of sympat het ic act ivat ion, pallor, sweat ing,
t achycardia
● Signs of vagal act ivat ion
* Bradycardia, vomit ing
● Signs of impaired myocardial funct ion:
* Hypot ension, Oliguria, cold peripheries
* Narrow pulse pressure
* Raised JVP
* Third heart sound
* Quiet first heart sound
* Diffuse apical impulse
* Lung crepit at ions
● Signs of t issue damage – Fever
● Signs of complicat ions
* Vent ricular fibrillat ion
* Vent ricular ect opics
* Mit ral regurgit at ion
* Pericardit is
* At rial Fibrillat ion
* Heart Block.
Treatment
● Bed rest
● Oral Aspirin – 150 – 325 mg
● High flow oxygen
● I nt ravenous access
● I nt ravenous Analgesics wit h opiat es
● I nt ravenous Morphine sulphat e 10 mg or Diamor-
phine 5 mg
● I nt ravenous Ant iemet ic
* Cyclizine 50 mg or Prochlorperazine 12.5 mg
● Consider t hrombolysis wit h int ravenous St rep-
t okinase or Alt eplase
● Defibrillat ion t herapy if necessary
St r ept oki nase
● 1.5 million unit s in 100 ml of saline as an int rave-
nous infusion over 1 hour
● The drug may cause hypot ension, which can be
managed wit h fluids and rest art ing t he infusion
at a slower rat e
● The drug is ant igenic.
Al t epl ase
ht pa (human t issue plasminogen act ivat or)
The regimen is given over 90 minut es (bolus dose of
15 mg followed by 0.75 mg/ kg of body weight and t hen
0.5 mg/ kg body weight over 60 minut es).
● Consider intravenous β – adrenoreceptor antag-
onist I nj . Met oprolol 5 mg I V every 2-5 minut es
for 3 doses and changed t o oral Met oprolol 50
every 6 hours for 48 hours, followed by 100 mg
every 12 hours
● Monit or ECG and cardiac enzymes
● Det ect and t reat complicat ions early
Ni t r at es
76
* Sublingual glyceryl trinitrate 300-500 μg
* I nt ravenous nit roglycerine 0.6 – 1.2 mg/ hour
* I sosorbide dinit rat e 1 – 2 mg/ hour
Ant i -coagul ant s
Subcut aneous Heparin 12,500 unit s t wice daily for
7 days is given in addit ion t o oral aspirin may prevent
re - infarct ion aft er successful t hrombolysis and reduce
t he risk of t hrombo-embolic complicat ions.
Contraindications to thrombolytic therapy
Absol ut e cont r ai ndi cat i ons t o t hr ombol yt i c
t her apy
● Act ive int ernal bleeding
● Previous sub-arachnoid or int ra-cerebral haem-
orrhage
● Non-haemorrhagic st roke wit hin t he last 1 year
● Uncont rolled hypert ension (syst olic
> 180mmHg,diast olic> 110mmHg)
Rel at i ve cont r a-i ndi cat i ons t o t hr ombol yt i c
t her apy
● Current use of ant i-coagulant s
● Recent (< 2 weeks) invasive surgical procedure
● Recent prolonged (> 10 min) cardiopulmonary
resuscit at ion
● Known bleeding diat hesis
● Pregnancy
● Hemorrhage prone opht halmic condit ions.
● Act ive pept ic ulcer disease
● Recent hist ory of severe hypert ension
St rept okinase should not be used, if given in t he
preceeding 5 days t o 2 years because of t he risk of
allergic react ions
Congestive Heart Failure (CHF)
Def i ni tion
CHF is a clinical syndrome of inadequat e cardiac
out put result ing in fluid ret ent ion in t he lungs, abdominal
organs and peripheral t issue.
Symptoms
● Fat igue, list lessness
● Poor effort t olerance
● Decreased urine out put
● Breat hlessness and pink frot hy sput um
● Swelling around ankles
Si gns
● Cold peripheries
● Low blood pressure
● Oliguria, Uraemia
● Ort hopnoea
● Paroxysmal Noct urnal Dysnoea (PND)
● Bilat eral basal inspirat ory crepit at ions
● Raised JVP
● S
3
summat ion gallop
● Peripheral oedema
● Ascit es
● Pleural effusion
● Profuse pink frot hy sput um
● Tender hepat omegaly
Fact or s t hat may pr eci pi t at e or aggr avat e hear t
f ai l ur e
● Myocardial ischaemia or infarct ion
● I nt ercurrent illness (eg) I nfect ion
CXR-Pulmonary oedema
77
● Arrhyt hmia
● I nappropriat e reduct ion of t herapy
● Drugs :– β – adrenoreceptor antagonist, Drugs
wit h fluid ret aining propert y (NSAI DS, St eroids)
● Pulmonary embolism
● Condit ions wit h increased met abolic demand
* Pregnancy
* Thyrot oxicosis
* Anaemia
● I nt ravenous fluid overload
Compensat or y changes i n hear t f ai l ur e
● Chamber enlargement
● Myocardial hypert rophy
● I ncreased heart rat e
Treatment
Gener al measur es
● Rest rict physical act ivit y
● Bed rest in propped up posit ion wit h a back rest
● Diet ary salt (sodium) rest rict ion. (2 – 3 g/ day)
● Avoid and discont inue NSAI DS, high dose Bet a
blockers and calcium channel blockers
● Fluid rest rict ion depending on out put and ot her
condit ions.
Dr ug t her apy
● Diuret ics
● Vasodilat ors
● ACE inhibit ors/ Angiot ensin I I recept or blockers
● Digoxin
● β-adrenoceptor antagonist
● Ot her drugs – Heparin, Ant i coagulant s t o pre-
vent t hromboembolism complicat ing at rial fibril-
lat ion.
Di ur et i cs
● I nj . Frusemide 40 – 80 mg I V st at every 2 t o 3
hours wit h maximum up t o 200 mg/ day. Maint e-
nance dose is 40 mg I V 12
t h
hourly.
● Tab. Spironolact one 25 – 200 mg / day (or)
● Tab. Chlort hiazide 250 – 500 mg/ day (or)
● Tab. I ndapamide 2.5 - 5 mg/ day (or)
● Tab. Benzt hiazide 25 mg + Tab. Triamt erene 50
mg/ day
Vasodi l at or s
● Venodilat ors – Organic nit rat es
● I so-sorbide mononit rat e
Angi ot ensi n – conver t i ng enzyme ( ACE)
i nhi bi t or s
● Tab. Enalapril 2.5 – 20 mg/ day (or)
● Tab. Lisinopril 2.5 – 10 mg/ day
Angi ot ensi n I I r ecept or ant agoni st
● Losart an 50 mg once daily
Di goxi n
● I s indicat ed in fast vent ricular rat e (e.g.) At rial
Fibrillat ion
● Tab. Digoxin 0.5 mg first day followed by 0.25
mg/ day
Hepar i n
● I nj . Heparin 5000 I U 12 hourly SC if pat ient is
bedridden
● Bet a blockers
* Tab. Carvedilol 3.125 – 25 mg per day in one
or t wo divided doses is useful in all sympt o-
mat ic or asympt omat ic heart failure and in
case of reduced ej ect ion fract ion (< 40 %.)
Moni t or i ng of CHF pat i ent
● St rict int ake – out put chart ing
● Daily weight and abdominal girt h measurement
● Serum elect rolyt es and uric acid
● Wat ch for any sympt oms of di gi t al i s t oxi ci t y
* Anorexia
* Nausea
* Vomit ing
* Worsening of heart failure.
*
78
Pulmonary Embolism
Causes
Ri sk f act or s
● Pat ient fact ors
* Age, obesit y, long air t ravel, immobilit y (>
4days)
* Smoking, Hypert ension, Diabet es Mellit us
* Pregnancy, Puerperium, Thrombophilia
* Ant i-phospholipid ant ibody syndrome
* Hypercoagulable st at es such as
» Prot ein C, Prot ein S deficiency
» Hyper-homocyst einemia et c.
* Drugs such as t hose given for hormone re-
placement t herapy.
● Disease or surgical procedures
* Trauma or surgery, especially of pelvis, hip or
lower limbs
* Cardiac failure
* Malignancy
* Nephrot ic syndrome
* St roke
* I ndwelling cent ral venous cat het ers et c.
Symptoms
● Depends on size of t he embolism and associat ed
co-morbidit y
● Sudden onset dyspnoea is t he most common
sympt om
● Tachypnoea is t he most common sign
● Pleurit ic chest pain and haemopt ysis are present
when infarct ion has occurred
● Hypot ension wit h acut e right vent ricular failure in
a pat ient wit h risk fact ors of pulmonary embolism
Clinical syndromes of Pulmonary embolism
* Massive pulmonary embolism
* Sub-massive pulmonary embolism
* Small t o moderat e pulmonary embolism
* Pulmonary infarct ion
* Paradoxical embolism
* Non-t hrombot ic embolism
* Mult iple recurrent pulmonary embolism
Feat ur es
* Cardiogenic shock
* RV hypokinesia, normal blood pressure
* Normal RV funct ion, normal blood pressure
* Feat ures of lung consolidat ion
* St roke wit h pulmonary embolism
* Commonly air, fat , amniot ic fluid, t umour,
right sided infect ive endocardit is
* I ncreasing breat hlessness over weeks or
mont hs
I nvesti gati ons
● Non-imaging met hods
● I maging met hods
Non-i magi ng met hods
[ Suspicion of t he illness is t he most import ant first
st ep]
Pulmonary embolism - ECG showing S
1
Q
3
T
3
pattern
S wave in lead I, Q wave and inverted T wave in lead III
79
Test
● Plasma d-DI MER ELI SA
● ABG- Art erial blood gas analysis
● ECG
Comment
● I f undet ect able, excludes pulmonary embolism
● Type I respirat ory failure
● Sinus t achycardia (common)
● RV st rain
● Ant erior T wave inversion,
● S
1
Q
3
T
3
pat t ern in ECG
I magi ng met hods
● Chest X-ray
* Can be normal
* Cardiomegaly, wedge-shaped opacit y, effu-
sion, oligemia, abrupt cut-off of pulmonary
art ery
● Echocardiography
* Det ect s RV overload and funct ion
● CT Scan (Mult i det ect or – row CT Scan)
* Can det ect even small pulmonary art ery
emboli
* Can surplant t he pulmonary angiography
● Pulmonary Angiogram
* Gold st andard t est ,
* Done if surgery is planned.
● MR Angiogram
* Useful if CT Angiogram is cont ra indicat ed
● Venous Ult rasonography
* May show t hrombosis of deep veins of t he
lower limb or pelvis
● Vent ilat ion/ Perfusion Scanning
* Reserved for pat ient s wit h Renal failure /
Cont rast allergy
Treatment
Management of Acut e pul monar y embol i sm
● Oxygen t herapy / NSAI Ds for pain relief
● Avoid Diuret ics, vasodilat ors
● Fluid / Dopamine support if hypot ension is
present
● Thrombolyt ic t herapy (St rept okinase): I n pulmo-
nary embolism wit h cardiogenic shock
● Ant icoagulat ion
* Heparin followed by oral ant icoagulat ion
» Life long if t here is pro-t hrombot ic risk
» For 3 mont hs if an ident ifiable reversible
risk fact or is present
» For 6 mont hs in idiopat hic pulmonary em-
bolism
» Heparin: LMWH is preferred
Enoxaparin: 1 mg/ kg 12 - hourly
Dalt eparin : 200 I U/ kg sc daily
» Warfarin 5 mg ( To maint ain I NR bet ween
2-3)
* I nferior Venacava filt ers: useful in recurrent
pulmonary embolism
* Surgical embolect omy
* I dent ify t he risk fact ors and t reat
● Prophylaxis for Venous t hrombo-embolism:
* Prevent ive measures such as early mobiliza-
t ion, int ermit t ent pneumat ic compression,
graded st ock compression.
* Ant icoagulat ion prophylaxis ( To be combined
wit h int ermit t ent pneumat ic compressions
and graded st ock compressions)
Exampl es
Ant i coagul at i on
pr ophyl axi s
Dr ugs
Hip/ Knee replacement s
Hip or Pelvic fract ure
Warfarin (I NR: 2 - 2.5)
For 4 - 6 weeks
LMWH (Enoxaparin) 30
mg sc B.D
Gynaec cancer surgery Warfarin (I NR: 2 -2.5)
Enoxaparin 40 mg sc
OD
Neurosurgery,
Opht halmic surgery
or any ot her surgeries
where ant i coagulat ion is
cont raindicat ed
I nt ermit t ent pneumat ic
compressions
and graded st ock
compressions
Medical condit ions Compression st ockings
Heparin 5000 I U q8h
Enoxaprin 40 mg sc OD
80
Cardiac arrhythmias
Causes
● Due t o disorders of impulse format ion (or)
● Due t o disorders of impulse conduct ion
● Arrhyt hmia can be:
* Brady arrhyt hmia or Tachy arrhyt hmia
* Paroxysmal or persist ent
* Hemodynamically st able or unst able
Symptoms
Pat ient s present wit h palpit at ions, light headedness,
hypot ension, dyspnoea, angina, syncope or fat igue.
Sudden onset and abrupt t erminat ion of palpit at ions
may indicat e t achyarrt hymia.
Hist ory of congenit al (Hypert rophic
Cardiomayopat hy,WPW syndrome, congenit al long
QT syndrome) or acquired st ruct ural heart disease
(I schemic Heart Disease, Cardiomyopat hy, valvular or
endocrine disease ( Thyroid disorder, adrenal disorders)
should be obt ained.
I nvesti gati ons
Physical examinat ion includes pulse, Blood pres-
sure, det ailed cardio-vascular examinat ion.
I nvest igat ions include – 12 lead ECG, cont inuous
ambulat ory ECG (Holt er) monit oring for 24 – 72
hours event recorder, His Bundle Elect rogram,
Excercise ECG, EPS (Elect ro physiology st udy).
Treatment
Treat ing t he acut e at t ack of arrhyt hmia
1. Treat ing t he precipit at ing causes
2. Treat ing t he underlying causes
3. Long t erm management , if necessary
Cardiac arrhythmias
Br ady Ar r hyt hmi a
Def i ni tion
Any heart rhyt hm wit h a rat e less t han 60 beat s/ min.
Causes
1. Sick sinus syndrome (caused by SA node dys-
funct ion)
Present s as
* Sympt omat ic sinus brady cardia
* Sino at rial block
* Sinus arrest
2. A.V. conduct ion disorders:
* First degree A V Block: Prolongat ion of PR
int erval
* Second degree A.V.Block
c. Mobit z Type I Block (Wencke back’s phenom-
enon)
» Progressive prolongat ion of PR int erval.
» Periodically one P wave is not followed by
QRS complex.
d. Mobit z Type I I block
» Periodically P wave is not following by QRS
complex
5. Third degree A V Block
* A V disosiat ion
* I ndependent at rial and vent ricular rhyt hm
Treatment
I n sympt omat ic acut e sit uat ion, t he heart rat e should
be increased t o alleviat e t he sympt oms by:
● I nj . At ropine 0.5 mg – 2 mg I .V (or)
● I nj . I soprot erenol 1 – 4 micro gram/ min I .V.
● On a long-t erm basis, t he appropriat e pat ient s
have t o be provided wit h a permanent pacemak-
er.
Tachyar r hyt hmi a
Def i ni tion
Any heart rhyt hm wit h a rat e more t han 100 beat s/
min
Types
They may be: Supravent ricular (or) Vent ricular
Supr avent r i cul ar t achycar di a
They occur paroxysmally. Onset is sudden wit h
abrupt t erminat ion.
Symptoms
● They may be asympt amat ic or sympt omat ic.
● Pat ient s present wit h palpit at ion, dizziness, an-
gina.
● Hypot ension may be present .
● Polyuria may follow aft er t he acut e episode.
81
I nvesti gati ons
1. ECG:
* SVT: Regular narrow QRS Tachycardia. Ven-
t ricular rat e may be 160 – 200 beat s/ min.
P wave may be buried in QRS or follow QRS
complex.
* SVT wit h aberrancy: Regular wide QRS Tachy-
cardia.
Mechani si m:
1. AVNRT (A.V. Nodal Re-ent rant t achycardia)
2. O – AVRT (Ort hodromic A.V. re-ent rant t achycar-
dia using accessory pat hway in WPW syndrome)
Treatment
Depends on t he haemodynamic st at us of t he pat ient .
I f he is haemodynamically st able:
1. Treat ment of acut e episode includes vagal ma-
noeuvres (Carot id sinus massage, valselva
maneuver)
2. I f t his measure fails, AV Nodal blocking drugs are
t ried.
* I nj . Adenosine 6 mg I V bolus followed by 10
ml saline flush.12 mg I V bolus can be repeat-
ed if no response aft er 2 minut es.
* Cont ra indicat ions: Sick sinus syndrome or
second or t hird degree A.V. Block
3. I nj . Met oprolol 5 mg I V. Can be repeat ed aft er 5
minut es
4. I nj . Verapamil 5 – 10 mg I V bolus over 2 – 3 min-
ut es. Can be repeat ed aft er 15 minut es
5. I nj . Dilt iazem 0.25 mg/ kg I V bolus over 2 min-
ut es. Followed by I V infusion at a rat e of 10 mg/
hour.
6. I f haemodynamically unst able, prompt synchro-
nized direct current (DC). Cardio version (using
10 t o 100 Joules) has t o be done.
Mai nt enance t her apy
Once sinus rhyt hm is est ablished, chronic
maint enance t herapy includes
1. Oral calcium channel blockers
* Dilt iazem – 30 mg t id (or)
* Verapamil – 40 mg t id
2. Bet a-adrenergic ant agonist
* Met oprolol 25 – 100 mg bid
* At enolol 25 – 100 bid
* Digoxin 0.125 – 0.5 mg od
Cur at i ve Ther apy
Curat ive t herapy for supravent ricular t achycardia
involving accessory pat hway is radio-frequency
ablat ion.
Ventricular tachycardia
Def i ni tion
Runs of t hree or more consecut ive idiovent ricular
beat s exceeding a rat e of 100 beat s/ minut e.
Types:
* Sust ained - I f vent ricular t achycardia per-
sist s for > 30 seconds.
* Non-sust ained - 3 beat s t o 30 seconds.
* Monomorphic - Configurat ion is uniform
* Polymorphic - Configurat ion varies from
beat t o beat
Symptoms
Pat ient s wit h vent ricular t achycardia may present
wit h st able haemodynamic st at us or feat ures of
hypot ension and syncope or pulseless st at e.
I nvesti gati ons
Echo and el ect r ocar di ogr aphy
AV Dissociat ion, capt ure or fusion beat s and an LBBB
morphology wit h right axis deviat ion.
QRS morphology in precardial leads in VT
Lead V1 Lead V6
I f t here is LBBB
pat t ern
R > 30 milli seconds QR or QS
R t o S > 60 milli
seconds
Not ched S wave
RBBB pat t ern Monophasic R R/ S < 1
QR or RS
Treatment
1. Pat ient s wit h non-sust ained VT wit hout organic
cardiac disease are asympt omat ic – need not be
t reat ed.
2. Pat ient s wit h sust ained VT in t he absence of car-
82
diac disease are sympt omat ic and require t hera-
py wit h Bet a blockers, verapamil, Class I A, I C or
I I I or amiodarone.
3. I n pat ient s wit h VT wit h organic cardiac disease,
if t here is haemodynamic inst abilit y, unsynchro-
nized 200 Joules DC cardioversion will t erminat e
t he arrhyt hmia.
4. I f haemodynamically st able, t he following drugs
can be t ried:
* I nj . Lidocaine – 1 mg/ kg I V bolus, 0.5 – 1 mg
/ Kg boluses may be repeat ed at 5 min int er-
vals followed by 2 – 4 mg/ min maint enance
infusion.
* I nj . Amiodarone may be t ried.
* I f t hese drugs fail, over drive pacing has t o
be done.
* To prevent recurrences, sust ained VT – I CD
implant at ion is effect ive.
Pr ognosi s
* Prognosis of vent ricular t achycardia depends
on t he underlying heart disease. Vent ricular
t achycardia and supravent ricular t achycardia
wit h aberrancy are t o be different iat ed, as t he
t herapy is different in bot h condit ions.
Atrial fbrillation
Common arrhyt hmia we see in pract ice
Types:
1. Paroxysmal
2. Persist ent
3. Permanent
4. Acut e (or) chronic
Causes
Seen in t he following condit ions:
* Pat ient s wit h valvular heart disease
* I schaemic and hypert ensive heart disease
* Chronic lung disease, hypoxia, hypercapnia
* ASD
* Thyrot oxicosis
* Lone at rial fibrillat ion occurring in pat ient s
wit hout heart disease
* Acut e alcoholic int oxicat ion
* Emot ional st ress, exercise
Symptoms
● Palpit at ion, hypot ension, angina, syncope or em-
bolic manifest at ions.
● Pulse : irregularly irregular
● JVP- Loss of ‘a’ waves.
● Varying int ensit y of first heart sound.
I nvesti gati ons
● ECG: No discret e ‘p’ wave, only ‘f ’ waves are
seen
● Varying RR int erval
● Rat e 350 t o 600 beat s/ minut e
Treatment
Acut e at r i al f i br i l l at i on
1. Treat ing t he precipit at ing fact ors.
2. I f t he pat ient is haemodynamically unst able,
elect rical cardioversion using 200 Joules is t he
t reat ment of choice.
3. I f haemodynamically st able, vent ricular rat e con-
t rol is adequat e by bet a blockers or calcium chan-
nel blockers.
4. Next st ep is t o convert at rial fibrillat ion t o si-
nus rhyt hm. I t consist s of ant i-coagulant prior
t o cardioversion and following t he cardioversion
and use of ant iarrhyt hmic drugs t o rest ore sinus
rhyt hm.
Chr oni c at r i al f i br i l l at i on:
1. Chronic at rial fibrillat ion cannot be convert ed
t o sinus rhyt hm or will not remain in t he sinus
rhyt hm.
2. I n t his case, rat e cont rol is sufficient by bet a
blockers, calcium channel blockers or digit alis.
3. To prevent recurrence of at rial fibrillat ion, Sot alol
and Amiodarone and can be used.
4. To prevent t he risk of embolism, eit her Aspirin or
Warfarin can be used depending upon t he pres-
ence of risk fact ors.
Sur gi cal met hods
1. Ablat ion around pulmonary veins.
2. MAZE procedure, t o creat e zig zag surgical scars
in t he at ria.
3. Cat het er ablat ion of at riovent ricular node wit h
pace maker implant at ion.
83
Haematology
Chapter 4
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
● Anemia
* Microcyt ic Anemia
* Normocyt ic Anemia
* Macrocyt ic Anemia
● Haemolyt ic Anemia
● Approach t o a bleeding pat ient
● Plat elet Disorders
● Acut e I TP
● Coagulat ion Disorders
● General Considerat ions
85
Anaemia-approach to diagnosis
Def i ni tion
Anaemia is defined as a reduct ion in t he number
of red blood cells, blood hemoglobin cont ent , or
hemat ocrit , below t he normal level for t he same age
and sex.
Ther e ar e t hr ee pr i mar y causes of anaemi a:
1. Reduced product ion of red blood cells in t he bone
marrow
2. Excessive dest ruct ion of red blood cells, and
3. Excessive blood loss.
When t o suspect anaemi a?
When t here are sympt oms and signs of weakness,
fat igue, palpit at ions, t achycardia, dyspnea, posit ional
dizziness, syncope, increased or new onset angina.
The di agnost i c appr oach consi st s of
1. Hist ory
2. Physical examinat ion and
3. Laborat ory evaluat ion.
Hi st or y
● Blood loss, int ake of Aspirin or ot her NSAI Ds,
● Menst rual hist ory or possible pregnancy in wom-
en
● Diet ary hist ory, including hist ory of pica
● Hist ory of alcohol abuse
● Family hist ory
● Hist ory of gast ric surgery, dist al parest hesias,
gait problems -consider B12 deficiency
● Hist ory of j aundice, t ransfusion, new medicat ion,
infect ion
● Hist ory of weight loss, fever and chills, cough,
dyspnea,
● Ot her diseases like cancer, HI V, rheumat oid ar-
t hrit is, t hyroid disease and renal disease
I nvesti gati ons
I nit ial laborat ory t est s for anaemia workup
● Complet e blood count profile, including red cell
morphology, whit e blood cell different ial and re-
t iculocyt e count .
● Biochemist ry profile-Renal and liver funct ion
t est s.
● Urine analysis: Hemat uria/ prot einuria in renal
disease, hemoglobinuria in hemolysis.
The Compl et e bl ood count and ot her r el at ed
t est s
Par amet er s i n nor mal adul t
1. He moglobin
Male= 15.5 (+ / - 2 mg/ dl)
Female = 13.5 (+ / -2)
2. Hemat ocrit
Male= 46.0 (+ / - 6%)
Female= 41.0 (+ / - 6%)
3. Red blood cell count
Male = 4.3 - 5.9 million/ uL
Female = 4.0 - 5.2 million/ uL
4. Whit e blood cell count 4500 - 11000 cells/ uL
5. Plat elet count 1.5 - 4.0 lakh cells/ uL
6. Ret iculocyt e count 0.5 - 1.5 %
Red cel l i ndi ci es
● Mean corpuscular volume 80 - 90 fl
● Mean corpuscular hemoglobin 27 - 32 picogram
● Mean corpuscular hemoglobin concent rat ion
30 - 36 gm/ dl
● Red cell dist ribut ion widt h 11.5 - 14.5
Fr om a pat hophysi ol ogi cal per spect i ve, anaemi a
i s ei t her due t o
● Decreased product ion
● I ncreased loss
Ret i cul ocyt e count
The r et i cul ocyt e count hel ps di f f er ent i at e
bet ween t hese t wo t ypes
● The ret iculocyt e must be correct ed for t he reduc-
t ion in red cell count t o accurat ely reflect marrow
product ion of eryt hrocyt es and is obt ained by t he
following formula.
Correct ed ret ic = observed ret ic x observed hemat ocrit
(%)
● Normal hemat ocrit : 45
86
● The normal correct ed ret iculocyt e percent age is
1-2%
● From a pract ical diagnost ic perspect ive, anaemia
is best classified according t o Mean corpuscular
volume (MCV) as
* Microcyt ic
* Macrocyt ic
* Normocyt ic
Classifcation of Anaemia based
on Red cell size
Mi cr ocyt i c (MCV < 80 fL)
● I ron deficiency anaemia
● Thalassemia
● Congenit al sideroblast ic anaemia
● Chronic inflammat ion
● Lead poisoning
Macr ocyt i c (MCV > 100 fL)
● Vit amin B12 deficiency
● Folat e deficiency
● Liver disease
● Hypot hyroidism
Nor mocyt i c (MCV 80-100 fL)
● See t able below
Approach to microcytic anaemia
Low MCV (<80 fL)
Low Ferritin+ Increased RDW
Hb electrophoresis
Normal
Anemia of chronic disease
Sideroblastic anemia
Abnormal
Thalassemia Beta/
Alpha/HbE/disease
Normal/ High
Ferritin
Serum Ferritin
Tr eat ment f o I r on def i ci ency anaemi a
Ai m of t r eat ment
1. Correct ion of anaemia
2. Replenishmint of st ores
3. Treat ment of t he cause of iron deficiency
* Transfusion of packed red cells is only indi-
cat ed if t here is significant ly sympt omat ic and
severe anaemia
* Ferrous sulphat e given as non - ent eric coat ed
t ablet s 150 - 200 mg of element al iron has
t o given daily in 1 - 3 divided doses. Adverse
effect s can be reduced by st art ing wit h sin-
gle t ablet per day and t hen increasing t he
dose slowly. The t ot al durat ion of t herapy is
6 mont hs.
* Parent eral iron- Rarely required
I ndi cat i ons
● Malabsorpt ion
● I nflammat ory bowel disease
Not e:
I ron surcrose can be administ ered as 200 mg in
100 ml of normal saline as infusion over 20 min-
ut es.
Tr eat ment of megal obl ast i c anaemi a
● 1 mg of int ramuscular Cyanocobalamin per day
for 3 days, 1 mg weekly for 4 weeks and t hen 1
mg once in 3 mont hs for 1 year for megaloblast ic
anaemia
● Megaloblast ic anaemia should never be t reat ed
wit h folat e alone as neurological disease is pre-
cipit at ed.
Approach to normocytic anaemia
Decreased production
Only red cells
Bone marrow examination
Pancytopenia
Erythroids absent/
Reduced/Purered
cell aplasia
Erythroids present/
increased MDS CDA
Aplastic anemia/In-
filrtative disorder
Hemorrhage Hemolysis
Congenital Acquired
Increased loss
Normocytic anemia
Mi cr ocyt i c anaemi as
An MCV of less t han 80 fL wit h pale, poorly
hemoglobinized red cells on peripheral smear
charact erizes t his group of anaemias.
87
Approach to macrocytic anaemia
Normal /not available
Bone marrow
Megaloblastic anemia
Non-megaloblastic
changes
Liver disease
Hypothyroidism
Myelodysplastic syndrome
Megaloblastic
changes
Low
High MCV (> 100 fL)
Vitamin B12 and Folate levels
Hemolytic anaemia
Anaemi a wi t h hi gh r et i cul ocyt e count
syst emat i c appr oach
1
st
st ep
Look for t he evidence of haemolysis (clinical and
laborat ory)
2
nd
st ep
I mmune versus Non-immune
3
rd
st ep
Peripheral smear examinat ion t o find a clue t o
t he diagnosis.
4
t h
st ep
Ask for confimat ory t est t o est ablish t he diagno-
sis.
Evi dence of hemol ysi s
Cl i ni cal evi dence
Chronic long st anding from childhood
● Skelet al Abnomalit ies
* Front al Bossing
* Macillary prominence
* Harrison’s sulcus
* Genu valgum
● Jaundice wit h acholuric urine
● Hepat osplenomegaly
● Chronic leg ulcers
I nvesti gati ons
Labor at or y evi dence
Hallmark of hemolysis is presence of an elevat ed
ret iculocyt e count , wit h st able or falling hemoglobin.
● Ot her findings include:
* Elevat ed indirect bilirubin
* Elevat ed serum lact at e dehydrogenase (LDH)
* Decreased Hapt oglobin levels
* Hemoglobinemia and hemoglobinuria
* Eryt hroid byperplasia in bone marrow
Approach to hemolysis
High corrected retic %
Negative
Non Immune hemolytic anemia
Peripheral smear examination
Refer for further investigations to tertiary centre

Autoimmue
hemolytic anaemia
Warm antibody
Cold antibody
Congential
Red cell membrane
Hereditary spherocytosis
Red cell enzymopathies
Hemoglobinopathies
Hb S Disease
Hb D Disease
Hb C Disease
Acquired
Intrinsic RBC
disorders
PNH
Lead toxicity
Infections
Extrinsic disorders
Microangiopathy
Chemicals
Postive
Coomb’s test
Management of hemolytic anaemias
Congent i al Hemol yt i c Anaemi a
Pat ient s wit h hemolyt ic anaemia should not be given
oral iron as t his may siad t o iron overload. Folic acid 205
mg / day should be administ ered.
Aut oi mmune Hemol yt i c Anaemi a
St eroids are t he mainst ayof t reat ment for pat ient s
wit h aut oimmune hemolyt ic anema. St art pred-nisolone
1 mg / kg / day for- weeks and t hen t aper over- weeks.
St eroids should not be cont inued beyond weeks.
88
Transfusion is warrant ed when cardiac or cerebral
funct ion is t hreat ened.
I f pat ient is st eroid dependent or if t here is
inadequat e response t o st eroids, Tab Azat hioprine t o be
st art ed at a dose of 1-2mg/ kg body weight for 6 mont hs,
wit h monit oring of leukocyt e count . Splenect omy
t o be considered, if not responding t o st eroids and
azat hioprine.
I nvesti gati ons
Recommended laborat ory I nvest igat ions in t he facilit ies
LEVEL 1:
● Primary healt h cent er
* Hemoglobin est imat ion using a spun hemat-
ocrit or colorimet er. Preipheral smear exami-
nat ion.
LEVEL I I :
● Dist rict hospit al
* Bood cell count er wit h 3 or 5 part different ial
and ret iculocyt e count
* Coomb’s t est .
LEVEL I I :
● Tert iary referral cent re
* Blood cell count er wit h 5 part different ial
* Facilit ies for bone marrow examinat ion includ-
ing t rephice
* Serum iron TI BC and ferrit in.
● Evaluat ion of hemolyt ic anaemia
* HPLC/ Hb elect ophoresis
* Osmot ic fragilit y
* Unst able hemoglobin
* Sickle preparat ion
* G6PD est imat ion
* Ham’s t est and
* Sucrose lysis t est
Approach to the bleeding patient
Haemost asis may be defined as t he process t hat
maint ains blood in a fluid st at e while prevent ing loss
of blood from sit es of vascular disrupt ion. A normal
haemost at ic mechanism maint ains a healt hy balance
bet ween bleeding and clot hing.
Pr i mar y haemost asi s is t he funct ion of a plat elet
plug at sit es of inj ury and occurs wit hin seconds of
inj ury.
Secondar y haemost asi s describes t he coagulat ion
syst em, result ing in fibrin format ion. This is part icularly
import ant in bleeding originat ing from large vessels and
in prevent ing recurrent bleeding hours or days aft er
init ial inj ury.
Haemorthagic disorders
Platelet disorders
Coagulation disorders
Acquired disorders are more common t han inherit ed
bleeding disorders.
I nvesti gati ons
The invest igat ion of a suspect ed bleeding t endency
may begin from t hree differnt perspect ives:
I nvest i gat i ng a cl i ni cal l y suspect ed bl eedi ng
t endency
● The invest igat ion begins wit h hist ory, which may
suggest an acquired or congenit al disorder of pri-
may or secondary haemost asis
● I f t he bleeding host ory of family hist ory is sig-
nificant , appropriat e specific t est sw and assays
should be performed.
Fol l owi ng up an abnor mal f i r st -l i ne t est
● Plat elet Count (Normal range - 1.5 lakhs t o 4.5
lakhs)
● Bleeding t ime (Normal range - 2 t o 8 mins)
● Prot hrombin t ime (Normal range - 11 t o 16 secs)
● Act ivat ed part ial t hromboplast in t ime (Normal
range - 26 t o 40 secs)
● The abnormalit ies already det ect ed will det er-
mine appropriat e furt her invest igat ions.
I nvest i gat i ons of acut e hamost at i c f ai l ur e
● This is oft en required in t he cont ext of an acut ely
ill or post operat ive pat ient
● I nvest igat ions are t herefore direct ed t oward de-
t ect ing disseminat ed int ravascular coagulat ion
(DI C) or a previously undet ect ed coagulat ion de-
fect (congenit al or acquired)
* The availabilit y of a normal pre-morbid coagu-
lat ion screen and furt her quest ioning t o det er-
mine a bleeding hist ory is ext remely useful in
89
t his sit uat ion.
Platelet disorders
Feat ur es:
● Purpura
● Bleeding t ime - prolonged
● Pat elet count - normal / abnormal
● PT,APTT - normal
● Bleeding rarely occurs when count s > 50,000 /
cu.mm
● < 50,000 / cu.mm - purpura
● < 20,000 / cu.mm - spont aneous bleeding includ-
ing high risk mucosal bleeds and int racerebral
haemorrhage
I nher i t ed qual i t at i ve Pl at el et di sor der s:
● Bleeding (usually muco - cut aneous)
* Purpura
* Ecchymosis
* Menorrhagia
* Gl bleeding since childhood
● Family hist ory of bleeding t endencies may be
post ive.
● Bleding t ime - prolonged.
● Clot ret ract ion - defect ive or absent .
● Plat elet count and peripheral smear st udy for
plat elet aggregat es and morphology
● PT, APTT - normal.
● (N.B: APTT could be prolonged in Von eillebrand
disease
● Plat elet aggregat ion st udies - abnormal in Glanz-
mann Thrombast henia and BSS.
Plat elet Disorders
S.No:
Quant it at ive Plat elet Disorders
(Low plat elet s/ t hrombocyt openia)
Qualit at ive Plat elet Disorders
(Normal plat elet count )
I ● Acut e I TP ● Congenit al
* Glanzmann’s-t hrombast henia
* Bernard - Soullier syndrome
I I ● Drug induced
* Cyt ot oxic Drugs
* Cephalosporins
* Ant i-mlarials
* Rifampin
● Acquired
* Uraemia
* Liver disease
* Myelo-proliferat ive disorders
* Cardiopulmonary by pass
* Drugs - Aspirin, Clopidogrel et c.
I I I ● SLE
I V ● I nfect ions
* Malaria
* Dengue
* HI V - 1
* I nfect ious Mononucleosis
V ● DI C
VI ● Sepsis
VI I ● Thrombot ic t hrombocyt openic purpura
VI I I ● Hemolyt ic-uraemic syndrome
I X ● Et hanol induced
X ● Heredit ary
90
Treatment
● Non-t ransfusional haemost at ic drugs and plat elet
t ransfusion are t he mainst ay of t herapy in con-
genit al disorders, for maj or bleeding.
● Aquired disorders require in addit ion, manage-
ment of t he primary problem.
Thr ombocyt openi a - non - i mmune
Poi nt s t o r emember :
1. Plat elet t ransfusion
* Random plat elet t ransfusion- 1unit / 10 kg
body weight ant icipat ed increase in plat elet s
is 10,000 / cu.mm.
* One unit of Single Donor Plat elet (SDP) t rans-
fusion is equivalent t o 6 unit s of Random
Plat ele t ransfusion. Single Donor Plat elet s de-
creases alloimmunizat ion.
2. Porphylact ic Plat elet s :
* Plat elet count s < 10,000 / cu.mm wit h act ive
bleeding or fever.
* Plat elet count < 50,000 / cu.mm if invasive
procedures are cont emplat ed.
Avoi d
● I nt ra muscular inj ect ions
● Ant i - Plat elet drug- NSAI DS.
Acute Idiopathic Thrombocytopenic
Purpura
● Bleeding (usually muco-cut aneous)
* Purpura
* Ecchymorrhagia
* Gast ro int est inal or urinary bleeding of short
durat ion.
● Presence of underlying disease (eg. SLE) or his-
t ory of drug int ake.
I nvesti gati ons
● Plat elet count-very low
● PT, APTT - normal
● Bone marrow - Normal wit h adequat e mega-
karyocyt es.
Treatment
● Count s > 30,000 / ul
* Cort icost eroids (short course - 2 weeks) if
bleeding and st eriod responsive. No t reat-
ment , if no bleeding.
● Count s < 30,000 / ul
* Wit hout serious bleed
» Prednisolone 1 mg / kg / day for 4 weeks
and t hen t aper over 2-4 weeks
» St eroids should not be cont inued beyond
6-8 weeks.
* Wit h serious bleeding
» Prednisolone 1 mg / kg / day plus
» I V gamma globulin 1 gm / kg / day for 2
days (if possible), or
» Rh-D immunoglobulin 50 - 75 mg / kg /
day given (if possible) I V once in 3-4 weeks
t o maint ain count s around safe level >
50,000 / ul, wit h appropriat e precaut ions.
● Splenect omy t o be considered in adult s, if not re-
sponding t o st eroids.
● Ot her drugs useful in I TP
* Azat hioprine 1-2 mg / kg / day for 6 mont hs
* Dapsone 2 mg / kg / day for 6 mont hs
● Those unresponsive t o above t herapies should be
referred t o a t ert iary cent re.
● Plat elet s t ransfusions are not indicat ed. However,
if t here is life t hreat ening bleeding such as int rac-
ranial bleeding, t hen 4-6 plat elet unit s, may be
given, if available.
Coagulation disorders
I nherit ed coagulat ion fac-
tor defciencies
Acquired coagulat ion
disorder
Fact or VI I I deficiency
-Haemophilia A
Fact or I X deficiency
-Haemophilia B
Von-Willebrand disease
Rare coagulat ion disorder
DI C
Liver disease
Vit amin K deficiency
Drugs (heparin,
warfarin)
Cl i ni cal f eat ur es
● Servere inherit ed disorders are associat ed wit h
bleeding since childhood.
● Bleeding int o j oint s - spont aneous, post t raumat ic
91
● Soft t issue including muscle bleeds
● CNS bleed can be life t hreat ening
● DI C is charact erised by :
* Generalized bleeding associat ed wit h feat ures
of underlying disease.
I nvesti gati ons
PT i s pr ol onged i n
● DI C
● Liver disease
● Vit K deficiency
● Warfarin t herapy
APTT i s pr ol onged i n
● DI C
● Liver disease
● Fact or VI I I deficiency / Fact or I X deficiency
● Lupus ant icoagulant
● Heparinized pat ient
Cor r ect i on Test s Usi ng t he PT or APTT
● I f t here is deficiency of a clot hing fact or - PT or
APTT performed on a 1: 1 mixt ure wit h normal
pooled plasma should give complet e correct ion
of prolonged t imes
● I t is t hen necessary t o ident ify t he specific
fact or(s) t hat are deficient
● I f PT/ APTT is prolonged, and normal plasma fails
t o correct ht e prolonged t ime, an inhibit or should
be suspect ed
● An inhibit or screen and t est s for an lupus ant ico-
agulant should be performed.
Speci f i c f act or y assay
● < 1% : severe deficiency
● 1 % - 5 % : moderat e deficiency
● 6% - 30 % : mild deficiency.
Not e:
N-Normal
PT- Prot hrombin t ime
APTT-Act ivat ed part ial t hrombo plast in t ime
TT-Thrombo plast in t ime
First-line tests used in investigating haemostatic failure
S.No: PT APTT TT Fibrinogen Plat elet Condit ion
1 N N N N N Normal haemost asis
Disorder of plat elet funct ion
Fact or XI I I deficiency
Disorder of vascular haemost asis
2 Long N N N N Early oral ant icoagulat ion
Fact or VI I deficiency
3 N Long N N N Von- Willebrand’s disease
Circulat ing ant icoagulant , e.g.lupus
Fact or VI I I , I X, XI , XI I deficiency
4 Long Long N N N Oral ant icoagulant s
Fact or V, X, or I I deficiency
Mult iple fact or deficiency and liver failure
Vit amin K deficiency
5 Long Long Long N or
Abnormal
N Liver disease
Fibrinogen deficiency/ disorder
Hyper-fibrinolysis
Heparin (large amount )
6 N N N N Low Thrombocyt openia
7 Long Long N N or
Abnormal
Low Liver disease
Massive t ransfusion
8 Long Long Long Low Low Acut e liver disease
Disseminat ed int ravascular coagulat ion
92
Treatment
1. Replacement t herapy
* Fact or VI I / I X concent rat es, if available, for
pat ient wit h haemophilia.
* Fresh Frozen Plasma (FFP) - 15-20 ml / kg
body wt .
* Cryoprecipit at e 1 bag / 10 kg body wt . - useful
in haemophilia A, VWD (Von-Willebrand Dis-
ease), DI C.
* Correct ion of anaemia.
2. Treat t he cause / precipit at ing fact or, if possible,
such as sepsis.
3. Avoid delet erious agent s such as ant i-plat elet
drugs
4. Local measures (for haemart hrosis in haemo-
philia)
* Pressure bandage
* Cold compression
* I mmobilisat ion
* Physiot herapy aft er pain subsides
5. Bleeding due t o ant icoagulant s
* Oral ant icoagulant s
» Ant i-dot e: I nj . Vit K 1 -2 mg, if bleeding
wit h I NR> 5.0
» Fresh frozen plasma- 10 - 15 ml/ kg if
bleeding or for int ervent ions.
» Wit hhold drug, t ill bleeding st ops.
* Heparin
» Ant i-dot e: Prot amine sulphat e 1 mg / 100
unit of heparin given I V
» Fresh frozen plasma - 10 - 15 ml/ kg if
bleeding or for int ervent ions.
I n bl eedi ng neonat es
1. Coagulat ion fact ors do not cross from mot her t o
fet us.
2. Physiological deficiencies of coagulat ion fact ors
can cause prolongat ion of PT and APTT.
3. Bleeding is more common and severe in pre-t erm
and low birt h weight infant s.
4. All new borns should receive Vit K 1 mg immedia-
t ily aft er birt h.
General considerations
1. Blood sample for coagulat ion profile should be
obt ained before t ransfusion of blood or blood
product s.
2. I f on ant icoagulat ion, t he same t o be not ed while
int erpret ing t he result s.
3. I f only whole blood is available, fresh blood
(wit hin 6 hours of bleeding) is preferred t o st ored
blood, aft er adequat e screening.
4. Plat elet concent rat es should be t ransfused imme-
diat ely aft er procurement from t he blood bank.
5. Ant i-fibrinolyt ics such as Trann-exemic acid can
be used for mucosal bleeds.
* For oral bleeding one t ablet of Trann-exemic
acid (500mg) t o be powdered and mixed wit h
10ml of wat er t o make a past e. This may be
kept in t he mout h for 10-15 mins and t hen
swallowed
* I f bleeding does not st op by local measures,
t ablet / capsule can be t aken orally
* Dose - 500 mg t hree - four t imes a day for an
adult init ially and can be increased t o 1 gm
every 6 hours (Dose in Children : 50-100 mg/
kg/ day). This may be cont inued t ill t he bleed-
ing st ops
* For epist axis, a roller gauze may be soaked in
t he same past e and t he nose packed wit h it .
Not e:
Syst emic Trann-exemic acid (oral/ int ravenous) is
cont ra-indicat ed in pat ient s wit h hemat uria.
Recommended facilit ies t o be available at various
levels of hospit als for evaluat ion of bleeding disorders:
1. Primary healt h cent re:
* Blood smear examinat ion for plat elet s
2. Dist rict hospit al, in addit ion t o t he above
* Complet e blood count .
* Bleeding t ime
* PT and APTT wit h correct ion st udies wit h
pooled normal plasma
* Thrombin t ime
* Fibrinogen (if possible)
* I nhibit or screening.
3. Tert iary referral Hospit al
93
* I n addit ion t o above
* Fact or assays.
* I nhibit or assays
* Von-Willebrand disease work up
* Plat elet aggregat ion st udies
* d-Dimer
95
Respiratory
medicine
Chapter 5
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
● Bronchial Ast hma
● COPD
● Bronchiect asis
● Pleural Effusion
● Cor Pulmonale
● Tuberculosis
● RNTCP
● Ext ra Pulmonary TB
● Special Sit uat ions
* TBM
* Pregnancy
● Vaccinat ion
97
Bronchial asthma
“Ast hma is a chronic inflammat ory disorder of t he
airways in which many cells and cellular element s play a
role, in part icular, mast cell, eosinophils, T Lymphocyt es,
Macrophages, neut rophils, and epit helial cells.
I n suscept ible individuals, t his inflammat ion causes
recurrent episodes of wheezing, breat hlessness, chest
t ight ness, and coughing, part icularly at night or in t he
early morning
These episodes are usually associat ed wit h
widespread but variable airflow obst ruct ion t hat is oft en
reversible eit her spont aneously or wit h t reat ment .The
inflammat ion also causes an associat ed increase in t he
exist ing bronchial hyperresponsiveness t o a variet y of
st imuli”.
Fact or s Pr eci pi t at i ng: -
Al l er gens: -
I nhaled (Dust , Pollen, House dust mit e)
I ngest ed (Fish, Nut s, St rawberries)
Food Addit ives
Pharmacologic St imuli: - NSAI D’s especially aspi-
rin, Bet a Blockers
Environment al and Air Pollut ion: -Cold Air, Tobac-
co Smoke, Dust , acrid fumes
Occupat ional Fact ors: - Grain dust , Wood dust
I nfect ions: - Viral, Bact erial
Exercise
Emot ional St ress
Cl i ni cal Mani f est at i ons: -
Sympt oms:
● Episodic breat hlessness
● Cough
● Chest Tight ness
● Wheezing
Si gns:
Tachypnea
Tachycardia
Diaphoresis
Use of accessory muscles
Pulsus paradoxus
I mpending respirat ory failure
Silent chest
Unable t o speak
Respirat ory muscle fat igue
Cyanosis
Shock
I nvesti gati ons
Spi r omet r y: -
FEV1 / FVC normally great er t han 0.75 t o 0.85%
Reduced FEV1
Reduced FEV1 / FVC rat io indicat es airflow
l imit at ion
FVC loop shows expirat ory flow limit at ion
FEV1 or FVC improve by at least > 200ml and >
12% of baseline following administ rat ion of short
act ing bronchodilat or indicat ive of reversibilit y.
Peak Expi r at or y Fl ow:
PEF measurement s are made using a peak flow
met er and can be an import ant aid in bot h diag-
nosis and monit oring of ast hma.
Useful in assessing :
Acut e ast hma diagnosis
Monit oring of chronic ast hma
Diagnosis of Ast hma - > 15% of diurnal variabilit y
Chest X-Ray: -
To R/ O ot her causes of wheezing
To R/ O presence of pneumot horax in severe
acut e ast hma
Si gns of hyper i nf l at i on: -
I ncreased lung volume
Hyperlucency
Depressed diaphragm
I ncreased ret rost ernal airspace
Focal at elect asis due t o mucus plugging
Treatment
Phar macol ogi cal t r eat ment : -
Bet a 2 – agonist s- salbut amol, t erbut alin, salmet erol,
formet rol. I nhalers are preferred over t ablet s since
t here are more effect ive and have less side effect s. The
short act ing bet a - 2 agonist s should be given only for
98
‘as and when required’ basis and not regularly. Bet a
agonist s can be combined wit h regular use of inhaled
cort icost eroids.
I nhaled cort icost eroids - budesonide,
beclomet hasone, flut icasone, and should be used in all
ast hmat ics except t hose wit h mild int ermit t ent ast hma.
Nedocromil and cromolyn sodium – Wit h t he advent
of more effect ive inhaled cort icost eroids t he role of
t hese agent s have come down.
Leukot riene recept or agonist s - Mont elukast ,
Zafirlukast , Zileut on
Theophyllines – Can be used if ast hmat ic is st ill
sympt omat ic when aft er giving inhaled cort icost eroids
and Long act ive bet a agonist s. Should not be used as
t he sole drug for t reat ing ast hma.
Oral cort icost eroids – Prednisolone – should be given
only during exacerbat ion. Oxygen
Non Phar macol ogi cal Tr eat ment : -
Environment al cont rol for reduce exposure t o al-
lergens
I mmunot herapy in select ed cases.
Educat ion
Cr i t er i a f or i mmedi at e r ef er r al t o hospi t al
● Any life t hreat ening feat ures:
● Silent chest
● Cyanosis
● Feeble respirat ory effort
● Bradycardia
● Hypot ension
● Exhaust ion
● Confusion
● Coma
Any feat ures of severe at t ack t hat persist aft er init ial
t reat ment cannot complet e sent ence in one breat h
Respirat ory rat e > 25/ min Pulse rat e > 110/ min
Pathogenesis of Bronchial Asthma
99
Compl i cat i ons: -
Respi r at or y
1. Mediast inal and Subcut aneous emphysema
2. Pneumot horax
3. Lobar collapse
Car di ac
1. Cardiac arrest
2. Myocardial infarct
3. Dysrrhyt hmia
Bi o-Chemi cal
1. Hypokalemia
2. Syndrome of I nappropriat e ADH Secret ion
Pr event i on of ast hma
I nt ervent ions are
1. Avoidance of house dust mit e (HDM) exposure.
2. Avoidance of cert ain food like cow’s milk, nut s,
eggs and fish
3. Combinat ion of t he t wo.
Chronic Obstructive Pulmonary Disease
I nt r oduct i on :
COPD is charact erized by airflow limit at ion t hat is
not fully reversible. The airflow limit at ion is usually bot h
progressive and associat ed wit h an abnormal response
of t he lungs t o noxious part icles or gases.
● COPD includes :
* Chronic bronchit is
* Emphysema
Chronic Bronchit is is defined as presence of cough
and sput um product ion for at least 3 mont hs in each of
2 Consecut ive years
Emphysema is defined as abnormal and
permanent enlargement of airspaces dist al t o
t erminal bronchioles wit h dest ruct ion of walls and
wit hout fibrosis of airspaces
Et i ol ogy :
● Tobacco smoke ﴾active and passive smoking﴿.
Recent evidence shows t hat upt o 40% of smok-
ers develop COPD.
● Smoke from biomass fuel. ﴾firewood petrol
diesel etc﴿
● Occupational chemicals ﴾ vapors and fumes﴿
Symptoms
● Cough
● Sput um product ion
● Dyspnoea
Si gns :
● Sit t ing and bending forward wit h hands on
knees.
● Pursed lip breat hing.
● Cyanosis ﴾Ominous sign﴿
● Dist ance bet ween st ernal and t hyroid not ch.
* Normal – 4 finger breat h COPD - less t han
3 finger
● Forced expirat ory t ime
* Normal 4 secs - COPD - 6 secs and above
● Barrel chest
● Hyper resonant chest
● Diminished breat h sound and bilat eral wheeze
Di agnosi s
Spiromet ry showing obst ruct ion (Fev1/ Fvc < 70%
even aft er bronchodilat or confirms t he diagnosis of
COPD.
Treatment
Non pharmacological
● Rehablit at ion
* Exercise
* Nut rit ion
* Educat ion
● Oxygen t herapy
● Avoid smoking
● Pharmacological
● Bronchodilat ors inhaled bronchodilat ors are
preferred t o oral formulat ions in view of bet t er
efficacy and lesser side effect s. I nhaled bron-
chodilat ors include short act ing bet a agonist s
(salbut amol, t erbut aline), long act ive bet a ago-
nist s (salmet erol, formot erol), short act ing ant i-
cholinergics (iprat ropium), long act ing ant icholin-
ergic (t iot ropium).
100
● Glucocort icoids - I nhaled cort icost eroids should
be given in severe COPD or in t hose wit h repeat-
ed exacerbat ion. syst emic cort icost eroids should
be given only in pat ient s wit h acut e exacerbat ion
of COPD.
● Ant ibiot ics only when t here is evidence of infec-
t ion in t he form of purulent sput um or fever.
● Surgical Bullect omy Lung t ransplant at ion.
Compl i cat i on:
● I nfect ion
● Cor pulmonale - Peripheral edema, pulmonary
hypert ension
● Respirat ory failure
● Polycyt hemia. PCV more t han 55%
Ref er r al and admi ssi on:
● I ncreased sympt oms despit e t reat ment
● Cyanosis and peripheral edema
● Peak expirat ory flow less t han 100 lit ers / min
● SaO2 less t han 90%
● Pneumonia
Ref er ences:
www.goldcopd.org
Bronchiectasis
I nt r oduct i on
Bronchiect asis is defined as permanent irreversible
dilat at ion and dist ort ion of medium sized bronchi.
Et iology
Congenit al, Acquired
Acqui r ed
Bronchial obst ruct ion: Foreign body, t umor, bronchial
st enosis / st rict ure ext rinsic lymph node compression
I nf ect i on
Post measles and whooping cough
Bact erial infect ion
Mycobact erium t uberculosis and non t uberculous
mycobact eria
Fungus (aspergillus species) Allergic broncho pul-
monary aspergillosis (ABPA)
Acquired immunodeficiency syndrome
Cyst ic fibrosis
Primary ciliary dyskinesia (Kart agener’s syn-
drome)
Pulmonary sequest rat ion
Alpha 1 ant it rypsin deficiency
Young syndrome (idiopat hic obst ruct ive azoo
spermia wit h chronic sinopulmonary infect ion)
Hypogammaglobulinemia (I gA/ I gG deficiency)
Symptoms
Cough wit h copious sput um mucoid t o mucopurulent
may be blood st ained foul smelling wit h post ural
variat ion. Dyspnoea and wheezing Fever during
exacerbat ions
Si gns
Clubbing, halit osis and sinus t enderness
Persist ent coarse leat hery crackles may alt er in
charact er wit h coughing
I nvesti gati ons
Sput um examinat ion
Macroscopically large quant it y of t hree layered
sput um
Microscopic examinat ion – Gram’s st ain, Ziel
Neelson t est for AFB, pyogenic cult ure and sen-
sit ivit y, fungal cult ure and cyt ology for malignant
cells.
Hemogram
Leukocyt osis in bact erial infect ions
Lymphocyt osis in chronic infect ions
Eosinophilia in ABPA
Lymphopenia in AI DS
Chest X-ray PA view
Di agnosi s:
HRCT scan is t he recommended invest igat ion t o
confirm t he diagnosis of bronchiect asis.
Treatment
Non – pharmacological
1. Chest physiot herapy - coughing, huffing, post ural
drainage – By t his procedure sput um / pus in t he
101
non dependant areas of lung is brought int o t he
main st em bronchi or t rachea by t he aid of grav-
it y. Then t he sput um is cleared by coughing.
2. Physical exercise t o be encouraged t o aids mu-
cous clearance
Phar macol ogi cal
1. Ant ibiot ics. t o Amoxicillin, Ampicillin, Cephalaxin
for t he bact erial infect ion . Ciprofloxacin or Gen-
t amicin for pseudomonal infect ions
Bronchodilat ors. Salbut amol, t heophylline when
wheeze is present . I nhaled drugs are preferred
over oral.
2. Expect orant s and mucolyt ics. N-acet yl cyst eine,
Ambroxol, Bromhexine, st eam inhalat ion t o t hin
out t he secret ions which can be lat er cleared by
chest physiot herapy.
3. Supplement al oxygen.
4. Vaccinat ion Pneumococcal and annual influenza
vaccinat ions in high risk cases may reduce t he
incidence of frequent exacerbat ions and hospi-
t alizat ions.
Sur gi cal
Surgery is only appropriat e when bronchiect asis
is localized. Emergency surgical resect ion may be
necessary for life – t hreat ening hemopt ysis but
embolisat ion of appropriat e bronchial art ery is usually
at t empt ed first .
Nat ur al Cour se
Bronchiect asis may progress slowly over many years
and qualit y of life is usually impaired.
Compl i cat i ons
1. Acut e exacerbat ions,
2. Haemopt ysis
3. Lung abscess
4. Empyema / Pyot horax
5. Met ast at ic abscess – like cerebral abscess
6. Respirat ory failure and cor pulmonale
7. Amyloidosis
Pr ognosi s
Nowadays t he nat ural hist ory of bronchiect asis has
changed and t he prognosis is much improved However,
pseudomonal infect ion is a bad prognost ic sign.
Pat i ent educat i on
Pat ient is advised t o perform post ural drainage at
least once daily and t o increase t he frequency t o t wice
or t hrice if t hey suffer an exacerbat ion.
Pr event i on
Vaccinat ion against childhood infect ions prevent s
post infect ion bronchiect asis.
Admi ssi on
● Acut e exacerbat ion,
● Hemopt ysis
Ref er r al t o hi gher cent r e
● Presence of persist ent haemopt ysis
● Disease uncont rolled wit h medical management
● Unilat eral and localized disease wit h repeat ed in-
fect ion.
Pul monar y Funct i on Test s
● Obst ruct ive pat t ern
Pneumonia
I nt r oduct i on : -
A syndrome of infect ion t hat is usually bact erial wit h
sympt oms and signs of consolidat ion of part s of t he
lung parenchyma .
Et i ol ogy : -
Pneumonia is not a single disease I t can have over
30 different causes There are five main causes of
pneumonia .
● Bact eria
● Viruses
● Mycoplasmas
● Ot her infect ious agent s, such as Fungi- including
pneumocyst is
● Various chemicals
Hi gh r i sk f act or s wi t h speci f i c pat hogens : -
Peni ci l l i n-r esi st ant and dr ug-r esi st ant
pneumococci
● Age 65 years
● Lact am t herapy wit hin t he past 3 mont hs
102
● Alcoholism
● I mmuno-suppressive illness (including t herapy
wit h cort icost eroids)
● Mult iple Medical co-morbidit ies
● Exposure t o a child in a day care cent er
Pseudomonas
● St ruct ural lung disease ( bronchiect asis)
● Cort icost eroid t herapy (10 mg of prednisone per
day )
● Broad-spect rum ant ibiot ic t herapy for 7 days in
t he past mont h
● Malnut rit ion
Ent er i c gr am-negat i ves : -
● Residence in nursing home
● Recent ant ibiot ic t herapy
Sympt oms and si gns
● Cough, oft en producing mucus (sput um) from
t he lungs
● Mucus may be rust y or green or t inged wit h
blood.
● Fever, which may be less common in older adult s
Shaking , “ t eet h-chat t ering” chills ( one t ime only
or many t imes).
● Fast , oft en shallow, breat hing and t he feeling of
being short of breat h.
● Fast heart uberculosiseat chest wall pain t hat is
oft en made worse by coughing or breat hing.
● Feeling very t ired (fat igue) or feeling very weak
(malaise).
● Nausea and vomit ing
● Diarrhoea.
Cl assi f i cat i on
Condit ion
Commonly Encount ered Pat ho-
gens
Exposure t o
animals and
birds
Hist oplasma capsulat um
Chlamydia psit t aci,
Crypt ococcus neoformans,
Francisella t ularensis
Coxiella burnet ii (Q fever)
Legionella species
Travel and
voyage
Coccidioidomycosis
Pneumonia, Legionella species
Burkholderia pseudomallei, avian
influenza,
SARS
Bacillus ant hracis (ant hrax),
Yersinia pest is (plague)
I nfect ive and
st ruct ural
disease of lung
P. aeruginosa, S. aureus
Anaerobes, S. pneumoniae, H.
influenzae,
Drug-resist ant pneumococci,
MRSA, fungal pneumonia.
M. t uberculosis, At ypical
mycobact eria
HI V infect ion
(early)
S. pneumoniae, H. influenzae,
M. t uberculosis
HI V infect ion
(lat e)
Crypt ococcus, Hist oplasma,
Aspergillus, At ypical mycobact eria
(especially Mycobact erium
kansasii)
COPD / Smoker S. pneumoniae,Hemophilus
influenzae
Moraxella cat arrhalis, Legionella
Nursing home /
Residency
H. influenzae, St aphylococcus
aureus,
Anaerobes, Chlamydia
pneumoniae,
Tuberculosis
I nvesti gati ons
● Complet e blood count
● Pret reat ment blood cult ure
● Pret reat ment sput um cult ure
● Rapid PCR( Chlamydia and Legionella )
● Cold agglut inin for Mycoplasma
● Chest X-ray
● CT chest
103
● Bronchoscopy
Treatment

Non: - Phar macol ogi cal
● Oxygen Therapy
● Nut rit ion
● Physiot herapy
● I V Fluids
Phar macol ogi cal : -
● Analgesics
● Empirical Ant ibiot ics
● Appropriat e ant ibiot ics aft er cult ure result s
Nat ur al Cour se
● Wit h t reat ment , most t ypes of bact erial pneu-
monia can be cleared wit hin t wo t o four weeks .
● Viral pneumonia may last longer .
● Mycoplasma pneumonia may t ake four t o six
weeks t o resolve .
● Pneumonia progresses t o bact eremia in about
20% and mort ialt iy is increased in such pat ient s.
Compl i cat i ons
● Pleural effusion
● Shock and DI C
● Bact eremia
● Lung abscess, pneumot horax ,empyema
● Pericardit s , endocardit is , myocardit is
● Respirat ory failure
● Meningo - encephalit is , Guillain - Barre Syn-
drome (GBS)
Pr ognosi s
Cr i t er i a f or cl i ni cal st abi l i t y : -
● Temperat ure < 37.8 C
● HR< 100 beat s/ min
● RR< 24 breat hs/ min
● Syst olic BP > 90 mm hg
● Art erial O2 sat urat ion > 90% ( or ) PO2 < 60 mm
Hg on room air
● Abilit y t o maint ain oral int ake
● Normal ment al st at us
Pr event i on
● Hand – washing ( hospit al set t ing )
● I dent ificat ion of sources of infect ion
● Vaccinat ion
● Ant ibiot ic prophylaxis
Ref er r al And Admi ssi on
● Pat ient s who fail t o respond t o amoxicillin or a
macrolide are frequent ly older have coexist ing
lung disease such as chronic bronchit is and em-
physema .
● Those who show inadequat e response t o oral an-
t ibiot ics .
● Respirat ory rat e > 30 breat hs/ min
● Mult ilobar infilt rat es
● Confusion/ disorient at ion
● Uremia (BUN level, > 20mg/ dl)
● Leukopenia (WBC count , 14000 cells/ mm3)
● Thrombocyt openia (plat elet count , 1100,000
cell/ mm3)
● Hypot ension requiring aggressive fluid resuscit a-
t ion
● Pat ient s who need invasive mechanical vent ila-
t ion
● Sept ic shock wit h t he need for vasopressors.
Ref er ences
www. webmd. com/ a- t o- gui des/ pneumoni a-
sympt oms American academy of family physic-
lans February 1, 2006 vol, 73 No. 3 Thorax, De-
cember 1, 2001: 56 ( 90004) : !
Pleural effusion
Symptoms
● Breat hlessness
● Cough
● Fever
● Pleurit ic chest pain
Si gns:
Decreased breat h sounds, dullness on percus-
104
sion, decreased vocal resonance
Types:
● Transudat e
* Congest ive cardiac failure
* Cirrhosis of liver
* Nephrit ic syndrome
* Myxoedema
* Perit oneal dialysis
● Exudat es
* I nfect ious diseases-Tuberculosis, ot her bact e-
rial, viral, fungal, parasit ic
* Neoplasm – met ast at ic disease, mesot helio-
ma, pulmonary embolism
* Collagen vascular disease-Rheumat oid
Art hrit is(RA), Syst emic Lupus Eryt hemat osus
(SLE)
* Gast roint est inal disease- Oesophageal perfo-
rat ion, Pancreat ic disease
* Uraemia
* Chylot horax, Hemot horax
* Drug induced- nit rofurant oin, dant rolene,
amiodarone
Di agnost i c aspect s
Chest radiography: lat eral decubit us, PA view,
lat eral view can be t aken
● Blunt ing of cost ophrenic angle
● Ellis S shaped in larger effusions
Ul t r asound chest
To det ect
● Small amount s of fluids
● Loculat ion
● Sept at ion
Treatment
Thor acocent esi s
● One space below t he maximum dullness in t he
post erior axillary line j ust above t he rib, should
be done.
● I f pat ient develops cough or chest pain, st op t he
procedure.
● Complicat ions: Pneumot horax (do check x-ray of
t he procedure)
Management of most common causes
● Tuberculosis
* St raw coloured effusion
* Cell count - lymphocyt e predominance
* Pleural fluid prot ein > 3g/ dl
* Cat egory I I I ATT
* Cat egory I ATT if presence of co morbid ill-
ness / bilat eral effusion or Chest X-ray infilt ra-
t ion , Parat racheal nodes
● Para pneumonic effusion
* Chest X-ray consolidat ion feat ures along wit h
effusion
* Cell count predominant ly neut rophilic
* Appropriat e ant ibiot ics.
* Thoracocent esis t o ensure t hat empyema has
not developed
● Malignant effusion
* Cyt ology posit ive
* Refer t o higher cent re
* Treat ment of underlying cause in heart failure
/ nephrot ic syndrome / liver cirrhosis
Cor Pulmonale
Def i ni tion
Hypert rophy of t he Right Vent ricle result ing from
diseases affect ing t he funct ion and / or st ruct ure of t he
lung.
105
Et i ol ogy
Parenchymal and I nt erst it ial Diseases
Chronic Sequelae
of Tuberculosis
Cough, expect orat ion
fever,loss of appet it e, loss of
weight night sweat s,
hemopt ysis.
Cyst ic Fibrosis
Neonat e or child – Failure t o
t hrive Meconium ileus, Rect al
prolapse Cough,Recurrent .chest
infect ion. GI T Dist urbances,
Sinusit is,Diabet es Mellit us,Male –
I nfert ile Female-Subfert ile
Pulmonary
Embolism
Acut e or Chronic,Circulat ory
Collapse, Dyspnoea, Hemopt ysis
,Pleurit ic pain, Tachypnoea
,Dyspnoea RR > 20
Pneumonect omy From Hist ory
Pneumoconiosis
Occupat ional hist ory, coal mining
foundary work, welding,
fireworks,armament and paint ing.
Clinical Feat ures, Cough, Sput um,
Dyspnoea on exert ion.
Airway Diseases
Ast hma
Wheeze, Noct urnal cough,
Episodic dyspnoea,Chest t ight ness
Triggering fact ors.
COPD
Dyspnoea, reduced exercise
t olerance, product ive cough,
Wheeze.
Bronchiect asis
Recurrent childhood infect ion,
Viral exant hema
Cough, Product ive sput um.
Vascular Disease
Pulmonary
Embolism
(Acut e Cor Pulmonale)
Primary
Pulmonary
Hypert ension
Exert ional dyspnoea, Chest Pain
Syncope, Palpit at ion Edema.
St ruct ural
Chest Wall
Abnormalit ies
Kyphoscoliosis
Neuromuscular disease
Symptoms
● Weight gain
● Right Upper Quadrant discomfort
● Noct uria
● Peripheral edema
● Easy Fat iguabilit y
Si gns
● Tachypnoea
● Accessory muscles of respirat ion act ing
● Cyanosis
● Neck vein dist ent ion
● Ascit es
● Pedal edema
● Liver – enlarged t ender
● CVS- Parast ernal syst olic lift
● Thud felt over Pulmonary area
● S2 accent uat ed
I nvesti gati ons
Chest X-ray
Enlarged Pulmonary art ery and underlying lung
disease
ECG
‘P’ Pulmonale, R axis deviat ion RV Hypert rophy
ECHO
To rule out Left V en t ricular failure from CAD /
Aort ic / Mit ral Valvular Disease, Congenit al Heart
Disease.
RBC
Polycyt hemia
ABG
PO2 < 90%
Treatment
● Non – Pharmacological
● Salt reduced diet
● Diaphragmat ic breat hing
● Breat hing exercises
● Long t erm O2
● Avoid smoking / Viral I nfect ions
● Prompt t reat ment of acut e respirat ory infect ions.
106
Phar macol ogi cal
● Bet a 2 – agonist s
● Cort icost eroids
● Diuret ics
● Digoxin
● Oxygen t herapy
Sur gi cal
● Phlebot omy
Pat i ent Educat i on
● Avoid smoking
● Avoid exposure t o cold and allergens
● Prompt t reat ment of acure respirat ory infect ions.
Ref er r al
● RR > 30
● ABG PO2 < 60
● Hypoxemia –Persist ent and Worsening
● Cardio – respirat ory failure.
● Pneumot horax.
Compl i cat i ons
● Respirat ory failure
● Circulat ory failure
● Congest ive hepat omegaly.
● Neurohypoxia
Pr ognosi s
● Poor.
Tuberculosis and RNTCP
( Revi sed Nat i onal Tuber cul osi s Cont r ol
Pr ogr am)
Tuberculosis is caused by Mycobact erium t uber-
culosis, which is primarily a pulmonary disease
but also affect s ot her syst ems of t he body.
I n I ndia, t here are 14million t uberculosis cases
out of which, 3.5million are sput um posit ive and
about 1million sput um posit ive cases are added
each year. About 1000 people per day and one
every minut e, die of Tuberculosis in our count ry.
Tr ansmi ssi on of di sease:
When a sput um posit ive pulmonary t uberculosis
pat ient coughs, he spreads Tuberculosis bacilli
int o air, in t he form of t iny droplet s of 1-5µm.I f
t hese droplet s are happened t o be inhaled by a
healt hy person, he may be infect ed wit h t uber-
culosis.
Effect ive t reat ment of smear posit ive t uberculosis
pat ient can help t o cont rol t he spread of disease.
Hence, it is t he t op priorit y under RNTCP. (Re-
virsed Nat ional Tuberculosis Cont rol Programme)
Goal of RNTCP
To cure at least 85% of all newly det ect ed sput um
posit ive cases.
107
Diagnostic algorithm for Pulmonary tuberculosis
Sputum smear Positive TB
(Anti-TB Treatment)
2 or 3 Positives
COUGH FOR 3 WEEKS OR MORE

3 Sputum smears

2 or 3 Positives

3 Negatives
Antibiotics 10-14 days
Cough Persists
Repeat 3 Sputum
Examinations
Negative
1 Positive
X-Ray
Suggestive of TB Negative for TB
X-Ray
Suggestive of TB Negative for TB
Sputum Smear-positive TB
(Anti-TB Treatment)
Non TB
Sputum Smear-Negative TB
(Anti-TB Treatment)
108
drugs are given under supervision during I P, t hrice
weekly on alt ernat e days. During CP, t he first dose of
each week is given under supervision.
Dosage St r engt hs:
Drug
Dose(t hrice a week)
I soniazid 600 mg H
Rifampicin 450 mg(600 mg if wt > 60 kg) R
Pyrazinamide 1500 mg Z
Et hambut ol 1200 mg E
St rept omycin 0.75 g I M(0.5 g if age> 50 years)

S
Not e:
Smear -negat i ve pul monar y Tuber cul osi s
Ser i ousl y i l l :
● Miliary Tuberculosis
● Ext ensive parenchymal infilt rat ion
● Co-infect ion wit h HI V.
● Pulmonary Disease wit h cavit at ions
● All forms of Paediat ric sput um smear-negat ive
pulmonary Tuberculosis except primary complex.
Extra - Pulmonary Tuberculosis
Tuberculosis can affect any part of body includ-
ing pleura, lymph node, bone and j oint s,genit o-
urinary t ract ,gast ro-int est inal t ract and cent ral
nervous syst em.
Diagnosis of ext ra pulmonary t uberculosis may
require specialized t est s such as FNAC, biopsy,
radiological invest igat ions or st rong clinical evi-
dence.
Di agnosi s
Any person wit h cough wit h expect orat ion for 3
or more weeks should be invest igat ed for t uber-
culosis. Sput um microscopy of at least 3 samples
is t he gold st andard invest igat ion t o confirm pul-
monary t uberculosis. I t also indicat es t he degree
of infect ivit y and helps t o monit or response t o
t reat ment .
Radiological invest igat ion is unreliable because
ot her pulmonary disease may oft en resemble t u-
berculosis and t he act ivit y of t he disease cannot
Not e:
* * Ant ibiot ics used in t he t reat ment should not
have Ant i Tuberculosis act ivit y ( e.g. co-t rimoxa-
zole. Avoid floroquinolones, rifampicin and st rep-
t omycin.)
RNTCP-DOTS:
Direct ly observed t reat ment , short course is t he
way Tuberculosis cases are t reat ed under RNTCP.
I t is ensured t hat pat ient s t ake medicines regu-
larly.
Cat egor i es and t r eat ment :
● Cat egory of t reat ment
● Type of pat ient
● Regimen
● Cat egory I
● New sput um smear-posit ive
Seriously ill new sput um smear-negat ive
Seriously ill new ext ra-pulmonary
● I nt ensive phase - 2H3R3Z3E3
● Cont inuat ion Phase - 4H3R3
● Cat egory I I
● Sput um smear-posit ive Relapse
● Sput um smear-posit ive Failure
● Sput um smear-posit ive Treat ment Aft er default
● Ot hers
● I nt ensive phase - 2H3R3Z3E3S3 + 1H3R3Z3E3
● Cont inuat ion phase - 5H3R3E3
Cat egor y I I I
● New Sput um smear-negat ive, not seriously ill
● New Ext ra-pulmonary, not seriously ill
● I nt ensive phase - 2H3R3Z3
● Cont inuat ion phase - 4H3R3
Not e:
The number before t he let t ers refers t o no. of mont hs
of t reat ment . The subscript aft er t he let t ers refers t o
no. of doses per week.
Pat ient s in cat egories I , I I who have a posit ive sput um
smear at t he end of int ensive phase should receive an
addit ional mont h of int ensive phase t reat ment .
I P – I nt ensive Phase, CP – Cont inuat ion Phase. All
109
be confirmed.
Ext r a pul monar y Tuber cul osi s ( EPTuber cul osi s)
Ser i ousl y i l l EPTuber cul osi s
● Meningit is
● Pericardit is
● Perit onit is
● Bilat eral or Ext ensive pleural effusion
● Spinal Tuberculosis wit h neurological involve-
ment .
● I nt est inal, Genit o-Urinary
● Co-infect ion wit h HI V
● All forms of paediat ric EPTuberculosis ot her t han
lymph node and unilat eral pleural effusion
Not Sever el y EPTuber cul osi s
● Lymph node
● Unilat eral pleural effusion
● Peripheral Joint s.
● Hospit alisat ion:
Ext r emel y i l l EPTuber cul osi s,
● Wit h significant hemopt ysis,
● Pneumot horax,
● Large pleural effusion
● Dyspnoea
● Hospit alisat ion and int ensive care.
Special Situations
Tuber cul osi s Meni ngi t i s:
● Pat ient s should be referred t o t he hospit al and
t reat ed under cat egory I t reat ment , wit h cont inu-
at ion phase last ing 6-7 mont hs.
● St eroids should be given init ially t o reduce me-
ningeal inflammat ion and t apered over a period
of 6-8 weeks.
Dur i ng pr egnancy:
● All ant i t uberculosis drugs used in RNTCP except
st rept omycin are safe during pregnancy.
● Breast feeding should be cont inued regardless of
mot her’s Tuberculosis infect ive st at us.
Chi l d cont act s - < 6 year s of age wi t h sput um
smear posi t i ve case:
● I f t he child has sympt oms of t uberculosis and if
it is confirmed by t he t reat ing physician – a full
course of ATT (CAT I I I ) should be given.
● I f t he child does not have sympt oms:
* Tuberculin t est : Not available – chemot hera-
phy for 6 mont hs I soniazid 5 mg/ kg.
* Tuberculin t est : Available – child should be
given I NH chemot herapy for 3 mont hs and
Tuberculin t est should be done, t hen t reat as
per t he not es given below.
Not e:
● I f indurat ion t o t uberculin t est < 6mm st op
prevent ive chemot herapy and vaccinat e wit h
B.C.G (if not vaccinat ed previously)
● I f indurat ion is > 6mm, cont inue I NH prevent ive
chemot herapy for anot her 3 mont hs.
Vacci nat i on:
BCG vaccinat ion does not prot ect an individual from
developing adult t ype pulmonary t uberculosis. But ,
several st udies indicat e t hat BCG prevent s serious forms
of Tuberculosis in children.
111
Gastroenterology
Chapter 6
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
● Apht hous Ulcers
● Acut e Esophageal Candidiasis
● GERD
● Pept ic Ulcer Diseases
● Vomit ing
● Const ipat ion
● I BS
● AGE
● Chronic Diarrhoae
● Ulcerat ive Colit is
● Amoebic Liver Abscess
● Pyogenic Liver Abscess
● Acut e Pancreat it is
● Chronic Pancreat it is
● GI Bleed
113
Aphthous ulcers
Symptoms
Apht hous ulcers in t he oral cavit y cause significant
pain during chewing food.
Causes
Minor apht hae are recurrent , painful t ypically single
or mult iple (1-15 mm) shallow ulcers surrounded by
eryt hemat ous mucosa occurring anywhere in t he oral
mucosa. These occur cyclically and heal wit hout a scar
in a week’s t ime. Larger and deeper ulcers known as
maj or apht hae, heal wit h a scar. Those t hat are vesicular
are called herpet iform apht hae and are more numerous.
Fever, adenopat hy, gast roint est inal sympt oms are
t ypically absent .
I mpor t ant not e
Ulcers occurring repeat edly at t he same sit e or slow
healing ulcers wit h syst emic sympt oms e.g. uveit is,
art hrit is, fever, adenopat hy are worrisome. Malignancy
should be excluded.
Treatment
Medical t herapy
Ant i bi ot i cs
1. Topical and syst emic ant ibiot ic t reat ment :
Tet racycline 250-mg ant ibiot ic capsule dis-
solved in 180 mL wat er and used as a “ swish
and swallow” or “ swish and spit ” t reat ment four
t imes per day for several days in adult pat ient s.
o r
Tet racycline suspension, 250 mg per 5 ml, used
in a similar fashion, wit h 5 ml swished four t imes
per day. (Avoid in children and in pregnancy)
2. Pro-biot ics:
The powder form can be used t wo or t hree t imes
a day, placed wit hin t he oral cavit y and swallowed
wit h sips of wat er
3. Ant i-inflammat ory agent s
Pellet s of Hydrocort isone 5 mg can be kept on
t he ulcer base and sucked every 4 hours for 3 t o
5 days. Most successful when ulcers are locat ed
in t he sulci where pellet can be left t o dissolve.
Triamcinolone 0.1 percent
● Applied t o ulcers t wo t o four t imes a day. The
past e can be applied unt il t he ulcer heals.
Bet amet hasone sodium phosphat e (Bet nesol
mout hwash)
● One 0.5 mg t ablet dissolved in 5 t o 10 ml of
wat er used as a mout hwash qid during ulcer at-
t ack. Must be held in mout h for a minimum of
3 minut es for maximum effect iveness; spit out
aft er use. Can be used 6 t imes a day under st rict
supervision.
Dexamet hasone elixir:
● 0.5 mg per 5 ml as a rinse and expect orat ed:
recommended for ext ensive oral ulcerat ion
● Warning: secondary fungal infect ion likely.
● Tab. Prednisolone 0.5 mg/ kg/ day for 3 t o 5 days.
I mmune modul at or s
● Hydrocort isone pellet s 5 mg can be kept on t he
ulcer base and sucked every 4 hours for 3 t o 5
days
or
Prednisolone 0.5 mg/ kg/ day for 3 t o 5 days.
● Levamisole
* Dose: 50 mg t wice a day for t hree consecu-
t ive days for 4 weeks; no medicat ion for next
t wo weeks
* Followed by Levamisole 150 mg t ablet : half a
t ablet t wice a day for t hree consecut ive days
for t wo weeks.
HI V posi t i ve pat i ent s
Thalidomide: 200 mg once t o t wice daily for t hree
t o eight weeks (cont ra-indicat ed in non-HI V ulcers:
significant side effect s and t erat o-genicit y)
Do’s and Don’t ’s
● Good oral hygiene: Repeat ed mout h wash wit h
plain wat er/ saline gargle especially aft er eat ing
● Ensure t oot hbrush has aligned brist les
● Avoid chewing bet el leaf and ot her condiment s
● Avoid excessive carbonat ed drinks and spicy or
sharp/ crispy foods
● Take plent y of green leafy veget ables. Leaves of
‘Manat hakali” when chewed for 10 minut es t wo
or t hree t imes a day, result s in spont aneous heal-
ing of ulcers
● Using a st raw can alleviat e pain
● Seek opinion of a dent ist , if ulcer fails t o heal.
114
Acute Oesophageal candidiasis
Causes
Commonly occurs as opport unist ic infect ion in
individuals wit h uncont rolled Diabet es mellit us or
immuno-compromised condit ions (AI DS, malignancy,
chronic st eroid t herapy, cyt ot oxic drugs). Usually caused
by Candida albicans.
Symptoms
Discret e or confluent curdy whit e adherent plaques
on t he oropharyngeal mucosa.
● Oral lesions are usually painless but oesophageal
lesions produce painful dysphagia
Ant ifungal t herapy for Esophageal Candidiasis
Ant ifungal
Agent
Form St rengt h Use
Topical
Nyst at in Suspension 100,000
U
5 ml, swish
and swallow
q.i.d.
Clot rimazole Oral
lozenge
10 mg Dissolve 1
lozenge 5
t imes/ day
Amphot ericin B Suspension 1 mg/ ml 1 ml, swish
and swallow
q.i.d.
Amphot ericin B Lozenge 100 mg q.i.d.
Amphot ericin B Tablet 10 mg q.i.d.
Syst emic
Ket oconazole Tablet 200 mg 1-2 t ablet s /
day b.i.d.
Fluconazole Tablet 100 mg 1 t ablet /
day
Fluconazole Solut ion 10 mg/ ml 10 ml / day
I t raconazole Capsule 100 mg 200 mg / day
I t raconazole Solut ion 10 mg/ ml 10-20 ml /
day b.i.d.
I nvesti gati ons
Diagnosis is confirmed by demonst rat ion of
pseudohyphae on wet smears or cult ure.
Treatment
Suspension Nyst at in local applicat ion in mout h
and 100, 000 unit s orally 4 hourly for 5 t o 7 days
or
Tab Fluconazole 100 mg / day for 10 t o 14 days
Dyspepsia
I t is a non-specific group of sympt oms relat ed t o
t he upper gast roint est inal t ract . I t is also referred t o as
‘non-ulcer dyspepsia’ / funct ional dyspepsia/ GERD
Symptoms
Common sympt oms include
● Upper abdominal sympt oms simulat ing an ulcer
disease, or heart burn wit h or wit hout regurgi-
t at ion simulat ing gast ro- oesophageal reflux dis-
ease, heaviness, post-prandial fullness or early
sat iet y (dysmot ilit y t ype). Sympt oms of ‘gas’ in
abdomen is not uncommon.
● Beware of red flag signs or ‘alarm’ sympt oms
such as anorexia, weight loss, anaemia, dys-
phagia, mass abdomen
● Age > 35 years (sout h I ndian), not responding t o
empirical ant i ulcer, ant i -GERD t reat ment
I nvesti gati ons
The above sympt oms suggest an organic disease
and are excluded by hist ory and upper endoscopy.
Treatment
Medi cal t her apy
St art empirical t herapy for pat ient s below 35
years and in absence of ‘alarm sympt oms’. UGI
scopy is indicat ed in non-responders.
● I n pat ient s wit h ulcer-like dyspepsia, cap.
Omeprazole 20 mg once a day 45 min-
ut es before breakfast for 4 t o 6 weeks
o r
Ranit idine 150 mg t wice a day 45 min. before
breakfast and dinner for 4 t o 6 weeks Ant acids 2
t o 3 t easpoon or 2 t abs (chewable) when symp-
t omat ic despit e above medicat ion
● For t hose wit h dysmot ilit y sympt oms
* Domperidone 10 mg t hree t imes a day 30
min. Before breakfast , lunch and dinner (op-
t ions: ot her prokinet ics: mosapride, it opride,
levosulpride).
* Avoid met oclopramide due t o ext rapyramidal
side effect s
● For reflux t ype dyspepsia
* Cap Omeprazole 20 mg 45 min. Before break-
fast 4 t o 6 weeks
* I f regurgit at ion is predominant one can add
115
Domperidone 10 mg half an hour before
breakfast and dinner (or any ot her prokinet ic)
Dur at i on:
Short courses of t herapy (4 t o 6 weeks) of t he
drug may be repeat ed or long-t erm t reat ment may
be cont inued for up t o a year. I nt ermit t ent t herapy or
biweekly PPI is also recommended in t hose requiring
long-t erm t reat ment .
Ant i -H pyl or i t r eat ment i s r ecommended f or
● Those on long t erm NSAI Ds
● Those wit h Duodenal / gast ric ulcers (complicat-
ed e.g. bleed).
Recommended t r eat ment f or H. Pyl or i
( For one week)
Combinat ion of
Omeprazole 20 t wice a day
+
Amoxicillin 500 mg t hrice a day
+
Met ronidazole 400 mg t hrice day
Fol l owed by
Omeprazole 20 mg once a day for t hree weeks
I t is desirable t hat t he ant i -H pylori regimen is
t aken for at least 5 days
Do’s and Don’t ’s
● Avoid excess t ea, coffee, fried food it ems.
● Abst ain from alcohol and smoking.
● Avoid unnecessary NSAI Ds; prefer Paracet amol
especially t hose wit h ulcer like sympt oms or
t hose wit h document ed duodenal/ gast ric ulcer.
● Follow meals at regular int ervals: 4 t h hourly (in-
cluding snacks).
● Daily exercise t o maint ain opt imum weight .
Gastro-Esophageal Refux Disorder
Causes
I t is a common disorder caused by ret rograde flow
of gast ric cont ent s t hrough an incompet ent gast ro-
oesophageal j unct ion.
Symptoms
Clinically pat ient present s wit h
● Ret ro-st ernal pain, heart burn and regurgit at ion
most ly aft er a meal
● Rare present at ions: chronic cough, laryngit is,
recurrent pulmonary infect ions, bronchospasm,
ot it is media et c
I nvesti gati ons
Diagnosis is confirmed by endoscopy which based
on severit y of disease may show mild (minimal or no
mucosal change) t o severe changes (linear ulcers wit h
or wit hout oesophageal st rict ure). Endoscopy is not
recommended as a rout ine for screening for GERD
since t here is a very poor correlat ion bet ween clinical
present at ion and endoscopy findings. pH st udy is t he
gold st andard.
Treatment
I f GERD is occasional i.e. once a week or t wice a
week:
For immediat e relief:
● Liquid ant acid wit h or wit hout alginat e 10 t o 15
ml or
● 2 t o 3 t ablet s chewed: 4 t o 6 t imes a day ½ t o 1
hr aft er a meal if sympt oms persist .
● There is no role for long-t erm maint enance t her-
apy. Ranit idine or Omeprazole will not relieve t he
sympt oms inst ant aneously.
For Mi l d GERD
1. Cap Omeprazole 20mg OD/ BD
2. (or Pant oprazole 40 mg OD,
3. Rabeprazole 20 mg OD,
4. Esomeprazole 40 mg OD, or
5. Lanzoprazole 30 mg OD) 45 minut es before a
meal for 4 t o 6 weeks.
6. I f individual is on mult i- drug t herapy, Pant opra-
zole or Rabeprazole is recommended.
7. Add pro-kinet ic: Domperidone 10 mg t hree t imes
a day 30 minut es before a meal for 2 weeks. if
regurgit at ion is significant .
8. Long-t erm t herapy wit h Omeprazole is not asso-
ciat ed wit h maj or side effect s. Drugs are oft en
an alt ernat ive t o surgery.
For moder at e t o sever e GERD
● Cap Omeprazole 20 mg or any of t he available
PPI s t wice a day 45 minut es before a meal for 4
116
t o 6 weeks i.e. “ double dosing”
Fol l ow-up
Maint enance dose
Recommended in few cases using half t he
recommended dose (Omeprazole 10 mg once a day half
- hour before break fast ).
For Sever e GERD
Long t erm maint enance t herapy / double dose wit h
PPI is recommended. Pat ient may event ually require
surgery.
Sur ger y
This is indicat ed in individuals who are young,
responding t o Prot on pump inhibit ors (PPI ) and are
likely t o require long t erm maint enance. I t is relat ively
cont raindicat ed in non-responders t o PPI
I mpor t ant not e
Do’s and Don’t s
Life st yle modificat ion
● Reduce fat int ake
● Weight reduct ion
● St op smoking
● Small regular meals
● Allow 3-hours bet ween last meal and ret iring at
night
● Avoid t ight corset s during sleep
● Avoid alcohol/ hot drinks before bed/ excessive
t ea/ coffee/ garlic pearls
● Combine wit h a PPI when on t reat ment for ast h-
ma, depression.
● Plent y of wat er is recommended while swallow-
ing doxycycline, t et racycline, NSAI Ds et c.
● Raise head end of bed by 10 cm using a block/
brick if noct urnal sympt oms are present . Do not
raise t he head using pillows
117
General measures and liquid ant acids as needed
Approach t o drug t herapy in GERD
Relief No relief aft er 4 weeks
Tab.Ranit idine 150 mg bd/ Cap.Omeprazole 20 mg OD for 12 weeks
Add Domperidone/ Mosapride/ I t opride if regurgit at ion dominat es
Cont inue PPI double dose
Consider ECG and referral t o t ert iary cent ers for pH
st udy, Esophageal manomet ry
Proceed for maint enance t herapy
(Half t he dose t hrice a week for
anot her 12 weeks)
No oesophagit is
No relief Relief
Esophagit is
St op PPI for 2 weeks: proceed for en
doscopy
Revise diagnosis
118
Non-Hel i cobact er pyl or i
Sympt omat i c t her apy
1. Any PPI for 4 t o 6 weeks, 45 minut es before
breakfast .
2. H2-Recept or ant agonist s
* Ranit idine (150 mg bd) / Famot idine (40 mg
od) equally efficacious but t akes longer t ime
for sympt om relief.
3. Maint enance dose wit h PPI for pat ient s on long
t erm NSAI Ds, I HD pat irent s
Do’s and Don’t s
St op smoking
Curt ail alcohol int ake
Avoid NSAI Ds, prefer Paracet amol
Avoid foods which aggravat e sympt oms; no role
for bland diet or excess milk
Meals at regular int ervals
Vomiting
Def i ni tion
Vomit ing is forceful expulsion of t he gast ric cont ent s
due t o cont ract ion of abdominal musculat ure and
simult aneous relaxat ion of gast ric fundus and lower
oesophageal sphinct er.
Nausea is an unpleasant feeling, t hat one is likely t o
vomit .
Regurgit at ion is effort less vomit ing wit hout forcible
cont ract ion of abdominal wall muscles.
Causes
1. Cent ral (due t o st imulat ion of vomit ing cent re)
neurological diseases, raised int racranial pressure
2. Vest ibular syst em disorders
3. Drugs and t oxins
4. Toxic and met abolic disorders such as ket oaci-
dosis,
5. Syst emic infect ions
6. Radiat ion exposure
7. Pregnancy and
8. Psychogenic vomit ing.
9. Peripheral
10. Obst ruct ive diseases of t he GI T
Peptic ulcer disease
Def i ni tion
There is ulcerat ion of t he gast ric or duodenal mucosa
due t o acid and pepsin.
Symptoms
● Pat ient present s wit h sharp gnawing epigast ric
pain, worsened (gast ric ulcer) or relieved by in-
t ake of food (in duodenal ulcer).
● Noct urnal pain commonly awakens t he pat ient
at midnight . Pat ient occasionally get s up in t he
morning wit h pain. Typically t here are relapses
and remissions.
● Complicat ions due t o an ulcer disease include an
upper GI bleed, perforat ion and gast ric out let ob-
st ruct ion.
● Helicobact er pylori is responsible for most of t he
duodenal and gast ric ulcers.
● Endoscopy is confirmat ory. Empirical t reat ment
is recommended in t hose wit h no “ alarm symp-
t oms.”
● Helicobact er pylori checking is not done rout inely.
● Rapid urease t est , hist ology of ant ral- mucosa is
adequat e.
Treatment
Medi cal t r eat ment
Ant i H.pylori t reat ment is recommended for pat ient s
on long t erm NSAI Ds, bleeding pepic ulcer
Preferred one-week t riple t herapy ( Table), followed
by PPI for 3 weeks.
H.pylori treatment
Drug Dose (mg)
Frequen-
cy
Durat ion
PPI
Clarit hromycin
Met ronidazole
*
500
400
BD
BD
BD
One
week
PPI
Amoxicillin
Met ronidazole
*
500
400
BD
TDS
TDS
One
week
PPI
Amoxicillin
Clarit hromycin
*
500
500
BD
BD
BD
One
week
* Choice of PPI : Pant oprazole 40 mg/ Rabeprazole
20 mg/ Lansoprazole: 30 mg
119
t rimest er
For mot ion sickness: Tab Cyclizine 50 mg 3 t imes
daily.
Pr event i on
● Avoid st ale food, cut veget ables/ fruit s kept in
open, drink pot able wat er only.
● Avoid NSAI DS, especially if ulcer sympt oms are
present .
● Prevent dehydrat ion: Encourage pat ient s t o t ake
sips of liquids at short int ervals t o prevent dehy-
drat ion.
● Endoscopy is necessary, if sympt om persist s.
● Prevent mot ion sickness by avoiding heavy meal
before t ravel.
Constipation
Causes
Commonest cause of const ipat ion is habit ual.
I mport ant fact ors include insufficient diet ary fibre,
physical inact ivit y, suppression of defecat ory urges
occurring at inconvenient moment s, prolonged st ress
et c.
Secondary causes include neurological, hormonal,
colonic, malignancy, depression. These causes should
be considered if t here is recent onset of const ipat ion or
severe sympt oms.
Symptoms
Clinically an individual is considered t o be chronically
const ipat ed if t here is decrease in frequency and
liquidit y of st ool compared t o t he normal pat t ern in a
part icular individual or st raining at defecat ion> 25%
of t imes, passing lumpy/ hard st ools and sensat ion of
incomplet e evacuat ion.
I nvesti gati ons
A rect al examinat ion wit h a short lengt h colonoscopy
is a must for all pat ient s wit h recent onset of const ipat ion
irrespect ive of bleeding per rect um.
When acut e, t he const ipat ion may be a part of a
serious illness such as acut e bowel obst ruct ion. These
pat ient s present wit h abdominal pain, vomit ing and
dist ension and non-passage of flat us are t he t ypical
present at ion. These pat ient s should be referred
immediat ely t o a higher cent er aft er rect al examinat ion,
passage of rect al t ube (for passage of flat us) and a
plain X-ray abdomen.
11. Acut e gast rit is, gast roent erit is
12. Severe UGI bleed et c.
13. Excessive vomit ing can result in elect rolyt e imbal-
ance.
14. Chronic recurrent vomit ing can result in malnut ri-
t ion.
15. Repeat ed nausea and ret ching may result in UGI
bleed oft en mild, consequent t o a mucosal t ear
in oesophageal-cardia j unct ion referred t o as a
Mallory-Weiss t ear.
I nvesti gati ons
● Evaluat ion should exclude CNS causes and an
Upper GI endoscopy t o rule out pat hology in t he
upper GI t ract . Screening up t o I I I part of duo-
denum is possible.
● Barium meal is recommended only when Upper
GI endoscopy is normal.
● Psychogenic vomit ing is diagnosed by exclusion
of organic causes only.
Treatment
Hospit alize t he pat ient t o give int ravenous fluids if
dehydrat ed. St art oral fluids as soon as t he pat ient can
t olerat e. Appropriat e analgesics if pat ient has severe
pain.
Acut e vomi t i ng
Rule out gast ric out let obst ruct ion t hen
I nj Met oclopramide 10 mg I / M, repeat aft er 6
hours if needed
or
Tab. Mozapride 5 mg t hree t imes a day
or
Tab. Domperidone 10 mg t hree t imes a day
or
Tab Met oclopramide 10 mg t hree t imes a day
or
I nj ect ion Prochlorperazine 5 mg I M. Repeat ed af-
t er 4-6 hours if needed
or
Ondanset ron 8 mg st at dose (oral/ parent eral)
and repeat ed 8-hrly if required
I n pregnancy avoid all drugs, if possible
Promet hazine 25 mg oral/ inj ect ion safe in t he first
120
Treatment
I f pain is predominant
Tab. Mebevaerine Hcl 270 mg t hree t imes a day
given for long t erm
or
Tab Drot averine 40 t o 80 mg 3 t imes a day
or
Tab Propant heline Hcl 15 mg 3 t imes a day
I n t hose wit h depressive sympt oms
1. Tab Amit rypt aline 10 mg HS for 4 t o 6 weeks
2. I n t hose wit h diarrhoeal sympt oms
3. Tab Loperamide 2 t o 4 mg daily for several days/
weeks depending on t he clinical response
4. Any I BS pat ient wit h change in present at ion e.g.
change in bowel habit requires re-evaluat ion.
Do’s and Dont ’s
● Diet should cont ain high fibre and supplement ed
wit h bulk forming agent s such as isaphghul husk
● Avoid caffeine and alcohol
● Avoid milk and ot her diet ary const it uent s, which
worsens t he sympt oms
● Psychot herapy may be helpful in select cases
Acute Gastro-enteritis( AGE)
Symptoms
I t is a self-limit ing illness charact erized by diarrhoea,
abdominal cramps, nausea and vomit ing, usually caused
by viruses or bact eria (E coli, V cholerae, St aph aureus,
Bacillus cereus et c). Most of t hese cause non-invasive
or t oxic diarrhoea.
Less commonly pat ient present wit h diarrhoea wit h
passage of mucous and / or blood in st ools. This may
be associat ed wit h significant sympt oms such as fever,
malaise et c. These pat ient s are more likely t o have
invasive diarrhoea caused by bact eria (E coli, Shigella,
salmonella, Campylobact er) or parasit e amoeba.
Treatment
I n acut e gast ro-ent erit is t he aim is t o correct
dehydrat ion and elect rolyt e imbalance. There is no
need t o invest igat e for t he et iology immediat ely. Furt her
invest igat ions are necessary if t here is bloody diarrhoea,
clinical evidence of t oxicit y or prolonged diarrhoea.
Treatment
Medical t reat ment may be given 2 t o 4 t imes a week.
Some pat ient s may require t hese for several weeks t o
mont hs
Lact ulose solut ion 15 t o 20 ml at night
or
Susp. Magnesium sulphat e 15 t o 20 ml at night
or
Bulk forming agent s such as ‘isaphgul husk’ or
‘psyllium seeds’ or
I sot onic polyet hylene glycol (PEG elect rolyt e) so-
lut ion 125 – 250 ml
Do’s and Don’t s
Advise pat ient s t o t ake plent y of fluids, high fiber
diet – green leafy veget ables, fruit s, avoid caf-
feinat ed drinks.
Regular walk and exercise ½ t o 1 hr daily, ab-
dominal exercise.
To use I ndian closet as far as possible (t his will
st raight en t he anorect al angle).
Avoiding suppression of urge t o defecat e, making
a regular habit ).
Avoid purgat ive frequent ly t o t reat const ipat ion,
as it may be habit forming.
Supposit ory or simple enema is preferred in I HD.
Irritable Bowel Syndrome (IBS)
Def i ni tion
A const ellat ion of gast roint est inal sympt oms
associat ed wit h lower bowel sympt oms t hat occur in
absence of an organic disease.
Symptoms
Clinically t he diagnosis is made when cont inuous or
recurrent sympt oms of abdominal pain associat ed wit h
any of t he t hree feat ures viz. Relief by defecat ion and
/ or onset wit h change in st ool frequency or consist ency
for at least 3 mont hs.
Support ive sympt oms of I BS include passage of
mucous, abnormal st ool passage (st raining, urgency,
feeling of incomplet e evacuat ion) and feeling of
abdominal fullness.
Exclude I BS if individual has alarm sympt oms such
as fever, weight loss, bleeding per rect um or anaemia.
121
● Barium meal may be of some help as also an
ult rasound of t he abdomen. A duodenal biopsy
from t he t hird part of duodenum may be in-
format ive.
Treatment
Medi cal t r eat ment
There is a role for long-t erm Tet racycline 250 mg
t hree t imes a day for 6 mont hs wit h Tab Folic Acid 5 mg
a day, when bact erial overgrowt h is suspect ed.
Ant i-cholinergics or nonspecific ant i-diarrheal agent s
are not recommended in t he absence of a proper
diagnosis.
Ot her recommended agent s
1. Tab Norfloxacin 400 mg BD or Tab Ciprofloxacin
500 mg BD or Cap Doxycycline 100 mg OD or I f
t he above ment ioned drugs are cont raindicat ed,
Tab Cot rimoxazole 960 mg BD.
2. Tab. Folic acid 5 mg BD
3. Pro-biot ics t wo t o t hree caps t hree t imes a day
for 2 weeks
The above t reat ment is given for 3-6 mont hs durat ion
depending upon pat ient ’s response. Ot her minor
nut rient supplement s are given if t here is evidence of
specific deficiency.
Ulcerative colitis(UC)
Symptoms
During t he first at t ack t he pat ient oft en present s
wit h bloody diarrhoea, wit h syst emic sympt oms of low
t o moderat e fever, backache, art hralgia.
The first at t ack is a close mimicker of acut e
infect ive diarrhoea. A st ool examinat ion followed by
sigmoidoscopy is mandat ory, especially if t he bloody
diarrhoea persist s for more t han a mont h. I t is import ant
t o exclude amoebic infect ion prior t o inst it ut ion of
st eroids.
Rect um is uniformly involved in t hese pat ient s.
Frequency of st ool can provide informat ion on severit y
of disease: mild (2-4 st ool/ day), moderat e (4-6 st ools/
day) or severe (> 6 st ools/ day).
During remission, pat ient may be asympt omat ic or
may have ext ra-int est inal sympt oms.
Treatment
These pat ient s require a referral t o a t ert iary unit .
Aim is induct ion of remission in acut e st age and t hen
maint enance of remission.
Medi cal t r eat ment
1. I ndicat ed only in very ill pat ient s wit h syst em-
ic sympt oms associat ed wit h bloody diarrhoea,
t raveller’s diarrhoea or in cholera infect ion. Tab
ciprofloxacin 500 mg t wo t imes a day for 3 t o 5
days
2. I n amoebic dysent ery Tab Met ronidazole 400 mg
t hree t imes a day for 5 t o 7 days or Tab Tinida-
zole 600 mg t wice a day for 3 t o 5 days
3. I n acut e Giardial infect ion
Tab Tinidazole 1000 mg single dose or Tab Met-
ronidazole 400 mg t hree t imes a day for 3 days
Hospit alizat ion is needed when t here are clinical
signs of dehydrat ion especially in young children
or in t he elderly, suspect ed cholera, immunosup-
pressed pat ient s and t hose wit h severe syst emic
sympt oms
Do’s and Dont ’s
I n absence of vomit ing pat ient should be asked
t o t ake sips of fluid
Fluids used at home can be j uices, soups and
ORS
Milk and relat ed product s are avoided for at least
2 weeks, because of secondary lact ase deficiency.
Chronic diarrhoea
Def i ni tion
A pat ient is considered t o have chronic diarrhoea if
diarrhoea persist s for more t han a mont h.
Causes
● Common causes of chronic diarrhoea are parasi-
t osis, sprue and t uberculosis.
● A person is considered t o have mal-absorpt ion if
t he st ools are bulky, greasy, frot hy, foul smelling
st ools associat ed wit h lot of flat ulence indicat ing
mal-absorpt ion.
● A large bowel diarrhoea is t ypically small volume,
loose, wat ery st ools mixed wit h mucus and/ or
blood.
I nvesti gati ons
● Aft er a preliminary blood sugar, t hyroid funct ion
t est s and st ool fat globules, pat ient should be re-
ferred t o a t ert iary cent re for furt her evaluat ion.
122
Mai nt enance of r emi ssi on
Lifelong maint enance t herapy is generally
recommended for all pat ient s, especially t hose wit h left
sided or ext ensive disease, and t hose wit h dist al disease
who relapse more t han once a year.
Discont inuat ion of medicat ion may be reasonable for
t hose wit h dist al disease who have been in remission for
2 years and are averse t o such medicat ion. However,
t here is some evidence t hat maint enance t herapy
reduces t he risk of colo-rect al cancer.
For t he maint enance of remission in UC:
● Oral Mesalazine 1–2 g daily or Balsalazide 2.5 g
daily should be considered as first line t herapy.
● Sulpha-salazine 2–4 g daily has a higher inci-
dence of side effect s compared wit h newer 5-ASA
drugs.
● Select ed pat ient s, such as t hose wit h a react ive
art hropat hy, may benefit .
● Topical Mesalazine 1 g daily may be used in pa-
t ient s wit h dist al disease wit h/ wit hout oral Me-
salazine, but pat ient s are less likely t o be compli-
ant .
● Most pat ient s require lifelong t herapy, alt hough
some pat ient s wit h very infrequent relapses (es-
pecially if wit h limit ed ext ent of disease) may re-
main in remission wit hout maint enance t herapy.
● The advant ages and disadvant ages of cont inued
t reat ment wit h amino-salicylat es are best dis-
cussed wit h t he pat ient , especially if a pat ient has
been in remission for a subst ant ial lengt h of t ime
(> 2 years).
● St eroids are ineffect ive at maint aining remission.
● Azat hioprine 1.5–2.5 mg/ kg/ day or mercap-
t opurine 0.75–1.5 mg/ kg/ day are effect ive at
maint aining remission in UC. However, in view
of t oxicit y t hey should be reserved for pat ient s
who frequent ly relapse despit e adequat e doses
of amino-salicylat es, or are int olerant of 5-ASA
t herapy. I t is common pract ice t o cont inue ami-
no-salicylat es wit h azat hioprine, but limit ed evi-
dence t hat t his is necessary.
● Pat ient s wit h gast roint est inal int olerance of aza-
t hioprine may be caut iously t ried on Mercapt opu-
rine before being considered for ot her t herapy or
surgery.
I mpor t ant Not e
Regular surveillance is necessary for UC last ing
Medi cal t her apy
Therapeut ic decisions depend on disease act ivit y
and ext ent . Pat ient s wit h severe disease require hospit al
admission, whereas t hose wit h mild/ moderat e disease
can generally be managed as out pat ient s.
Di sease ext ent can br oadl y be di vi ded i nt o di st al
and mor e ext ensi ve di sease.
Dist al disease (proct it is/ proct o-sigmoidit is):
Topical management is appropriat e.
Ext ensive disease:
Oral or parent eral t herapy is t he mainst ay of
t reat ment .
Choi ce of dr ugs:
Mesalamine preparat ions and St eroid prepara-
t ions
Treat ment of act ive left sided, or ext ensive UC:
● Mesalazine 2–4 g daily or Balsalazide 6.75 g daily
are effect ive first line t herapy for mild t o moder-
at ely act ive disease.
● Sulpha-salazine has a higher incidence of side
effect s compared wit h newer 5-ASA drugs. Se-
lect ed pat ient s, such as t hose wit h a react ive ar-
t hropat hy, may benefit .
● Prednisolone 40 mg daily is appropriat e for pa-
t ient s in whom a prompt response is required, or
t hose wit h mild t o moderat ely act ive disease, in
whom Mesalazine in appropriat e dose has been
unsuccessful.
● Prednisolone should be reduced gradually ac-
cording t o severit y and pat ient response, gener-
ally over 8 weeks. More rapid reduct ion is associ-
at ed wit h early relapse.
● Long-t erm t reat ment wit h st eroids is undesir-
able. Pat ient s wit h chronic act ive st eroid depend-
ent disease should be t reat ed wit h azat hioprine
1.5–2.5 mg/ kg/ day
● Topical agent s (eit her st eroids or Mesalazine)
may be added t o t he above agent s. Alt hough
t hey are unlikely t o be effect ive alone, t hey may
benefit some pat ient s wit h t roublesome rect al
sympt oms.
● Severe UC: close monit oring at a t ert iary cent re.
123
days
2. I f t he pat ient is very t oxic,
I nj . Met ronidazole 500 mg given 8 t h
hourly unt il pat ient improves. Swit ch
over t o oral t herapy whenever possible.
Followed by Diloxanide furoat e (luminal agent for
cyst s) 500 mg t hree t imes a day for 10 days.
3. Chloroquine
Chloroquine 600 mg orally daily 2 days, followed
by 300 mg daily for 2 weeks; dose is calculat ed
as chloroquine base. Drug is act ive against E. his-
t olyt ica t rophozoit es
I ndi cat i ons f or dr ai nage of an abscess:
1. I f pyogenic abscess cannot be excluded
2. No improvement wit h medical t herapy in 72 hours
3. I mpending rupt ure of abscess (severe pain, pleu-
rit ic pain, hiccups)- one very close t o t he surface
of t he liver
4. Large left lobe abscess, t o prevent rupt ure in t o
t he pericardium
Fol l ow-up:
1. Monit or t he pat ient for resolut ion of sympt oms
wit h medical t reat ment and aspirat e if any indi-
cat ion.
2. Abscess cavit y may persist for several weeks
even aft er cure of infect ion. Frequent US scan
is unnecessary unless pat ient develops fever et c.
Scan may be repeat ed aft er 4-6 weeks, aft er t he
pat ient becomes asympt omat ic.
3. Tab. Di-loxanide furoat e 500 mg 3 t imes a day
for 1 week may be given aft er a course of Met-
ronidazole
Do’s and Don’t s
1. Avoid t aking alcohol, specifically if on t reat ment
wit h Met ronidazole
2. Avoid cont aminat ed food and drinking wat er.
Veget ables should be cooked or washed well.
3. Use boiled wat er (kills t he cyst ) or bot t led wat er
from a known source.
4. Maint ain good hygiene during food int ake t o pre-
vent ent eric infect ions
Ref er ences
for more t han 10 years.
Explain t o t he pat ient t he chronic nat ure of t he
disease and cont inuat ion of maint enance t reat-
ment for life wit h regular follow-up. Risk of co-
lonic cancer aft er 10 years of disease onset must
be explained
Do’s and Don’t ’s
Milk is preferably avoided during t he acut e phase of
illness.
Amoebic liver abscess
Causes
Liver abscess is t he commonest ext ra-int est inal form
of amoebiasis, caused by E. hist olyt ica. The disease
usually affect s young males, part icularly chronic
alcoholics, in endemic areas.
Causes
● Clinical manifest at ions are high grade fever, RUQ
pain, which may be dull aching or pleurit ic in na-
t ure.
● Sympt oms are oft en chronic wit h int ermit t ent fe-
ver and const it ut ional sympt oms.
● Jaundice is uncommon. Liver abscess is less com-
mon in t he elderly.
Compl i cat i ons
I nclude rupt ure of abscess int o pleural, pericar-
dial or rarely perit oneal cavit y.
I nvesti gati ons
● The diagnosis is made by an elevat ed t ot al
count ,ESR and serum alkaline phosphat ase,
● One or more hypo-echoic lesions in liver on ult ra-
sonography.
● St ool is post ivie for E hist olyt ica in 30%.
● Ant ibodies t o E. hist olyt ica is high.
● Examinat ion of pus for t he parasit e is usually
negat ive.
Treatment
1. Tab. Met ronidazole 800 mg t hree t imes orally (or
I V, if necessary) daily for 5-10 days
or
Tab. Tinidazole 600 mg 2 t imes a day for 7-10
124
St andar d dosage
● Ceft riaxone 2 g int ravenously every 24 hours, or
cefot axime 2 g int ravenously every 8 hours.
● I nit ial empirical t reat ment should include broad-
spect rum ant ibiot ics.
● Various combinat ions recommended are:
Met ronidazole : 500 mg I / V t hree t imes daily
Ampicillin : 2 g I / V 6 hourly
Gent amicin : 2 mg/ kg load, t hen adj ust for renal
funct ion
Ciprofloxacin : 400 mg I / V 12 hourly for 10 days
or
I nj . Ceft riaxone 1-2 g I V every 24 hours t imes
a day
or
I nj . Cefot axmine 2 g 8-hrly for 10 days Co m -
binat ion of Amoxycillin + Ciprofloxacin + Met roni-
dazole is also a recommended schedule
I n t he elderly or t hose wit h renal impairment : a
Penicillin (such as amoxicillin) plus an inj ect able
Cephalosporin (such as cefot axime or cefuroxi-
me) plus met ronidazole is recommended
I n penicillin –allergic pat ient s: ciprofloxacin plus
clindamycin
● Once t he sensit ivit y is known, ant ibiot ic t herapy
is amended accordingly. Durat ion of t herapy is
usually from 2–4 weeks or longer depending on
number of abscesses and t he clinical response.
Fol l ow-up:
1. Monit or for clinical improvement and modify t he
t herapy based on cult ure sensit ivit y report
2. Abscess should always be drained.
3. Surgery considered if no improvement wit h medi-
cal t reat ment and percut aneous drainage in 4-7
days.
I mpor t ant Not e
1. Avoid t aking alcohol, specifically if on t reat ment
wit h Met ronidazole.
2. Maint ain good hygiene regarding food int ake t o
prevent ent eric infect ions.
1. Sharma MP, Ahuj a V. Management of amebic and
pyogenic liver abscess. I ndian J Gast roent erol
2001; 20: 33-6
2. Amoebiasis and infect ion wit h free living amoe-
ba. I n: Harrison’s Principles of I nt ernal Medicine,
Kasper DL, Braunwald E, Fauci AS et al (eds),
16t h edit ion, 2005, McGraw Hill Company I nc.,
New York, pp 1214-18
3. Seet o RK: Amebic liver abscess: epidemiology,
clinical feat ures, and out come. West J Med 1999,
170: 104-109. I ndicat ions foe aspirat ion of amoe-
bic liver abscess
4. Hughes MA: Amebic liver abscess. I nfect Dis Clin
Nort h Am 2000, 14: 565-582.
Pyogenic liver abscess
Liver abscess const it ut es about 48% of all visceral
abscesses.
Causes
Pyogenic liver abscess is usually caused by spread
of infect ion from perit oneum, abdominal viscera such
as appendicit is/ divert iculit is/ port al pyemia or disease
of biliary t ract . I t is most commonly caused by coliform
organisms.
Symptoms
Fever, abdominal pain, t oxaemia, feat ures of
associat ed problems such as appendicular pain/ mass
et c. Most ly abscesses are small and mult iple.
I nvesti gati ons
Diagnost ic invest igat ions include t ot al count s, US
scan of t he abdomen, blood cult ure, pus cult ure. CECT
and MRI is seldom indicat ed.
Treatment
1. Drainage- percut aneous cat het er or open surgi-
cal- remains t he mainst ay of t reat ment for large
abscess
2. Pat ient should be kept nil by mout h and given I V
fluids if t oxic and sick.
Recommended ant i bi ot i cs
Met ronidazole plus ampicillin and gent amicin,
ciprofloxacin, or a t hird-generat ion cephalosporin
(eg, ceft riaxone or cefot axime).
125
back, crouched post ure.
● I n severe cases, t here is paralyt ic ileus, vomit ing
abdominal dist ent ion, j aundice and fever.
I nvesti gati ons
1. Diagnosis is confirmed by an elevat ed serum
amylase t o more t han 3 t imes t he normal. One
needs t o exclude ot her causes of acut e abdomen
like gut perforat ion or infarct ion. A repeat assay
is done aft er 48 hours.
2. Serum lipase elevat ion is more specific for pan-
creat it is. USG or CT scan furt her helps t o confirm
t he diagnosis
Compl i cat i ons
* Necrosis
* Haemorrhage
* Pseudo-cyst
* Abscess
* Pleural effusion and
* Ot her end organ failure.
Treatment
● I f t he disease is mild and t here are no signs of
hypovolemia: St art int ravenous fluids
* I nfusion Ringer lact at e followed by 4 t o 6
pint s of I / V normal saline, maint aining a good
urine out put
* I nj KCl 60-80 mmol (20 mmol added t o 50 ml
of I V fluid)
● Pat ient is kept nil oral unt il bowel sounds appear
or pat ient cont inues t o vomit .
● Oral feeds are init iat ed at t he earliest , when t he
general condit ion is st able i.e. wit hin 72 hours
● The diet should be low in fat and prot ein.
● Analgesics are recommended for pain relief
* I nj Diclofenac Sodium 75 mg I M 2-3 t imes a
day;
* I f pain is not relieved, I nj Tramadol 50 mg
I / M, repeat ed hourly if needed
● Ant ibiot ics are not t o be given as a rout ine. There
is no role for oct reot ide/ somat ost at in.
● I f gallst ones wit h st ones in common bile duct are
det ect ed on ult rasonogram, emergency ERCP is
warrant ed t o disimpact t he dist al st one.
Pyogenic liver abscess suspected through abdominal imaging
Aerobic and anaerobic blood cultures
Amebic precipitins if any risk factors for amebic liver abscess
are present
Guided drainage of abcess
Submit for Gram’s stain, and aerobic and anaerobic cultures
Work up for predisposing factors
Consider ERCP if bililary disease suspected
Gradual clinical improvement
Remove percutaneous catheter when drain-
age is minimal
Intravenous antibiotics for 2 weeks followed
by oral antibiotics for 4 weeks
Repeat imaging at the end of therapy
Initiate broad spectrum intravenous antibiotics
Drainage and antibiotics
Review microbiologic data to exclude
amoebic abscess
Ensure coverage for group D streptocooci
Repeat CT and drain any large collection
No clinical improvement
Re-evaluate diagnosis
Examine for concomtiant illness (eg. chol-
angitis)
Consider surgical drainage
Approach to Pyogenic Liver Abscess
Ref er ence
● Sharma MP, Ahuj a V. Management of amebic and
pyogenic liver abscess. I ndian J Gast roent erol
2001; 20: 33-6
● I nt ra-abdominal I nfect ions and Abscesses. I n:
Harrison’s Principles of I nt ernal Medicine, Kasper
DL, Braunwald E, Fauci AS et al (eds), 16t h edit ion,
2005, McGraw Hill Company I nc., New York, pp
749-54
Acute Pancreatitis
Causes
Acut e inflammat ion of t he pancreas, usually caused
by alcohol or gall st ones get t ing impact ed at t he
ampulla. Rare causes include
* Trauma
* I nfect ions such as mumps, ascariasis and
* Drugs such as diuret ics and azat hioprine.
Symptoms
● Acut e upper abdominal pain, radiat ing pain t o t he
126
● I nt erval cholecyst ect omy is recommended aft er
resolut ion of acut e pancreat it is.
● I n case t here is det eriorat ion in general condi-
t ion or pat ient has evidence of severe necrot iz-
ing pancreat it isof t he pat ient referral t o a t ert iary
cent re is recommended.
Markers of severe Pancreatitis include
1. WBC count > 15 000 cells/ cu mm
2. Blood urea > 16 mmol/ l
3. Calcium < 2.0 mmol/ l
4. Albumin < 3.2 g/ dl
5. Glucose > 10 mmol/ l
6. pO2 < 8 pKa (60 mm Hg)
7. AST> 200 iu/ l
8. LDH > 600 iu/ l
9. C-react ive prot ein > 150 mg/ l
Management of acut e pancr eat i t i s
All pat ient s wit h (amylase > 4-fold elevat ed)
Analgesia (Pet hidine, not morphine)
Nil by mout h
Plain abdominal and erect chest x-ray (exclude
perforat ion)
Urinary cat het er
Nasogast ric t ube if vomit ing
Assess severity by objective criteria
Mild Severe
Less t han 3/ 9 markers
of severit y
More t han 3/ 9 markers of
severit y
Admit Transfer t o higher cent er
I / V cryst alloids (oft en
sufficient )
Peripheral venous line
Rest art diet aft er 48 t o
72 hours if improving
Urgent ult rasound t o
exclude gallst ones
No gall st ones
Remove cat het er at 24 hours
Consider ot her causes of
acut e pancreat it is
Ref er ence
1. Approach t o t he pat ient wit h Pancreat ic disease.
I n: Harrison’s Principles of I nt ernal Medicine,
Kasper DL, Braunwald E, Fauci AS et al (eds),
16t h edit ion, 2005, McGraw Hill Company I nc.,
New York, pp 1891-1906
2. Acut e and Chronic Pancreat it is. I n: Harrison’s
Principles of I nt ernal Medicine, Kasper DL, Braun-
wald E, Fauci AS et al (eds), 16t h edit ion, 2005,
McGraw Hill Company I nc., New York, pp 1895-
1906
Chronic Pancreatitis
Causes
Usually caused by chronic alcohol consumpt ion or
due t o t ropical calcific pancreat it is.
Symptoms
Typically pat ient s present wit h pancreat ic t ype of
pain, st eat orrhoea and Diabet es mellit us. Diabet es is
oft en non-ket ot ic, t hough blood sugar levels are grossly
elevat ed.
I nvesti gati ons
The diagnosis is confirmed by plain x-ray abdomen
(for calcificat ion in bed of pancreas),st ool examinat ion
for fat globules and a CECT.
Treatment
Medical t reat ment
Treatment Algorithm for chronic Pancreatitis
Pain
AXR
USG
CECT
Management
• Diet
• Analgesics
• ERT- Protease
• Endotherapy
Steatorrhea
Motion fat globules
AXR/USG
CECT
Management
ERT- Lipase
Diabetes
HbA1C levels
• Insulin
• End organ damage
127
Di et
Daily diet of 2000-3000 calories, consist ing of 1.5-2
g/ kg of prot ein, 5-6 g/ kg of carbohydrat es, and 20-25%
of t ot al calories consumed as fat (about 50-75 g) per
day.
Oral supplement at ion of fat soluble vit amins (A, D,
E, and K) and vit amin B-12 is recommended.
Small frequent , low fat meals
Medium chain t riglycerides
Coconut oil based
Micronut rient supplement at ion
Diabet ic diet
Dr ugs
● Pancreat ic enzyme replacement t herapy
● High prot eases cont aining preparat ion
● Adequat e dose t o be t aken along wit h a meal
● For non-ent eric coat ed preparat ion combine wit h
pre-meal H2RA/ PPI t herapy
● Treat ment cont inued unt il 8 weeks
● I f no response: refer t o higher cent re for endo-
t herapy
● Ot hers
* Analgesics: Tramadol
* For St eat orrhoea:
* Medium chain t riglycerides
* Coconut oil based
* Enzyme preparat ion 25,000 unit s t o 30,000
unit s of lipase
* Wit h every main meal
* 10,000 unit s wit h every fat t y snack
* Ant ioxidant s
Enzyme Preparat ions...local brand
Brand Form Lipase Prot
ease
Amylase
Panlipase Micropearls
2mm
10000 37500 33200
Creon Minimicro
spheres
10000 37500 33200
Digemax EC t ab 20000 1500 15000
Fest al Ec t ab 8000 18000 18000
Pankreoflat Ec t ab 6500
Enzar
Fort e
Ec t ab 4000 15000 15000
Ref er ence
Acut e and Chronic Pancreat it is. I n: Harrison’s
Principles of I nt ernal Medicine, Kasper DL, Braunwald
E, Fauci AS et al (eds), 16t h edit ion, 2005, McGraw Hill
Company I nc.,
New York, pp 1895-1906
Gastrointestinal (GI) bleeding
Def i ni tion
Gast roint est inal (GI ) bleed may present as a frank or
an occult bleeding.
Upper GI bleed is defined as bleeding from any
sit e from pharynx t o duodeno-j ej unal (DJ) flexure and
usually present s as haemat emesis or melaena (at least
50 mL of blood in st ool).
A malenic st ool is black, t arry, st icky and foul
smelling. I t is necessary t o exclude int ake of iron,
charcoal cont aining t ablet s or bismut h salt s.
Lower GI bleed is defined as bleeding occurring
beyond t he ligament of Triet z is referred t o as a lower
GI bleed.
Symptoms
Any individual present ing wit h haemat emesis or
melena
● Assess degree of bleed
* A pat ient walking int o t he casualt y wit h no
hist ory of giddiness is likely t o have 500 mL
of blood loss
* Those wit h giddiness, post ural hypot ension
are likely t o have had approximat ely 1000 t o
1500 mL of blood loss
* Those coming in a st at e of shock are likely t o
have lost more t han 1500 mL of blood.
Treatment
Resuscit at ion is t he key t o management of any GI
bleed especially if moderat e t o massive. An UGI scopy
will not be helpful t o deal wit h an act ive massive bleed.
First assess t he clinical st at us of t he individual:
● Assess pulse, blood pressure, post ural change in
blood pressure
● Pass a ryles t ube t o exclude ongoing bleed
128
Acute upper gastrointestinal haemorrhage
Resuscitation
Endoscopy
Varices Peptic ulcer (vascular
malformation
Mallory- weiss tear)
Sclerotherapy or
banding plus
intravenous
terlipressin
Bleeding
controlled
Bleeding
continues
or recurs
TIPSS or
surgical referral
Reassess
endoscopically
at 24 hours
Consider
angiography,
colonoscopy,
operative
enteroscopy
Conservative
management
and
early discharge
Bleeding continues
or recurs
Surgery
Minor
bleed
Major
bleed
No obvious cause
No major
SRH
Major SRH
Endoscopic injection,
heat appliction
or combination
Bleeding controlled
1. Banding Programme
2. Assess and manage
underlying liver disease
3. Consider propanolol
I nvesti gati ons
● Collect blood samples for Hb, TC, plat elet s, co-
agulat ion profile, renal and liver funct ion t est s,
blood grouping and cross mat ching; Repeat Hb
aft er 6 hrs
● St art normal saline. I / V Ringer lact at e, and ar-
range for blood t ransfusion if post ural hypot en-
sion is present .
● Replace blood as soon as possible if moderat e or
severe bleed or act ive bleed.
● I nt ravenous Pant oprazole 40 mg as a st at dose.
(I f t here is a hist ory of NSAI Ds or pat ient is a
known case of pept ic ulcer disease, immediat ely
give)
I mpor t ant Not e
Do not at t empt t o give a st omach wash. t his can
displace a blood clot overlying an ulcer.
● I n case t he pat ient is a known case of chron-
ic liver disease wit h port al hypert ension,
I nj Oct reot ide 50 mcg I V immedi-
at ely followed by 25 mcg/ hr infusion.
o r
Somat ost at in infusion: 250 micro gm st at fol-
lowed by hrly dose inj ect ion for at least 5 days
I nsert ion of Sengst aken Blakemore t ube can be
life saving. Pat ient can be t ransferred t o a higher
cent re wit h t he t ube in sit u.
Ref er ence:
Gast roint est inal bleeding. I n: Harrison’s Principles of
129
I nt ernal Medicine, Kasper DL, Braunwald E, Fauci AS et
al (eds), 16t h edit ion, 2005, McGraw Hill Company I nc.,
New York, pp 235-8
131
Neurology
Chapter 7
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
● Headache
● Dement ia
● Epilepsy
● Facial Nerve
● Parkinson’s Disease
● GBS
● St roke
* Hemiplegia
* Paraplegia
* Quadriplegia
● Acut e Bact erial Meningit is
● TBM
● Herpes Simplex Encephalit is
● Japanese Encephalit is
● Neurocyst icercosis
● Vert igo
* Peripheral Vest ibulopat hy
* Ot it ic Herpes Zost er
* Meniere’s disease
* Vest ibular Neuronit is
133
Head ache
I nt r oduct i on
Many causes of headache have been described in
medical lit erat ure over t he years. For pract ical clinical
purposes, however, all headaches can be classified as one
of t he primary headache syndromes or as a headache
t hat is caused by or secondary t o an underlying disease
process or condit ion. Because primary headaches
are t he most common, t his discussion focuses on t he
diagnosis and management of t hose syndromes.
Def i ni tion
The primary headache syndromes are migraine,
t ension-t ype, and clust er. Migraine and clust er
headaches are episodic and recurring condit ions.
● Tension-t ype headache is usually episodic but
may be chronic, occurring daily or almost daily
for more t han 15 days a mont h.
● None of t hese headaches are associat ed wit h de-
monst rable organic disease or st ruct ural neuro-
logic abnormalit y.
● Laborat ory and imaging t est result s are gener-
ally normal; however, if an abnormalit y is found,
it most likely is not t he cause of t he headache.
Similarly, physical and neurologic examinat ion re-
sult s also are usually normal, but abnormalit ies
found are not relat ed t o t he headache.
● During t he headache, however, clust er and mi-
graine pat ient s may have some abnormal clini-
cal findings, and many pat ient s wit h t ension-t ype
headache will have demonst rable t ight ness in t he
cervical muscles, wit h limit at ion of neck mot ion
and/ or scalp t enderness.
● Secondary headaches are usually of recent onset
and associat ed wit h abnormalit ies found on clini-
cal examinat ion. Laborat ory t est ing and/ or imag-
ing st udies will confirm t he diagnosis.
● Recognizing headaches relat ed t o a condit ion or
disease is crit ical not only because t reat ment of
t he underlying problem will usually eliminat e t he
headache but also because t he condit ion causing
t he headache may be life-t hreat ening.
Pr eval ence
● Primary headaches account for more t han 90%
of all headache complaint s and, of t hese, episod-
ic t ension-t ype headache is t he most common.
Almost everyone has had an occasional headache
of t his t ype. Alt hough chronic t ension-t ype head-
ache occurs in only slight ly more t han 2% of t he
populat ion, it account s for a large number of vis-
it s t o t he physician’s office and missed work days.
● Several epidemiologic st udies conduct ed in vari-
ous areas of t he world indicat e t hat t he preva-
lence of migraine headache ranges from 12% t o
18% of t he populat ion. Migraine is t hree t imes
more common in females. The prevalence of
clust er headache is not known. This uncommon
condit ion probably affect s less t han 0.5% of t he
populat ion but is underdiagnosed and is oft en
believed t o be a sinus problem.
● Clust er headache affect s men eight t o t en t imes
more frequent ly t han women. Because t he t hree
primary headache syndromes t end t o begin in
persons younger t han 50 years, anyone older
t han 50 wit h a recent onset of headaches should
have a t horough examinat ion and t est ing t o look
for an underlying cause.
Symptoms
Mi gr ai ne
● Most migraine pat ient s do not have an aura; mi-
graine wit h aura occurs in only 15% t o 20% of
sufferers.
* The aura is a well defined visual or neurologi-
cal deficit last ing less t han 1 hour and is fol-
lowed by t he headache wit hin an hour.
* Most auras are visual, wit h phot opsia (flash-
ing light s) being most common.
* The aura is init ially small, t hen enlarges or
moves across t he visual field.
* A t ypical migraine aura may occur wit hout a
headache. This phenomenon t ends t o begin
lat er in life.
* Occasionally, a neurologic aura will occur, wit h
a t ingling or weakness t hat slowly spreads up
or down an ext remit y.
● Many pat ient s wit h migraine will have prodromal
sympt oms for many hours or even a day or so
before t he onset of an at t ack. These prodromal
sympt oms are generally changes in mood or per-
sonalit y. Fat igue also is common, and occasion-
ally hyperact ivit y occurs.
● The migraine at t ack last s 6 t o 72 hours. This
pounding, t hrobbing pain of moderat e t o severe
134
int ensit y is generally unilat eral, but some pat ient s
will experience bilat eral pain. Pain caused by mi-
graine worsens wit h physical act ivit y.
● Phot ophobia and phonophobia are very common,
wit h sensit ivit y t o odors being a lit t le less com-
mon. Migraine is a sick headache.
● Nausea occurs in most pat ient s, and vomit ing is
very common.
● Dehydrat ion may occur, which will increase t he
pain and disabilit y of t he condit ion. Migraineurs’
want t o be quiet , inact ive, and in a darkened area
during t he at t ack.
● Approximat ely 60% of women experience t heir
worst migraine at t acks in conj unct ion wit h t heir
menst rual period.
Tensi on-t ype headache
● Tension-t ype headache is charact erized by gen-
eralized pressure or a sensat ion of t ight ness in
t he head.
* The discomfort level is usually mild t o moder-
at e and does not worsen wit h act ivit y.
* Alt hough nausea and phot ophobia or pho-
nophobia may occur, t hey generally are not
prominent feat ures.
* Tension-t ype headache can be episodic (less
t han 15 days a mont h) or chronic (more t han
15 days a mont h).
* Poor post ure is oft en evident , which may play
a role in causing t ension-type headache.
Cl ust er headache
● Clust er headache causes int ense pain t hat is gen-
erally st eady and boring behind one eye.
* The pain may spread t o t he t emple, face, and
even back int o t he upper neck.
* I t is so int ense t hat most sufferers will pace
t he floor or do vigorous exercises during t he
at t ack.
* The at t acks are short (usually less t han 3
hours in durat ion) and oft en last only 30 t o
45 minut es.
* They occur from one t o several t imes a day
for a period of several weeks or mont hs, t hen
remit , leaving t he pat ient pain free for several
mont hs or years, only t o recur.
* During a clust er headache cycle, t he at t acks
of pain oft en occur at t he same t ime each day,
most oft en waking t he pat ient in t he early
morning hours.
* Eight y percent of clust er sufferers experience
unilat eral t earing, wit h conj unct ival inj ect ion
and ipsilat eral nasal congest ion.
* About 20% of clust er pat ient s have a part ial
Horner’s syndrome wit h pt osis and meiosis of
t he affect ed eye. These sympt oms clear as
t he at t ack leaves.
* Alcohol will bring on an at t ack wit hin a few
minut es in a pat ient .
I nvesti gati ons
● Hist ory
● Clinical examinat ion
● Laborat ory St udies t o exclude met abolic or endo-
crine fact ors
● A high eryt hrocyt e sediment at ion rat e in a pat ient
older t han 50 years wit h new headache onset
suggest s t emporal art erit is. This diagnosis must
be confirmed by t emporal art ery biopsy.
● CT Scans can be performed t o exclude int rac-
ranial causes of headache or t o rule out lesions
t hat cause neurologic or visual abnormalit ies as-
sociat ed wit h headache. Comput erized t omogra-
phy scanning of t he paranasal sinuses is useful
in evaluat ing t he role of acut e or chronic sinus
infect ion in t he et iology of t he headache.
● Magnet ic resonance imaging is current ly t he best
scan for viewing t he post erior fossa and occipit al
areas of t he brain.
Treatment
Mi gr ai ne Management
● Some migraine headaches can be relieved wit h
* The use of cold packs
* Pressure on t he t emple, and sleep
* However, most require prevent ive or abort ive
medicat ion.
● Educat ing t he migraine pat ient t o recognize and
avoid headache t riggers helps t o reduce t he fre-
quency of at t acks.
● Common migraine t riggers include
* Weat her changes
135
* The est rogen cycle
* Bright light s
* St rong odours
* St ress
* Food and food addit ives, and t he skipping of
meals
● Migraineurs do bet t er and have fewer headaches
by following regular eat ing and sleeping pat t erns.
Mi gr ai ne Pr event i ve Medi cat i on
● Drugs used for migraine prophylaxis
● Bet a-blockers
● Calcium channel blockers
● Nonst eroidal ant i-inflammat ory drugs (NSAI Ds)
● Ant i-depressant s
● Ant i-epilept ic drugs
Ot her s
Large doses of riboflavin or magnesium oxide
and t he serot onin agonist Met hysergide
Mi gr ai ne abor t i ve medi cat i on
● All migraine pat ient s suffering an acut e at t ack
need t o t ake an abort ive drug, whet her or not
t hey are t aking a prophylact ic agent .
● For mild at t acks, over-t he-count er analgesics (es-
pecially t hose cont aining caffeine) may be useful.
● Effect ive agent s available by prescript ion include
a
* Combinat ion of isomet hept ene mucat e
* Dichloralphenazone
* Acet aminophen
* Ergot amine t art rat e combined wit h caffeine
* Dihydroergot amine mesylat e and t he t ript ans.
● Large doses of rapid-act ing NSAI Ds, such as
meclofenamat e, ibuprofen, or naproxen sodium,
can also prove helpful in mild at t acks.
● Ergot amine t art rat e combined wit h caffine (oral,
supposit ory) is quit e effect ive but oft en causes
nausea. Dihydroergot amine (DHE 45) is a very
effect ive abort ive agent when used parent erally.
I t is also available as a nasal spray.
● I nt ravenous DHE, Prochlorperazine, Divalproex
sodium, magnesium and Ket orolac can be very
effect ive in st opping a migraine at t ack
Tensi on-t ype headache management
● The occasional t ension-t ype headache can be
alleviat ed by a hot shower, massage, sleep and
t hrough pat ient recognit ion and avoidance of
st ress fact ors.
● Episodic t ension-t ype headache is usually well
t reat ed wit h analgesics such as aspirin, acet ami-
nophen, and NSAI DS or combinat ions of t hese
agent s wit h caffeine or sedat ives.
● Some pat ient s, part icularly t hose wit h t ension-
t ype headache caused by st ress, may benefit
from relaxat ion t echniques or biofeedback t rain-
ing. Physical t herapy may decrease chronic neck
pain caused by increased cervical muscle spasm
or post ural abnormalit ies.
● The most effect ive group of drugs for t reat ment
of chronic t ension-t ype headaches is t he t ricyclic
ant idepressant s. Amit ript yline HCl, doxepin HCl
and nort ript yline HCl are t he most commonly
used.
● Muscle relaxant s such as cyclobenzaprine HCl, or-
phenadrine cit rat e, and baclofen may be helpful
at t imes, part icularly if increased muscle spasm
is present .
● I n recent clinical t rials, t he cent ral-act ing muscle
relaxant t izanidine HCl was found t o be effect ive
in t reat ing chronic headaches, eit her t ension-
t ype or coexist ing migraine and t ension-type.
Cl ust er headache t r eat ment
● Because t he onset of clust er headache at t acks
is rapid and may occur several t imes a day, t he
best approach t o t reat ment is wit h daily preven-
t ive drugs.
● Effect ive prophylact ic medicat ions include vera-
pamil HCl, prednisone, lit hium carbonat e, met hy-
sergide, and t he ant iepilept ic drugs divalproex
and t opiramat e. High doses of verapamil (480 mg
t o 720 mg / day) may be necessary.
● Prednisone and met hysergide work quickly and
oft en will be used wit h verapamil or lit hium at on-
set , for a quick response and t hen t apered while
verapamil or lit hium is cont inued. Prednisone is
usually prescribed at 60 mg / day init ially and
t hen t apered over 2 t o 3 weeks.
● The use of 100% oxygen by mask at a flow rat e
of 8 t o 10 L/ min for up t o 10 minut es will abort
136
an acut e clust er headache in 50% t o 60% of pa-
t ient s.
● Ergot amine t art rat e, DHE and any of t he t ript ans
usually are very effect ive, but are inappropriat e in
pat ient s who suffer several at t acks a day.
● Fort unat ely, clust er headache pat ient s do not
appear t o develop rebound headaches from fre-
quent use of ergot amine t art rat e or t he t ript ans,
as do migraine sufferers.
Dementia
Dement ia denot es a det eriorat ion of int ellect ual
or ment al abilit y wit h lit t le or no dist urbance of
consciousness and is usually associat ed wit h behavioural
and personalit y changes.
I t is generally considered as a disease of t he elderly,
(senile dement ia > 65 year age) t hough cases occur
in t he slight ly younger age group (pre-senile dement ia
age < 65 years).
Def i ni tion
Dement ia is defined as a decline in memory and
at least one ot her cognit ive funct ion such as aphasia,
apraxia, agnosia or decline in an execut ive funct ion such
as planning, organizing, sequencing or abst ract ion.
● This decline impairs social or occupat ional func-
t ioning in comparison t o previous funct ioning.
● The deficit should not be at t ribut ed t o delirium or
psychiat ric illness.
[ According t o t he Diagnost ic and st at ist ical manual
of ment al disorders–I V (DSM–I V) crit eria]
I nci dence
● 1.03% of t he whole populat ion
● > 4% of persons more t han 65 years, 20% in
persons > 85 years.
● > 50 – 60% of pat ient s wit h dement ia are due t o
Alzheimer’s disease.
Causes
Degener at i ve
● Alzheimer’s disease
● Lewy body disease
● Parkinson’s disease
● Front o-t emporal dement ia
● Progressive supra-nuclear palsy
● Mult isyst em at rophy
● Hunt ingt on’s disease
Vascul ar
● Mult iple infarct s
● Binswanger’s disease
● Normal pressure hydrocephalus (NPH)
● Subarachnoid hemorrhage
● Vasculit is
MRI of Hydrocephalus due to Aqueduct stenosis
Dilated Lateral Ventricles Sagittal image
137
● Single infarct s at st rat egic locat ions
I nf ect i ons
● Fungal meningit is
● AI DS dement ia
● Syphilis
● Cruet zfeldt – Jacob disease
Toxi c or met abol i c
● Vit amin B
12
deficiency
● Thyroid deficiency
● End organ damage (Liver, Kidney et c.)
● Alcohol Abuse
Tr aumat i c
● Subdural hemat oma
● Anoxic brain inj ury
● Closed head inj ury
Tumor
● Glioblast oma
● Lymphoma
● Met ast at ic t umour
Ot her s:
● Sympt omat ic hydrocephalus
Not e
Each of t he diseases in degenerat ive dement ias
has specific crit erias t o diagnose.Memory problems are
common among t he elderly but do not always herald
t he onset of dement ia. I solat ed memory impairment
(or) mild cognit ive impairment (MCI ) progresses t o
dement ia at a rat e of about 10% per year. But people
wit h MCI have normal act ivit ies of daily living and
normal general cognit ive funct ioning.
Symptoms
Hi st or y
I t is essent ial t o t ake hist ory not only from t he pat ient
but also from an independent informant . Enquiries
about t he memory and t he difficult ies, t he pat ient has in
carrying out his Act ivit ies of Daily Living (ADL) at home
and work place are made. Act ivit ies relat ed t o shopping,
hobbies, handling money, food preparat ion, dressing
et c are enquired about .
Et iology direct ed quest ions such as risk fact ors
for vascular disease, t oxin exposure, head inj ury,
medicat ion, syst emic illness, and alcohol exposure are
asked.
Exami nat i on
● Because dement ia must be prompt ly dist in-
guished from delirium, at t ent ion is assessed first .
I f t he pat ient is overt ly dist ract ible or ot herwise
unable t o maint ain at t ent ion, t he diagnosis is
likely t o be delirium, alt hough dement ia impairs
at t ent ion especially in t he lat er st ages.
● The abilit y t o regist er informat ion is evaluat ed by
present ing t he names of t hree obj ect s t o pat ient s,
who are asked t o repeat t he names immediat ely.
I f pat ient s cannot do so, t he problem is usually
at t ent ion not memory.
● I f pat ient s can regist er informat ion, short t erm
memory is t est ed aft er 5 minut es. Asking t he
pat ient t o name obj ect s wit h cat egories (e.g.
Alzheimer’s Disease
( section of Neo cortex shows amyloid deposits in
plaques in brain substance (arrow A) and in blood
Vessel wall ( arrow B)
138
animals, art icles of clot hing, furnit ure) is anot her
useful t est .
● Funct ional act ivit ies quest ionnaire is used t o eval-
uat e whet her cognit ive impairment affect s a pa-
t ient ’s abilit y t o perform inst rument al and ot her
complex act ivit ies of daily living.
Several versions of bedside ment al st at us t est ing are
available. Folst eins Mini-Ment al st at us examinat ion is
t he most widely used.
Mini - Mental status examination
5 For
Orient at ion t o t ime (year, season, mont h,
dat e and day)
5 For
Orient at ion t o place (st at e, count ry, t own,
hospit al and floor)
5 For
At t ent ion (eit her serial subt ract ion in 7s
wit h one point for each of t he first five
subt ract ions)
3 For
Regist rat ion of t hree it ems (e.g. Tree, Ball,
Gold)
3 For Recall of t hree it ems aft er 5 minut es
2 For Naming a pencil and a wat ch
1 For Repeat ing “ no it s, and or but s”
3 For Following a t hree – st aged command
1 For
Following a print ed command “ close your
eyes”
1 For Writ ing a sent ence
1 For
Copying a diagram of t wo int ersect ing
pent agons
The MMSE consist s of 30 point s, t he low – normal
cut off is est imat ed t o be 19 for uneducat ed people,
23 for element ary graduat es, 27 for high school
graduat es, 29 for college graduat es. Age fact or also
should be considered.
A full neurologic examinat ion has t o be done wit h
special at t ent ion t o visual fields, paresis, at axia, sensory
dist urbance, ext rapyramidal dist urbance et c.,
I nvesti gati ons
Recommended f or al l pat i ent s:
Complet e blood cell count , chemist ry panel such as
sugar, urea, creat inine, elect rolyt es, liver funct ion t est s,
t hyroid funct ion t est s, chest x-ray, vit amin B
12
level,
syphilis serological t est ing, comput ed t omography or
magnet ic resonance imaging and neuropsychological
evaluat ion.
Recommended f or sel ect ed pat i ent s:
Lumbar punct ure, Elect roencephalography, heavy
met al screening, HI V t est , SPECT, drug screening, et c.,
Treatment
● The primary import ance of t he physician is t o
ident ify any t reat able causes (reversible demen-
t ia) for t he sympt om. For example vit amin sup-
plement s for t he B
12
deficiency st at es, abst inence
of alcohol and vit amin supplement s for alcohol-
induced dement ia, t reat ment of depression, sur-
gical t reat ment for NPH, t umours, ART for AI DS
dement ia and t reat ment of infect ions such as
syphilis. Aft er about 6-12 weeks of t reat ment ,
reevaluat ion has t o be done and improvement
should be document ed.
● Once it is est ablished t hat t he pat ient has any un-
t reat able dement ing brain disease and t he diag-
nosis is sufficient ly cert ain, a responsible member
of t he family should be informed of t he medical
fact s and prognosis and assist ed in t he init iat ion
of social and support ive services.
● The value of newer, cent rally act ing cholinergic
agent s and glut amat e ant agonist s in t he t reat-
ment of Alzheimer disease is clear, but mod-
Pick’s disease showing atrophied brain areas “Pick bodies” seen as cytoplasmic inclusions
139
est and should be weighed against t he need,
side effect s and economical back ground. The
cholinest erase inhibit ors Donepezil, Rivast igmine
and Galant amine are somewhat effect ive in de-
laying t he progression of AD and dement ia wit h
lewy bodies and also in ot her forms. Memant ine,
an NMDA ant agonist , may help delay progression
of moderat e t o severe dement ia and can be used
wit h ot her drugs.
● Treat ment of dement ia does not st op wit h phar-
macot herapy alone. Environment measures such
as not exposing t he pat ient t o newer places,
keeping dangerous t hings such as guns, sickles,
power t ools and sharp obj ect s away from reach,
closing t he wells and t anks, prevent ing him from
driving et c has t o be adopt ed. Pat ient s are t o be
encouraged t o have regular meals, exercise and
clean habit s.
● Care giver st ress is common. Healt h care profes-
sionals must provide support for family members
in medical and non-medical issues including fi-
nancial planning.
● As dement ia worsens, highly aggressive int erven-
t ions and hospit al care provide less benefit and
may not be wort h t heir cost s, discomfort s and
risks. Palliat ive care should be rout inely offered.
Decision about art ificial feeding and t reat ment of
acut e disorders are best discussed before such a
sit uat ion occurs and t hen discussed again when
t he sit uat ion arises. I n severe dement ia, maxim-
ising comfort may be more appropriat e t han at-
t empt s t o prolong life.
Ref er ences
● Principles of Neurology - Adams and Vict ors
● Neurology in Clinical Pract ice - Bradley
● Neurological Different ial Diagnosis - John Pat t en
Epilepsy
I CD Code number : G 40.9
Def i ni tion
Sei zur e
Defined as uncont rolled elect rical act ivit y in t he
brain, which may produce a physical convulsion, minor
physical signs, t hought dist urbances or a combinat ion
of sympt oms.
I t manifest s as sudden and t ransit ory abnormal
phenomenon which can be in t he form of alt ered
consciousness, mot or, sensory, aut onomic and psychic.
Epi l epsy
I t is a disease charact erized by t he t endency t o
develop recurrent seizures due t o abnormal / refract ory
underlying st at e
Epi demi ol ogy
● Around 50 million people in t he world have epi-
lepsy.
● I t is t he commonest and most serious neurologi-
cal condit ion.
● Annual incidence is around 50 – 70 per 100,000
populat ion.
● I t is more in t he developing count ries due t o
primit ive obst et ric services, CNS infect ions and
head t rauma.
● I ncidence varies according t o age. I t is more in
t he early childhood and older age above 65 yrs.
● Point prevalence is 1 % of t he general popula-
t ion.
Cl i ni cal aspect s
Classifcation of Seizures
[ I LAE: I nt er nat i onal l eague agai nst epi l epsy]
● Part ial Seizure:
* Simple Part ial (wit h no LOC)
* Complex Part ial (wit h impaired conscious-
ness)
* Part ial leading t o Secondary generalizat ion.
● Generalized seizure:
* Absence – Typical, At ypical seizures
* Tonic seizures
* Clonic seizures
* Tonic – Clonic seizures
* Myoclonic seizures
* At onic seizures
* Unclassified seizures
Sympt oms
Si mpl e par t i al sei zur e
Depend on t he sit e of origin of elect rical discharges.
140
Consciousness is normal.
Mot or  Tonic, clonic movement s of opposit e
arm, leg and face.
Sensory  Parest hesia, olfact ory, visual and au-
dit ory hallucinat ions.
Aut onomic  Sweat ing and fear.
Psychic  Euphoria, panic, de j avu, j amais vu.
Compl ex Par t i al Sei zur e
Also called as t emporal lobe epilepsy.
I t st art s wit h aura or warning followed by vacant
st are, unresponsiveness, “ t onic and clonic” j erks
followed by aut omat ism in t he form of repet it ive semi-
purposive behavior such as facial grimacing, gest uring,
lip smacking, chewing, snapping t he fingers, repet it ive
words, walking, running and undressing. I t last s for 3
–5 minut es wit h t he post - ict al st at e of few minut es t o
hours.
Gener al i zed sei zur e
I t is due t o widespread involvement of bilat eral
cort ical regions.
Toni c–Cl oni c sei zur e ( GTCS)
Pat ient develops an ict al cry followed by t onic
post uring of all four limbs and t hen clonic j erks of bot h
upper and lower limbs, upward gaze, t ongue bit e and
urinary incont inence followed by post ict al confusion.
Absence Sei zur e
Sudden onset of vacant st are, unawareness, eye
blinking and lip smacking last ing for 5 – 10 seconds
occurring in clust ers.
Myocl oni c Sei zur e
Sudden, brief muscle cont ract ion occurs singly or in
groups.
At oni c Sei zur e ( Dr op At t acks)
Sudden loss of muscle t one leading t o fall and
inj uries t o face.
Febr i l e Sei zur e
● I t occurs in t he age group bet ween 6 mont h t o
6 years.
● Sudden cessat ion of act ivit y wit h uprolling of
eyes, part ial or generalized t onic clonic seizures
(GTCS).
● I t develops on t he first day of fever wit h no evi-
dence of CNS infect ion.
● Clinically confirmed by Cerebrospinal fluid analy-
sis when required
Di f f er ent i al Di agnosi s
● Syncope
● Migraine
● Transient ischemic at t ack
● Transient global amnesia
● Psychogenic Seizure (Pseudo-seizure)
● Non-Epilept ic at t ack disorder.
I nvesti gati ons
Diagnosis remains essent ially clinical. But few
invest igat ions may be useful.
El ect r o encephal ogr aphy ( EEG)
I t is helpful in t he classificat ion of seizure and
epilepsy, t o diagnose non-convulsive st at us epilept icus
and pseudo seizures. Video EEG is ideal as it links EEG
act ivit y and clinical manifest at ion.
CT Br ai n
Useful for ident ifying calcificat ion and t umors.
MRI Br ai n
● The invest igat ion of choice in epilepsy and is su-
perior t o CT
● I t is very helpful t o diagnose
* Malformat ions of cort ical development
* Hippocampal sclerosis
* Art erio-venous malformat ions
* Low grade glioma
Ot her s
● Complet e hemogram
● Renal Funct ion Test s
● Sereum elect rolyt es, are needed rout inely t o rule
out met abolic causes
● Cerebrospinal fluid analysis may be occasionally
done if CNS infect ion is suspect ed
Treatment
Medical, Surgical.
Medi cal
141
* Ant i epilept ic drugs (AED) play an import ant
role in t he management of epilepsy.
When t o st ar t Ant i epi l ept i c dr ugs?
● Aft er second GTCS or aft er first part ial seizure.
● Aft er first GTCS when associat ed wit h increased
chance of recurrence like presence of CNS lesion,
birt h t rauma, abnormal EEG and posit ive family
hist ory.

Choice of AED: First Line AED Second Line AED
Part ial Seizure CBZ, PHT, SVP, PHB LTG, TPM.
Absence Seizure SVP, LTG ESM, CZP
Myoclonic Seizure SVP CZP, TPM, Zonisamide,
Valproat e, Lamot rigine
GTCS SVP, CBZ, PHT, PHB LTG, TPM.
At onic Seizure SVP LTG.
Unclassifiable SVP LTG
Febrile Seizure – I nt ermit t ent Clobazam or diazepam.
CBZ, Phenyt oin are cont raindicat ed in Absence, Myoclonic and At onic Seizure.
[ CBZ- Carbamazepine, SVP-Sodium Valproat e, PHT-Phenyt oin, PHB-Phenobarbit one, LTG-Lamot rigine, TPM-Topiramat e, CZP-Clonazepam,
ESM-Et hosuximide]
Anti-epileptic drugs
Dosage Schedule: St art ing dose Maint enance dose Frequency
Sodium Valproat e Children: 10 mg/ kg/ day 20 –40 mg/ kg/ day bd –t ds
Adult s: 400 mg/ day 400 – 3000 mg/ day bd –t ds
Carbamazapine Children: 5 mg/ kg/ day 10 – 25 mg/ kg/ day bd –t ds.
Adult s: 200 mg/ day 400 – 2000 mg/ day bd –t ds
Phenyt oin Children: 5 mg/ kg/ day 5 – 8 mg/ kg/ day od –bd.
Adult s: 200 mg/ day 200 – 700 mg/ day od –bd
Phenobarbit one Children: 5 mg/ kg/ day 5 – 8 mg/ kg/ day od –bd
Adult s: 60 mg/ day 60 –240 mg/ day od –bd
Clonazepam Children: 0.025 mg/ kg/ day 0.025 – 0.1mg/ kg bd –t ds
Adult s: 1 mg/ day 2 –8 mg/ day od –bd
Clobazam Children: 0.25 mg/ kg/ day 0.5 – 1.0 mg/ kg/ d od - bd
Adult s: 10 mg/ day 10 -40 mg/ day od –bd
Lamot rigine Children: 0.5 mg/ kg/ day 2 –8 mg/ kg/ d od - bd.
Adult s: 12.5 - 25 mg/ day 100 -800 mg/ day od –bd
Topiramat e Children: 0.5 –1 mg/ kg/ day 5 – 9 mg/ kg/ d bd.
Adult s: 25 – 50 mg/ day 100 -500 mg/ day bd
142
Whi ch Ant i epi l ept i c dr ug?
Principles of AED Therapy:
● I t depends on t he t ype of seizure, age of t he pa-
t ient and comorbid illness.
● Monot herapy is always ideal. Polypharmacy is
needed in occasional cases
● St art at a low dose, slowly t it rat e over few weeks
t o est ablish effect ive and t olerable regimen
Strategies for treatment of newly diagnosed
epilepsy
Newly diagnosed epilepsy

First AED ⇒ Seizure free (47 %)

Second AED ⇒ Seizure free (13 %)
↓ 40 %
Refract ory

Add on AED or Surgery.
Dur at i on of AED
● I t should be given for at least a 2 –3 years seizure
free period, t hen slowly t apered and st opped
over t he next 6 mont hs.
● Monit or for drug side effect s and drug-wit hdrawl
seizure.
Sur ger y
I ndi cat i ons:
● Refract ory Epilepsy
● Polypharmacy and int olerable side effect s
Types:
● Ant erior t emporal lobect omy
● Amygdalat omy
● Lesionect omy
● Rarely Corpus callosot omy and
● Sub-pial mult iple resect ion
Pr ognosi s
Maj orit y of t he epilept ic pat ient s have a good
prognosis. 60 – 70 % become seizure free wit h AED.
Around 30 – 40 % cont inues t o have seizure wit h
varying frequency and severit y. Aft er drug wit hdrawal,
10 % can develop a relapse.
I ndi cat or s of poor pr ognosi s
● Sympt omat ic seizure
● High frequency of seizures
● Family hist ory of epilepsy
Mor t al i t y
I t is 2 –3 t imes above t hat of t he general populat ion.
SUDEP (Sudden Unexpect ed Deat h in Epilepsy) is
responsible for 17 % of t ot al deat hs.
When t o admi t ?
For evaluat ion of first seizure, recurrent seizures and
drug modificat ion.
When t o r ef er ?
Persons wit h Refract ory epilepsy on polypharmacy
and wit h int olerable side effect s.
Ref er ences
● Williams H. Trescher and Ronald P. Lesser, 2004,
The Epilepsies, Bradley’s Neurology in Clinical
Pract ice, 4
t h
edit ion, pp 1953 – 1990.
● Mart in J Brodie, St even C, Pat rick Kwan, 2005,
Fast fact s in Epilepsy, 3
rd
edit ion.
● Allan H.Ropper, Robert H.Brown, Epilepsies and
ot her seizure disorders, Adam’s Principles of Neu-
rology, 8
t h
edit ion, pp 273 – 299.
Facial Nerve Paralysis
I CD Code number : G 51.0
Def i ni tion
Facial nerve paralysis can be caused by lower mot or
neuron level or upper mot or neuron level lesions.
Epi demi ol ogy
I t is t he most common disease of t he facial nerve.
I ncidence rat e is around 23 / 100,000 annually. I t affect s
males and females equally occurs in all age groups. I t
is more common in diabet ic and hypert ensive pat ient s.
Causes
Lower mot or neur on pal sy
● Bell’s palsy - I diopat hic
● Viral infect ions
143
* HSV - Herpes simplex virus
* HZV - Herpes zost er virus
* HI V
* I nfect ious mononucleosis
* Polio
● Bact erial
* Tuberculosis of mast oid bone or middle ear
* Lyme disease
* Syphilis
● Trauma like t emporal bone fract ure
● Tumors of parot id gland
Upper mot or neur on pal sy
● St roke
● Demyelinat ion
● Brain t umors
Feat ur es of l ower mot or neur on ( LMN) pal sy:
(On t he same side of lesion)
● I t is charact erized by acut e onset of illness.
● I t reaches maximum paralysis in 48 hours in 50
%, in almost all by 5 days.
● I t is usually preceded by pain behind t he ear by
one or t wo days.
● Complet e paralysis of all muscles required for fa-
cial expression.
● Deviat ion of angle of mout h t o opposit e side,
absence of wrinkling of forehead.
● Effacement of creases and folds, widening of
palpebral fissure.
● I nabilit y t o close t he eye wit h int act Bell’s phe-
nomenon.
● Saliva dribbles from t he corner of t he mout h.
● Lacrimat ion and salivat ion may be affect ed in
some cases.
Feat ur es of upper mot or neur on ( UMN) pal sy
(On t he opposit e side of lesion)
● Upper part of face is spared
● Dissociat ion of emot ional and volunt ary face
movement s
● Preservat ion of facial reflexes
● Tast e and lacrimat ion is normal
I nvesti gati ons
I t remains essent ially clinical. But few invest iga-
t ions may be useful when UMN lesion is suspect-
ed
MRI Br ai n wi t h Gadol i ni um cont r ast
CT scan / MRI Brain would reveal t he cause of
t he upper mot or neuron palsy
Treatment
● Prednisolone:
* 1 –2 mg/ kg/ day (60 – 80 mg/ day) for 10 –14
days followed by slow t apering over next 2 – 4
weeks is useful.
* I t is highly effect ive if st art ed wit hin 3 days of
onset of illness.
● Prot ect ion of eyes during sleep using eye pads
● Splint ing of t he lower face t o prevent t he droop-
ing
● Massaging of weak muscles.
● Facial ret raining (mime t herapy) wit h biofeed-
back.
● Transcut aneous nerve st imulat ion
Pr ognosi s
80 % of t he pat ient s recover complet ely in one
or t wo mont hs. I ncomplet e weakness at t he onset
of illness is good prognost ic sign. Tast e recovery and
part ial mot or recovery at t he end of first week indicat es
good recovery.
I ndi cat or s of poor pr ognosi s
● Complet e facial palsy
● No recovery in t hree mont hs
● Age over 60 years
● Severe pain
● Nerve conduct ion st udies
* Lack of excit abilit y of facial nerve aft er 10
days and amplit ude difference bet ween t he
abnormal and normal more t han 50 %
● EMG showing denervat ion aft er 10 days
Compl i cat i ons
● Facial synkinesis
● Crocodile t ears
144
● Hemi-facial spasm
When t o admit ?
Can be managed as out pat ient most of t he t ime.
When t o refer?
No recovery wit hin 3 weeks, suspicion of second-
ary causes.
Ref er ences
● Pat rick J, Sweeney and Maurice R. Hanson, 2004,
Cranial Neuropat hies, Bradley’s Neurology in Clin-
ical Pract ice, 4
t h
edit ion, pp 1953 – 1990.
● Allan H.Ropper, Robert H.Brown, Facial nerve pal-
sies, Adam’s Principles of Neurology, 8
t h
edit ion,
pp 1181-1183.
Parkinson’s disease
I nt r oduct i on
By t he year 2040, neuro-degenerat ive diseases are
expect ed t o become t he second most common cause of
deat h in t he elderly. One of t he most common neuro-
degenerat ive disorders is Parkinson’s disease (PD).
Def i ni tion
Parkinson’s disease was described by James
Parkinson in 1817 as a clinical syndrome present ing
wit h bradykinesia, t remor, and slow, shuffling gait wit h
post ural inst abilit y. Rigidit y was described lat er, but is
included as a key clinical feat ure in t he current diagnosis
of Parkinson’s disease.
Parkinsonian disease is charact erized by a t et rad
known as TRAP:
● Rest ing Tremor
● Cogwheel Rigidit y
● Bradykinesia / Akinesia
● Post ural reflexes
Epi demi ol ogy
As a rule Parkinson’s disease (PD) begins bet ween
t he ages of 40 and 70, wit h peak age at onset occurring
in t he sixt h decade. Onset at younger t han age 20 is
known as j uvenile Parkinsonism, which has a different
pat t ern of nigral degenerat ion and is oft en heredit ary
(Parkin gene) or caused by Hunt ingt on’s or Wilson’s
disease. Parkinson’s disease is more common in men,
wit h a male-t o-female rat io of 3: 2.
Causes
The exact cause of parkinson’s disease remains
unclear. A combinat ion of fact ors is probably responsible
for t he development of parkinson’s disease. Various
t heories include
● Accelerat ed aging
* Decline in pigment ed neurons in subst ant ia
nigra
● Oxidat ive st ress
* Combined effect s of mult iple fact ors culminat-
ing in damage from free radicals.
● Genet ic suscept ibilit y
* I ncreased incidence of a family hist ory of Par-
kinson’s disease is observed in affect ed indi-
viduals (16% vs. 4% of cont rols)
● Environment al t oxins
* Cyanide
* Manganese
* Carbon disulfide
* Pest icides
* Well wat er
* Met hanol and
* Organic solvent s
● Medicat ions
* Met oclopramide
* Domperidone
* Reserpine cont aining ant ihypert ensive and
* Neuro-lept ics
Symptoms
● I nsidious onset , slowly progressive unilat eral rest
t remors at a frequency of 4-6 Hz in t he hands
is t he mode of onset of PD in more t han 85%
pat ient s.
● Slowness of mot or act ivit ies, masked facies, de-
creased eye blinking, cogwheel rigidit y, st ooped
post ure and decreased arm swing while walking
are present in t he early st ages.
● Early sympt oms may be weakness and fat igue,
nonspecific pains and discomfort . Soft speech,
micro-graphia, shuffling gait and post ural inst a-
bilit y and falls can also occur. These are t he mo-
t or manifest at ions.
145
● Non-mot or manifest at ions such as insomnia,
sleep dist urbances (night mares, rest less leg syn-
drome, periodic leg movement s, excessive day-
t ime sleepiness), aut onomic dist urbances such
as ort host at ic hypot ension, const ipat ion, urinary
urgency and frequency, excessive sweat ing and
seborrhea are common.
● Neuropsychiat ric manifest at ions can be mood
changes, depression, cognit ive and behavioral
dist urbances.
Di f f er ent i al di agnosi s:
● Wilson’s disease: I f t he onset is less t han 40
years (even 60 years) serum ceruloplasmin, urine
copper levels should be done
● Normal pressure hydrocephalus: different iat ed
by doing a CT scan - brain.
● Drug-induced Parkinsonism: can be ident ified by
det ailed hist ory.
● Vascular Parkinsonism: predominant ly in lower
limbs wit h hist ory of st roke and CT scan of brain
showing infarct s in basal ganglia.
I nvesti gati ons
Usually t he invest igat ions such as CT brain, MRI
brain, blood invest igat ions for Wilsons are done t o
exclude ot her causes. PD is usually a clinical diagnosis
not warrant ing sophist icat ed invest igat ion.
Nat ur al hi st or y
The disease progresses inspit e of t reat ment and
wit hin 10 years t he response t o t reat ment will be
reduced leading t o dykinesias of various t ypes and t he
pat ient will become bedridden wit hin 15 years.
Treatment
Ref Table 1 and Flowchart 1
146
Concl usi on
Diagnosis is easy as Parkinson’s disease, is usually
diagnosed wit h clinical examinat ion. Secondary causes
and ot her different ial diagnosis should be ruled out
by invest igat ions. Treat ment usually doesn’t alt er t he
course of t he illness and has only sympt omat ic value.
Ref er ences
● Jancovic J , The ext ra pyramidal disorders,Cecil Text
book of Medicine 20
t h
Edit ion Philadelphia,Pa: WB
Saunders Co 1996: 2042-2046
● Harrison’s I nt ernal Medicine -16
t h
Edit ion
● Adam’s Principles of Neurology-8
t h
Edit ion.
● Manual of Neurologic Therapeut ics-7
t h
Edit ion,
Lippincot Williams.
Guillain-Barre syndrome (GBS)
I CD Code number: G61.0
Def i ni tion
● Guillain - Barre syndrome(GBS) is a het erogenous
grouping of immune mediat ed processes gener-
ally charact erized by mot or, sensory and aut oim-
mune dysfunct ion.
● I n t he classic form, GBS is an acut e inflammat ory
demyelinat ing polyneuropat hy charact erized by
* Progressive symmet ric ascending muscle
weakness
Medical treatment of Parkinson’s disease
Drug Type Dose
Common Side
effect s
Special
feat ure
Selegiline Mono amino
oxidase inhibit or
5mg-15mg I nsomnia,
hypot ension
I nit iat ing t herapy
Tri-hexyphenidyl Ant i-choloinergic 2mg t ds Dry mout h,
confusion
Younger pat ient s
wit h t remors
Amant adine NMDA ant agonist 100mg-300mg Hallucinat ion Effect ive for
t remors
Levodopa/
Carbidopa
(4: 1)
10/ 100mg-25/ 200mg
4-6 t imes a day
Hypot ension,
Hallucinat ion,
confusion, dyskinesias
aft er 5 years of
disease
Mainst ay of
t reat ment
Pergolide DOPA agonist 0.05mg-0.5mg t ds Hypot ension,
Hallucinat ion,
confusion, pedal
oedema
Bromocript ine DOPA agonist 2.5mg t ds-20 mg t ds Hypot ension,
Hallucinat ion,
confusion, pedal
oedema
Ropinrole D2/ D3 agonist 0.25mg t ds -1-3mg/
t ds
Somnolence High
dose(> 16mg)
for monot herapy,
avoid driving
vehicles
Pramipexole D2/ D3 agonist 0.125mgt ds-0.5-
0.75mgt ds
Somnolence High dose(> 3mg)
for monot herapy,
avoid driving
vehicles
Ent acapone and
Tolcapone
COMT inhibit ors 100mg
100-200mg
Hepat ot oxicit y,
diarrhoea
To be given
wit h Levodopa/
carbidopa
147
* Flaccid paralysis, and
* Hyporeflexia wit h or wit hout sensory or aut o-
nomic sympt oms
● I n severe cases muscle weakness can lead t o res-
pirat ory failure and deat h.
Gener al Consi der at i ons
I n 1859, Landry described a neuropat hy charact erized
by ascending paralysis. Subsequent ly, Guillain-Barre
and St rohl not ed t he areflexia and albumino-cyt ological
dissociat ion in t he cerebrospinalfluid(Cerebrospinal
fluid) associat ed wit h t his neuropat hy.
Ot her names for t his condit ion are:
* Acut e post infect ive polyradiculoneuropat hy,
* Acut e infect ious polyneurit is
* Landry-Guillain- Barre- St rohl syndrome
* Post infect ious polyneurit is
Epi demi ol ogi cal aspect s
● GBS is t he most common cause of acut e general-
ized weakness wit h an annual incidence ranging
from 1-4/ lakh populat ion.
● Male t o female rat io is 1.5: 1.
● A Swedish epidemiological st udy indicat ed in-
cidence of GBS is lower during pregnancy and
increases in t he mont hs immediat ely following
delivery.
● GBS occurs at all ages, but a bimodal dist ribut ion
wit h peaks in young adult hood (15-35y) and in
elderly persons(50-75y) appears t o exist
● Epidemiological st udies from Japan show an
ant ecedent Campylobact er j ej uni (C.j ej uni) in a
great er percent age of GBS pat ient s.
Causes
Et i ol ogy
* A mild respirat ory infect ion or gast roint est inal
infect ion precedes t he neuropat hic sympt oms
by 1-3 weeks.
* Campylobact er j ej uni is t he most frequent
ident ifiable ant ecedent infect ion. Ot her
ant ecedent illness include viral exant hems and
viral infect ions(Cyt omegalovirus, Epst ein-Barr
virus, HI V), bact erial infect ions (Mycoplasma
pneumoniae, Borrelia burgdorferri) and lym-
phomas.
* Cert ain vaccines known t o cause GBS are
out moded ant irabies vaccine, A1 or New
Jersy(Swine) influenza vaccine, Menact ra
Meningococcal conj ugat e vaccine
* Anecdot al associat ion include
» SLE
» Sarcoidosis
» Surgery
» Renal t ransplant at ion
» Thrombolyt ic use and
» Snake bit es.
Pat hogenesi s
* GBS is believed t o be an aut oimmune re-
sponse, bot h humoral and cell mediat ed, t o a
recent infect ion. I t s relat ion t o ant ecedent in-
fect ions and ident ificat ion of various ant igan-
glioside ant ibodies suggest s t hat “ molecular
mimicry” may serve as a possible mechanism
for t he disease.
* The ant ibodies formed against t he ganglioside
like epit opes in t he lipopolysacharide layer
of some infect ious agent s cross-react wit h
ganglioside surface molecules of peripheral
nerves.
* Sympt oms generally coincide pat hologically
wit h various pat t erns of lymphocyt ic infilt ra-
t ion and macrophage mediat ed demyelina-
t ion, depending on t he subtypes.
* Recovery is t ypically associat ed wit h remyeli-
nat ion. I n axonal form of GBS, myelin sparing
axonal damage in t he form of direct cellular
immune at t ack on t he axon it self is seen.
Major Pathological Subtypes
AI DP * Acut e I nflammat ory Demyelinat ing
Polyneuropat hy.
AMAN * Acut e Mot or Axonal Neuropat hy.
AMSAN * Acut e Mot or Sensory Axonal Neuropa-
t hy.
MFS * Miller Fisher Syndrome
* Acut e Panaut onomic Neuropat hy.
BBE * Bickerst aff ’s Brain-st em Encephalit is
148
Acut e i nf l ammat or y demyel i nat i ng
pol yneur opat hy
● Most common. Nearly 40% of pat ient s are serop-
osit ive for Campylobact er j ej uni
● Lymphocyt ic infilt rat ion and macrophage me-
diat ed demyelinat ion of peripheral nerves are
present . Sympt oms generally resolve wit h re-
myelinat ion.
AMAN
I t is a purely mot or subt ype, more prevalent amongst
paediat ric age groups. Nearly 70-75% of pat ient s are
seroposit ive for Campylobact er. AMAN is generally
charact erized by rapidly progressive weakness, ensuing
respirat ory paralysis, more prot ract ed course and
delayed recovery.
AMSAN
Acut e severe illness similar t o AMAN but also affect s
sensory nerves and root s. Pat ient s are adult s wit h bot h
mot or and sensory dysfunct ion, marked muscle wast ing
and poor recovery.
MFS
I t is a rare variant t hat present s wit h classic t riad
of at axia, areflexia and opht halmoplegia. Pat ient s may
also have pt osis, facial palsy, mild limb weakness and
bulbar palsy. Ant i GQ1b ant ibodies, reduced or absent
sensory nerve act ion pot ent ials (SNAP) and absent t ibial
H reflex are charact erist ic of MFS. Recovery occurs
generally wit hin 1-3 mont hs.
BBE
Bickerst aff ’s Brain-st em Encephalit is
● A Variant of GBS
● Acut e onset of opht halmoplegia, at axia, dist ur-
bance of consciousness, hyperreflexia or Babin-
ski’s sign.
● Course of t he disease is monophasic or remit t ing
t o relapsing
● Prognosis is good
● MRI is diagnost ic
Acut e Pan-aut onomi c Neur opat hy
Rarest of all variant s. Cardiovascular involvement
is common. Dysrhyt hmias are a significant source of
mort alit y in t his form of disease. Recovery is gradual
and oft en incomplet e.
Ot her var i ant s of GBS
Regi onal
Cervico-brachio pharyngeal, oft en wit h pt osis,
oculopharyngeal weakness, bilat eral facial and abducens
weakness wit h dist al paraest hesias, Opht halmoplegia
wit h GQ1b ant ibodies and predominant paraparesis.
Funct i onal
Generalised at axia wit hout dysart hria or nyst agmus,
pure sensory, pure mot or, Pan-dysaut onomia and
axonal.
Symptoms
● I n GBS, t he maximum deficit develops over
days(maximum 28 days), followed by a plat eau
phase and a gradual recovery.
● Pat ient s may init ially present wit h paraest hesias,
sensory sympt oms and weakness. The fairly sym-
met rical weakness of t he lower limbs ascends
proximally over hours t o several days t o involve
arm, facial, oropharyngeal muscles and in severe
cases t he respirat ory muscles. Progression ends
by 1-4 weeks.
● Aut onomic sympt oms such as palpit at ion, pos-
t ural giddiness, facial flushing, venous pooling,
urinary ret ent ion and const ipat ion can occur.
Si gns
● Acut e flaccid quadriparesis, hypo or areflexia,
impaired propiocept ion and pain, cranial nerve
palsies in t he form of ophalmoplegia, pupillary
abnormalit ies, bi-facial, palat al and pharyngeal
weakness, and dysart hria.
● I n severe cases respirat ory muscle paralysis oc-
curs which is charact erized by poor respirat ory
effort , reduced vit al capacit y ( < 10ml/ kg ) and
reduced single breat h count < 20.
● Papilloedema, paralyt ic ileus and urinary ret en-
t ion can occur.
Di agnost i c Cr i t er i a
Feat ures required for diagnosis
● Progressive weakness of bot h legs and arms.
● Areflexia.
Cl i ni cal f eat ur es suppor t i ve of di agnosi s:
149
● Progression over days t o 4 weeks.
● Relat ive symmet ry of signs.
● Mild sensory sympt oms or signs.
● Cranial nerve involvement (bifacial palcies).
● Recovery beginning 2 weeks aft er progression.
● Aut onomic dysfunct ion.
● Absence of fever at onset .
I nvesti gati ons
● Elevat ed Cerebrospinal fluid prot ein wit h< 10
cells/ microlit re.
● Elect ro-diagnost ic feat ures of nerve conduct ion
slowing or block.
Not e: Feat ures support ing an axonal process are seen
in AMAN and AMSAN.
I nvesti gati ons
Cer ebr ospi nal f l ui d exami nat i on and ser i al
el ect r ophysi ol ogi cal st udi es are crit ical for
confirming t he diagnosis of GBS.
● Elevat ed or rising prot ein levels on serial lumbar
punct ure and 10 or fewer mononuclear cells/ mm
3
st rongly support diagnosis.
● Most common elect rophysiological abnormalit ies
include prolonged dist al mot or and F wave lat en-
cies, absent or impersist ent F waves, conduct ion
block, reduct ion in dist al CMAP amplit udes, wit h
or wit hout t emporal dispersion and slowing of
mot or conduct ion velocit ies.
● I n cases of axonal degenerat ion, reduced CMAP
and SNAP amplit udes are found.
● MRI - Lumbosacral MRI may demonst rat e Gado-
linium enhancement of lumbar root s.
● Serum- Elevat ed serum ant ibodies t o Mycoplas-
ma, C.j ej uni and cyt omegalovirus can pinpoint
t he preceding infect ions.
● Ant ibodies t o GM1 ganglioside are seen in AMAN.
● Ant ibodies t o GQ1b are seen in MFS and opht hal-
moplegia.
● Ant ibodies t o GD1a and GT1b are diagnost ic of
pharyngo brachial cervical variant .
● Biochemist ry
* Abnormal LFT in 1/ 3
rd
of pat ient s.
* Hyponat remia in vent ilat ed GBS pat ient s.
Di f f er ent i al di agnosi s
● Acut e neuropat hies
* Porphyrias
* Dipht heria
* Crit ical illness neuropat hy
* Toxins-Arsenic, lead, organophosphorus com-
pounds, t hallium, neurot oxic fish and shell
fish (ciguat oxin, t et radot oxin, saxit oxin), t ick
paralysis, vasculit is and lymes disease.
● Neuromuscular j unct ion disorders
* Bot ulism
* Myast henia gravis
● Myopat hies
* Hypokalemia
* Hypophosphat emia
* Polymyosit is
* Rhabdo-myolysis
● CNS disorders
* Rabies
* Poliomyelit is
* Transverse myelit is
* Basilar art ery t hrombosis.
Treatment
Emergency depart ment care
● Monit or airway, breat hing, circulat ion. I V fluids,
oxygen and assist ed vent ilat ion form t he init ial
management .
● Clinical indicat ions for t he need of int ubat ion in-
clude hypoxia, rapidly declining respirat ory func-
t ion, poor or weak cough reflex and suspect ed
aspirat ion.
● Typically int ubat ion is indicat ed whenever t he
FVC is less t han 15 ml/ kg (usually a single breat h
count of 20 is equivalent t o VC of 1.5 l), and max-
imum inspirat ory pressure is < 30 cm of wat er.
● I nt ravenous infusion and use of vasopressor
agent s in pat ient s wit h hypot ension due t o dy-
saut onomia.
● Correct ion of hyponat remia and use of heparin t o
prevent pulmonary embolism.
● Plasma exchange (PE) and int ravenous immu-
150
noglobulin (I v I g). Bot h t herapies have been
shown t o short en recovery t ime by as much as
50%.
Pl asma exchange
● Dosage
* 200 t o 250 ml/ kg of plasma in 4-6 t reat ment s
on alt ernat e days.
* The replacement fluid is saline combined wit h
5% albumin.
I ndi cat i on
I f t he pat ient is unable t o walk unaided, if he
shows significant reduct ion of vit al capacit y and
signs of oropharyngeal weakness.
Pr edi ct or s of r esponsi veness
Younger pat ient s and pat ient s wit h preserved
CMAPs prior t o inst it ut ion of t reat ment respond
bet t er.
Advant age
I n pat ient s who are t reat ed wit hin 2 weeks of
onset , t here is approximat e halving in period of
hospit alizat ion and in t ime required for independ-
ent ambulat ion.
Compl i cat i ons
● Need large bore venous access(subclavian or in-
t ernal j ugular cat het erizat ion) which may cause
pneumot horax, infect ion and haemorrhage.
● During and aft er t he procedure, hypot ension,
hypo-prot hrombinemia wit h bleeding, and car-
diac arrhyt hmias can occur.
I nt r avenous i mmunogl obul i n
● Dosage
* 0.4g/ kg/ day for 5 consecut ive days.
● Complicat ions
* Renal failure
* Prot einuria
* Asept ic meningit is
* Anaphylaxis can occur in pat ient s wit h con-
genit al I gA deficiency.
Not e
* Performing plasma exchange aft er int rave-
nous immunoglobulin does not make sense
and hence follow exchanges aft er int ravenous
immunoglobulin.
Cor t i cost er oi ds
● Are ineffect ive as monot herapy.
● Two randomised cont rolled t rials, one wit h con-
vent ional dose prednisolone and anot her wit h
high dose Met hylprednisolone have failed t o
demonst rat e any beneficial effect .
Pr ognosi s
● Approximat ely 3-5% of pat ient s do not survive
t he illness even in best equipped hospit als.
● I n early st ages deat h is due t o cardiac arrest
relat ed t o dysaut onomia, ARDS, pneumo or
haemot horax.
● Lat er in t he illness, pulmonary embolism and res-
pirat ory failure are t he main causes of deat h.
● Maj orit y of pat ient s recover complet ely but in
10% residual disabilit y is pronounced.
Fol l ow Up
● Average period of mechanical vent ilat ion has
been 22 days and period of hospit alizat ion is 50
days in pat ient s wit h respirat ory failure.
● Speed of recovery varies and t he pace is st eady.
I t oft en occurs wit hin few weeks t o mont hs.
● I n pat ient s wit h axonal degenerat ion, regenera-
t ion may require 6-18 mont hs or even longer.
When t o admi t ?
Since pat ient condit ion may det eriorat e unpre-
dict ably and rapidly in first few days of illness, vir-
t ually all but t he mildest cases should be admit-
t ed t o t he hospit al for observat ion of aut onomic,
mot or and respirat ory funct ions.
When t o r ef er ?
Pat ient s wit h significant respirat ory dist ress and
cardiovascular aut onomic inst abilit y need I CU
care by skilled personnel and hence t hey should
be referred t o higher inst it ut ions wit h facilit ies for
mechanical vent ilat ion and I CU care.
Ref er ences
● Allan H. Ropper, Robert H. Brown, Diseases of t he
151
peripheral nerves, Adams and vict or’s PRI NCI -
PLES OF NEUROLOGY, 8
t h
edit ion, pp1117-1126.
● E.Pet er Bosch and Benn E. Smit h, Disorders of
Peripheral Nerves, Walt er G. Bradley’s NEUROL-
OGY I N CLI NI CAL PRACTI CE, 4
t h
edit ion, pp2336-
2345.
● Art icle from E medicine(www.emedicine.com.)
on GBS from int ernet .
Stroke
Epi demi ol ogy
Cerebro vascular disease is a maj or public healt h
problem. The crude prevalence rat e varied from 45-
843 per 100,000. There are large human and monet ary
cost s involved in caring for pat ient s wit h st roke. At least
one-t hird of pat ient s survive wit h significant disabilit y.
Symptoms
A syst emat ic approach is required t o evaluat e a
pat ient wit h a cerebrovascular problem. St roke usually
is sudden in onset wit h rapid progression t o maximal
deficit . Tr ansi ent i schemi c at t ack is defined as
a t emporary episode of focal ischemic neurological
dysfunct ion t hat resolves complet ely wit hin 24 hours.
This has t o be different iat ed from ot her st roke mimics
such as migraine and seizures. St rokes can be classified
as ischemic and haemmorrhagic st roke.
Causes
● Maj or causes of cerebral ischemia are cardiac dis-
ease, large vessel disease, small vessel disease,
and hemat ological disease
● I schemic st roke can be classified as t hrombot ic,
embolic and lacunar infarct ions.
● I nfarct ions can be art erial or venous
● Fi ve common l ocat i ons of haemor r hage ar e
* Epidural and subdural (secondary t o t rauma),
* Sub-arachnoid haemorrhage (AVM or aneu-
rysmal rupt ure)
* I nt ra-cerebral and int ra-vent ricular hemor-
rhage (secondary t o hyper t ension, AVM, an-
eurysm)
Symptoms
Hi st or y
One should different iat e st roke / TI A from pot ent ial
mimics
● Sympt oms may include mot or weakness, sensory
dist urbances, cranial nerve dist urbances, cogni-
t ive abnormalit ies, seizures, unst eadiness, head-
ache, et c depending on sit e of ischemia.
● Hist ory of heart disease, at herosclerot ic risk fac-
t ors such as hypert ension, diabet es, hyper-lipi-
demia, smoking, sedent ary lifest yle, family hist o-
ry of at herosclerot ic disease should be asked for.
● Hist ory of pain in neck, face, head; pain might
suggest art erial dissect ion.
● Hist ory of fever, chills, cardiac sympt oms, drug
abuse might indicat e infect ive endocardit is.
Exami nat i on
● Blood pressure, cardiac rhyt hm, carot id pulses,
bruit s, heart sounds, murmurs are recorded.
● Neurological examinat ion allows classificat ion
int o one of t he st roke syndromes.
Maj or st r oke syndr omes i ncl ude
● Middle cerebral art ery syndrome wit h cont ra lat-
eral gaze paresis, hemi paresis, hemi sensory
loss, cont ra lat eral visual field loss and aphasia
wit h left sided neglect wit h right-sided lesions
● MCA branch syndromes
* Non-fluent aphasia if involving ant erior divi-
sion and fluent aphasia if involving post erior
division of left side.
● Ant erior cerebral art ery syndrome wit h predomi-
nant ly leg weakness and sensory deficit s cont ra
lat erally and sparing of vision.
● Post erior cerebral art ery syndrome wit h cont ra
lat eral homonymous hemianopia wit h associat ed
memory loss.
● Lacunar syndromes suggest ing occlusion of small
vessels result ing in pure mot or, sensory, isolat ed
dysart hria syndromes
● St roke mimics
* Acut e Migraine at t acks
* Seizures
* Hypert ensive encephalopat hy
* Met abolic causes
* Syncope
152
Management of Stroke
I nvest i gat i on
● Recommended t est s in acut e st roke are
* Serum glucose
* Blood count
* Serum elect rolyt es
* Renal funct ion t est s
* Coagulat ion st udies and
* ECG
Neur o i magi ng
● Emergency non-enhanced CT helps t o det ect
haemorrhage which appears hyper dense
* The abilit y of CT t o reveal an ischemic lesion
depends on t he size, locat ion of lesion, t ime
aft er onset of sympt oms
* CT may be normal in small infarct ions in pos-
t erior circulat ion, infarct s < 5mm and in acut e
infarct ions
* I schemic st roke is seen as an area of hypoden-
sit y t hat appears 12 t o 48 hours aft er st roke.
● Mult imodal MR imaging is
* Useful in det ect ing acut e st roke, post erior cir-
culat ion st roke and lacunar st rokes
* I t is more sensit ive t o ischemic brain damage
t han is t he CT scan
* While t he lat t er reveals hemorrhage immedi-
at ely aft er it occurs, soft ened t issue cannot be
seen unt il several days have elapsed
* On t he ot her hand, MRI reveals ischemic
damage wit hin a few hours, in bot h whit e and
gray mat t er, and diffusion-weight ed MRI t ech-
niques do so even earlier (wit h in minut es).
● By MR angiography
* One can see all t he maj or cervical and int rac-
ranial art eries and may det ect t he irregular lu-
men or occlusion of at herosclerosis and even
embolic occlusions in more dist al vessels
* This met hod has t o a large ext ent has re-
placed convent ional angiography, which is re-
served for cases in which t he diagnosis is in
doubt (e.g., suspect ed angiit is) or when sur-
gical int ervent ion or long-t erm ant icoagulant
t herapy is cont emplat ed.
Treatment
Acut e t her apy of I schemi c st r oke
● Time is prime fact or and awareness should be
creat ed for early medical at t ent ion t o t hese pa-
t ient s.
● I n general blood pressure should not be lowered
unless:
* Blood pressure lowering is necessary t o fulfill
crit eria for safe t hrombolysis.
* Acut e myocardial infarct ion being associat ed.
* Hypert ensive crisis wit h end-organ involve-
ment .
* The consensus guidelines from American
SPECT showing Caudate infarct
CT scan - MCA infarct
153
St roke Associat ion suggest t hat t herapy be
wit hheld unless Diast olic Blood pressure > 120
or syst olic Blood pressure > 220.
● Suppl ement al oxygen when SpO
2
l ess t han
95%.
● Hypert hermia and hyperglycemia t o be correct ed.
● When pat ient s pr esent wi t hi n 3 hour s, I V
t hr ombol ysi s wi t h r t PA i mpr oves st r oke out -
comes.
● Acut e use of lowdose Aspirin improves st roke
out come.
● Ant icoagulant s are useful in cardioembolic st roke,
cort ical vein t hrombosis and art erial dissect ions.
● Ant i-oedema measures are used when signs or
sympt oms of cerebral edema is present . Manni-
t ol, furosemide, hypervent ilat ion, Head elevat ion
is useful in management of cerebral edema.
● I f acut e st roke present s wit hin 3-6 hours int ra-
art erial t hrombolysis improves out come and so
pat ient can be referred t o specialt y cent ers for
t he same
Paraplegia and Quadriplegia
Def i ni tion
Paraplegia means weakness of bot h lower limbs and
quadriplegia is weakness of all four limbs.
Causes
Paraplegia or quadriplegia may be caused by lesions
of cerebrum, spinal cord, mot or root s, peripheral nerves,
myoneural j unct ion, or muscles. The causes include:
● Trauma
* Usually acut e onset (seconds or minut es)
* Cord t ransect ion –may be complet e or incom-
plet e
* Disc heriniat ion/ ext rusion
* Shock cord syndrome or spinal concussion,
may present wit h complet e cord syndrome,
but largely reversible.
* may be associat ed wit h vert ebral fract ure
● Acut e Transverse myelit is
● Ant erior spinal art ery infarct ion – at herosclerosis,
embolism, hypot ension, angiography, vasculit is
● Spinal cord hemorrhage – int ramedullary, sub-
arachnoid, subdural or epidural
* Haemat omyelia is usually due t o t rauma.
* Ot her et iologies include
CT scan - Lacunar infarction CT scan - Peripherial infarction from
a occlusion of MCA
154
» Art eriovenous malformat ion
» Venous infarct ion
» Blood dyscrasias
● Acut e immune disorders – includes
* GBS
* Myast henia gravis
* ADEM
* Para-neoplast ic myelopat hy, and
* Acut e polymyosit is
● I nfect ious disorders such as acut e epidural ab-
cess.
● Heredit ary met abolic disorders
* Hypokalemic and hyperkalemic periodic pa-
ralysis
* Acut e int ermit t ent porphyria.
● Toxins/ miscellaneous
* Tick paralysis
* Aminoglycosides
* Organophosphat es
● Cerebral causes of paraplegia such as
* Unpaired ant erior cerebral art ery t hrombosis,
* Superior sagit t al sinus t hrombosis
* Front al lobe t umours
● Hyst erical paraparesis.
Recur r ent par apl egi a
e.g. Mult iple sclerosis, Vascular malformat ions of
cord.
Chr oni c par a or quadr i par esi s
● Compressive myelopat hy
* Disc herniat ion
* Chronic degenerat ive art hrit is and spinal canal
st enosis
* Tumour
* Abscess
● I nflammat ory or demyelinat ing lesions
* Mult iple sclerosis
* CI DP
* Para-neoplast ic myelopat hy
* Spinal arachnoidit is
* Neuro-sarcoidosis
● I nfect ions
* HI V vacuolar myelopat hy
* Lyme disease
* Tuberculosis
● Met abolic or Toxic
* Vit B12 deficiency causing subacut e combined
degenerat ion
* Post radiat ion t herapy myelopat hy
* Lat hyrism
● Heredit ary and congenit al condit ions
* Cerebral palsy
* Heredit ary spast ic paraplegia
* Arnold-Chiarri malformat ion wit h or wit hout
syringomyelia
● Cent ral cause of paraplegia such as
* Para-sagit t al meningioma
* Chronic hydrocephalus.
Spi nal cor d syndr omes
Brown-sequard syndrome (cord hemisect ion)
Ant erior cord syndrome
Cent ral cord syndrome
Post erior cord syndrome
Conus medullaris syndrome
Cauda equina syndrome
Spinal` cord lesion has t he following t riad of clinical
feat ures:
● Sensory level (t he hallmark of spinal cord dis-
ease)
● Spast ic weakness
● Bladder and bowel dysfunct ion
Symptoms
The uppermost level of spinal cord lesion can
be localized by ‘segment al si gns’ like a band of
hyperalgesia at t he upper end of t he sensory level,
fasciculat ion or at rophy of muscles of one or more
segment s and diminished or absent DTR. They indicat e
a spinal cord lesion part icularly when accompanied by
long t ract signs.
The st at e of ‘spi nal shock’ wit h flaccid areflexic
limbs, result ing from severe and acut e t ransverse
155
lesions, may last for days or rarely weeks and should
not be mist aken for a LMN lesion like polyneuropat hy.
Slow spinal cord compression affect s t he pyramidal
t ract first , t he post erior column next and t he
spinot halamic t ract last .
I n occlusion of t he ant erior spinal art ery, t he
infarct ion is associat ed wit h spinot halamic t ract and
pyramidal t ract involvement wit h sparing of post erior
column.
Maj or concerns regarding mort alit y/ morbidit y due t o
spinal cord lesions depend on localizat ion.
● Respirat ory depression may occur wit h cranio-
cervical and cervical cord lesions.
● Aut onomic inst abilit y may occur wit h cord lesions
at t he mid t horacic level or above.
● Urinary ret ent ion.
When t he onset of paraplegia is acut e, vascular,
t raumat ic, inflammat ory and demyelinat ing causes
should be t hought of. I t represent s a ‘Neur ol ogi cal
emer gency’. Non-spinal causes should also be included
in t he different ial diagnosis.
Spinal epidural abscess is oft en missed and
misdiagnosed, somet imes wit h disast rous result s . Low
grade fever and low back pain followed by radicular
pain, present ing wit h rapidly progressive paraplegia or
quadriplegia , is charact erist ic.
I nvesti gati ons
● X-rays
* spine-AP and lat eral views
* Chest X-ray-PA
● TLC, DLC, ESR, Hb%
● CPK
● ECG
● Cerebrospinal fluid Analysis
● Rheumat ology work up
● CT Scan-may not be very informat ive.
● MRI spine wit h cont rast focusing on t he clinical
level of lesion.
● MRI of brain is ordered if hemispheric or cort ical
signs like seizures and confusion are present , in
t he absence of sensory level on t runk.
● Nerve conduct ion st udies
* EMG
* RNS. if lower mot or neurone involvement is
suspect ed. (RNS syst em is a deep brain st imu-
lat ion t reat ment )
Treatment
● Many disorders of t he spinal cord are t reat ed
if recognized early as ot herwise t he result s are
devast at ing.
● I f a spinal cord disease is associat ed wit h ab-
sence of demonst rable compression by imaging
t echniques, it is designat ed as non-compressive
myelopat hy.
● I n case of compressive lesions of t he spinal cord,
cauda equina or nerve root s, surgical t herapy is
usually required.
● Replacement of pot assium for hypokalemic pe-
riodic paralysis; I nj . Neost igmine for myast henia
gravis; vent ilat ory support for GBS;
● Hyst erical paralysis associat ed wit h ret ained DTR,
lack of at rophy and give way weakness should be
different iat ed from organic lesions causing para-
plegia.
● I n all cases of spinal inj ury, associat ed head in-
j ury and ot her inj uries such as abdominal inj ury
should be excluded and movement (especially
flexion) of t he cervical spine should be avoided.
The pat ient should be placed on a firm, flat sur-
face.
● Once t he degree of inj ury t o spine and cord has
been assessed, high dose Met hyl prednisolone in-
j ect ion is given – bolus of 30mg/ kg followed by
5.4 mg/ kg/ hour, for 23 hours, usually beginning
wit hin 8 hours of inj ury. Though acut e decom-
pressive surgery is done for haemat omas and
ot her sources of compression amenable t o sur-
gery, most surgeons do not favour surgery wit h
complet e spinal cord lesions.
● The spinal epidural abcess, if not surgically t reat-
ed by laminect omy and drainage at t he earliest
possible t ime, before t he onset of paralysis, t he
spinal cord lesion which is part y due t o ischemia
becomes more or less irreversible. Broad spec-
t rum ant ibiot ics in large doses should be given
init ially.
● I n t uberculosis, oft en t here is epidural compres-
sion from caseous granulat ion t issue get t ing ex-
t ruded from an infect ed vert ebra and it requires
ATT.
● Post infect ive and post vaccinal acut e t ransverse
myelit is is best t reat ed wit h high dose cort icos-
156
t eroids, plasma exchange, or I V immunoglobulin.
● Bladder care and avoidance of pressure sores are
import ant .
● Physiot herapy, assist ed devices, ort hot ics and
wheel chairs may all be beneficial in improving t he
funct ional abilit ies of pat ient s wit h paraplegia.
Ref er ences :
1. Neurological different ial diagnosis – A priorit ized
approach – Roongroj Bhidayasiri.
2. Principles of neurology – Adams and vict or.
Acute Bacterial Meningitis
Most common organisms responsible for bact erial
meningit is are
● Haemophilus influenzae
● Neisseria meningit idis and
● St rept ococcus pneumoniae, which account for
about 75 percent of sporadic cases.
● I nfect ion wit h L. monocyt ogenes is now t he
fourt h most common t ype of nont raumat ic or
nonsurgical bact erial meningit is in adult s.
● The following are less frequent causes
* St aph. aureus and group A and group D
st rept ococci, usually in associat ion wit h brain
abscess, epidural abscess, head t rauma,
neurosurgical procedures, or cranial t hrom-
bophlebit is
* E. coli and group B st rept ococci in newborns;
and t he ot her Ent erobact eriaceae such as
Klebsiella, Prot eus, and Pseudomonas, which
are usually a consequence of lumbar punc-
t ure, spinal anest hesia, or shunt ing proce-
dures t o relieve hydrocephalus
* Rarer meningeal pat hogens include Salmonel-
la, Shigella, Clost ridium, Neisseria gonorrhoe-
ae, and Acinet obact er calcoacet icus, which
may be difficult t o dist inguish from Haemo-
philus and Neisseria.
Epi demi ol ogy
Pneumococcal, influenzal (H. influenzae), and
meningococcal forms of meningit is have a worldwide
dist ribut ion, occurring mainly during t he fall, wint er,
and spring and predominat ing in males. Each has a
relat ively const ant yearly incidence, alt hough epidemics
of meningococcal meningit is seem t o occur roughly in
10-year cycles. Meningococcal meningit is occurs most
oft en in children and adolescent s but is also encount ered
t hroughout much of adult life, wit h a sharp decline in
incidence aft er t he age of 50. Pneumococcal meningit is
predominat es in t he very young and in older adult s.
Causes
● Meningococcal Meningit is occurs as a cyclical
out break (New Delhi and Nort hern part s of I ndia)
or sporadically.
● Remember environment al causes for meningit is
and look for t ickborne, zoonosis or ornit hosis; ask
for exot ic t ravel or t ravel t o endemic areas; ex-
posure t o airborne organism; and elicit behaviour
for cont act wit h carriers.
● Whenever cases of meningit is occur, search for
infect ion in t he adj acent areas.
● Bact erial meningit is among migrant populat ion
and t ravellers are not uncommon.
Cl i ni cal aspect s
Symptoms
● Meningit is is a medical emergency
● One should not expect all clinical sympt oms and
signs in every case of meningit is, as t hese are
influenced by t he age, biological st at us, previous
exposure and immune response of t he individual
on one side, and t he nat ure, number and viru-
lence of t he organism on t he ot her side.
● The classical clinical feat ures and laborat ory find-
ings may not be demonst rable in many cases
now, as t he cases are diagnosed on t he basis of
probabilit y and t reat ment is st art ed very early
before adequat e t ime is given for immunological
response.
● I f immuno-compromised individuals develop
meningit is, t hey may not show classical findings
of meningit is.
● I ndividuals wit h deficiency in complement com-
ponent s appear t o be suscept ible t o meningococ-
cal infect ion.
● Pat ient s wit h acut e bact erial meningit is seek
medical at t ent ion usually wit hin one t o t wo days
aft er t he onset of sympt oms.
● Asept ic meningit is has a benign course and is self
limit ed. I t is most ly caused by
157
* Viruses: Ent ero-viruses
* I nfect ious mononucleosis
* Lept ospirosis
* Disseminat ed Lyme’s disease
* Secondary syphilis, et c.,
● Wat ch for ot her syst em involvement during t he
course of t he meningit is or while present at ion in
every case of meningit is.
● I n ever y suspect ed t uber cul osi s meni ngi -
t i s, l ook f or BCG scar , ask for previous his-
t ory of pulmonary t uberculosis or elicit det ails on
t reat ment .
● Always look for neurological and non-neurologi-
cal complicat ions, as t hese cannot be predict ed
in a given case.
● Deat h in meningit is is most ly relat ed t o raised I n-
t ra cranial pressure (I CP).
● Lumbar Punct ure is essent ial when t here are in-
dicat ions.
● The frequency of Cerebrospinal fluid examinat ion
depends on t he clinical out come but a repeat ed
examinat ion should be done in 24 t o 48 hours, if
t here has not been sat isfact ory improvement or
if t he causat ive micro organism is more resist ant .
● Rout ine “ End of t reat ment ” Cerebrospinal fluid
examinat ion is unnecessary.
● Meningit is pat ient s may develop convulsions at
any point of t ime. Hence, medi cal per sonal
whi l e t r ansf er r i ng a case t o hi gher cen-
t r e must t ake car e t o manage convul si ons
whi l e on t r ansf er .
● Meningit is pat ient s who have respirat ory compli-
cat ions, mult i-organ failure or involvement and
det eriorat ing neurological signs require int ensive
care management , if available.
● I n view of t he immediat e and lat e complicat ions
due t o meningit is, care should be t aken t o t reat
t he pat ient s wit hout any delay.
I nvesti gati ons
● Cerebrospinal fluid (Cerebrospinal fluid) should
be sent immediat ely t o t he laborat ory for cyt o-
logical, bio-chemical, immunological and micro-
biological analyzes.
● Normal Cerebrospinal fluid in a suspect ed case
does not rule out meningit is.
● Ant ibiot ics given 4 hours before obt aining Cer-
ebrospinal fluid probably do not affect cult ure
result s.
● I n bact erial meningit is, posit ive rat e for gram
st aining vary from 60 t o 90%, and cult ure in
about 90%. Hence effort s must be made for bac-
t eriological st udies, if suspect ed.
● Cerebrospinal fluid sugar may be normal in List e-
ria mono-cyt ogenes infect ion.
● Cerebrospinal fluid sugar will be around 60% of
t he blood sugar of an individual normally.
● Cerebrospinal fluid prot ein may be elevat ed nor-
mally in diabet ic pat ient s
● I n uncont rolled diabet ics wit h cent ral nervous
syst em infect ion, t he Cerebrospinal fluid sugar is
less desirable
● Along wit h Cerebrospinal fluid glucose, est imat e
simult aneous blood glucose level.
● Depending upon t he clinical scenario, proceed
wit h mult iple invest igat ions t o ident ify t he cause
for meningit is.
● Encourage blood cult ure in suspect ed cases of
meningit is.
● Meningit is due t o opport unist ic pat hogens and
ot her newer organisms are at t ract ing clinicians,
micro biologist s and communit y medicine special-
ist s. Also, t hey need special media for isolat ion
and ident ificat ion.
● Various Salmonella serot ypes can cont ribut e t o
epidemic meningit is.
● As meningit is due t o more t han one organism
was report ed in one and t he same individual
rarely, one should not ignore t he isolat es as con-
t aminant s.
Treatment
● Meningit is pat ient s require empirical ant imicrobi-
al t herapy in high doses and it should be st art ed
immediat ely and be adj ust ed aft er t he microbio-
logical result s arrive.
● St eroids are administ ered amidst cont roversies in
view of t he pot ent ial benefit s and for short dura-
t ion.
● Type of ant i-microbial required, dose and dura-
t ion are decided by invading organism.
● I n Crypt ococcal meningit is Cerebrospinal fluid is
158
oft en at high pressure and management may re-
quire regular removal of 10 t o 15 ml of Cerebros-
pinal fluid t o prevent feat ures of raised I CP.
Pr event i on
● Vaccinat ion against meningit is is available for few
infect ions only.
● Observe for infect ion and assess carrier st at us
among ot her members living or in cont act wit h
t he case of Meningococcal meningit is.
● Fami l y member s have t o be gi ven chemo-
pr ophyl axi s, i f t he case t ur ned out t o be
meni ngococcal i nf ect i on.
● Healt hcare workers may be a carrier for t he oc-
currence of meningococcal Meningit is.
I mpor t ant not e
● Risks involved and ant icipat ed complicat ions
have t o be explained t o t he care givers of t he
pat ient s, as case fat alit y cannot be predict ed.
● Timely administ rat ion of medicat ions, vigilant
observat ion for complicat ions, good nursing care
and adequat e support ive measures enhance re-
covery wit h minimal complicat ions.
● Meni ngi t i s due t o not i f i abl e agent s has t o
be r epor t ed t o t he publ i c heal t h aut hor i t y
i mmedi at el y.
● I nclude microbiologist s and public healt h person-
nel in t he t eam when you are confront ed wit h
meningit is.
● I n every case of meningit is look for a cause and
a source.
● Ocular fundus examinat ion should be done be-
fore lumbar punct ure and should be ent ered in
t he medical records.
● Performance of CT scan brain before lumbar
punct ure is cont roversial but is not generally re-
quired if meningit is is considered in non-elderly
or immuno-compet ent individuals.
● Every case of meningit is invariably has predis-
posing / precipit at ing fact ors.
● Be empat het ic wit h pat ient s and care givers but
never give assurance.
● Lumbar punct ure has t o be carried out aft er ob-
t aining a writ t en informed consent .
● Suspect ed meningit is case has t o be referred t o
a higher cent re aft er assessment and providing
support ive care along wit h a det ailed writ t en re-
port .
● As t he implicat ions of meningit is on t he individual
are many- family, social, professional, nat ional
and legal, t he document at ion of cases should be
clear, specific and well writ t en.
Resear ch aspect s
Meningit is is a fascinat ing area for research from
t he point of view of epidemiology, clinical, t herapeut ic,
prevent ive, social, and economical aspect s.
Tuberculous Meningitis
Tuberculosis present ing as meningit is is t he most
common form of CNS t uberculosis and const it ut es a
medical emergency, as a diagnost ic and t herapeut ic
delay may have very serious consequences.
Nearly 50% of pat ient s wit h advanced CNS disease
fail t o survive and t here is a high incidence of serious
neurological complicat ions in t hose who survive.
Causes
Most cases of Tuberculous meningit is are in young
children, but primary infect ion can be acquired at a lat er
age and, in recent years, a large proport ion of pat ient s
wit h t his condit ion have been adult s. The disease is
uncommon, but severe, in pregnant women. There has
been an increase in t he incidence of t uberculosis relat ed
t o t he epidemic of HI V infect ion. HI V-infect ed pat ient s
wit h t uberculosis are at increased risk of meningeal
involvement .
The disease commences wit h t he rupt ure of a
meningeal or subcort ical lesion wit h liberat ion of t ubercle
bacilli int o t he Cerebrospinal fluid and t he development
of many t ubercles on t he meninges.
The ensuing meningeal inflammat ion, part icularly at
t he base of t he brain, leads t o t he secret ion of t hick
exudat es which may lead t o st rangulat ion of t he cranial
nerves, especially t he opt ic and audit ory nerves at t he
base of t he brain and t o raised int racranial pressure due
t o obst ruct ion t o t he flow of Cerebrospinal fluid.
Raised int racranial pressure is a maj or complicat ion
of t uberculous meningit is and some degree of
hydrocephalus occurs in lat e st ages.
Symptoms
Clinically, cases are classified int o t hree st ages:
St age 1
159
● The pat ient is fully conscious and rat ionale wit h
non-specific sympt oms such as general malaise,
low-grade fever apat hy, irrit abilit y, personalit y
changes, depression and int ermit t ent headache
but wit h no focal signs and lit t le or no evidence
of meningit is
● Sympt oms may be limit ed or even absent in im-
muno suppressed pat ient s, including t hose who
are HI V-posit ive.
St age 2
● The pat ient is ment ally confused and/ or has focal
neurological signs such as cranial nerve palsies.
● Ot her sympt oms include more severe and per-
sist ent headache and vomit ing and some degree
of phot ophobia.
St age 3
● The pat ient is deeply st uporous or comat osed
and or has complet e hemiplegia, paraplegia or
quadriplegia.
I nvesti gati ons
● Examinat ion of Cerebrospinal fluid is essent ial al-
t hough t his should be performed carefully aft er
ruling out raised int racranial pressure
* This may reveal
* Lymphocyt es
* A raised prot ein level and
* Decreased glucose level, but t hese param-
et ers may he normal
* I n some cases t here is a high polymorph
count , which suggest s t uberculous meningi-
t is of rapid onset or a non-acid-fast bact erial
infect ion.
● A chest X-ray may be helpful as pulmonary t u-
berculous lesions are evident in about half t he
pat ient s
● The diagnosis is confirmed by t he microscopic
det ect ion of acid-fast bacilli in cent rifuged sam-
ples of Cerebrospinal fluid, alt hough a very t hor-
ough search only det ect s such bacilli in 10-30%
of case. Where a Cerebrospinal fluid ‘c1ot ’ of fi-
brin is present , acid-fast bacilli may be seen in it
● Cult ure of Cerebrospinal fluid is far t oo slow, even
wit h t he use of aut omat ed syst ems but , where
facilit ies are available, PCR and relat ed nucleic
acid amplificat ion t echniques may be useful
● I f i n any doubt as t o t he di agnosi s, ant i t u-
ber cul osi s t her apy shoul d be commenced
i mmedi at el y.
● CT and MRI , where available, are of value in t he
invest igat ion of t uberculous meningit is as t hey
det ect
* Crypt ic lesions
* Raised int racranial pressure
* Hydrocephalus and
* Cerebral infarct ions
● Clinically, t he different ial diagnosis should include
* Various subacut e or chronic meningit is, in-
cluding part ially t reat ed bact erial meningit is,
fungal meningit is para-meningeal infect ions,
* Neoplast ic and granulomat ous infilt rat ions of
t he meninges (for example carcinomas, leu-
kaemias. lymphomas, sarcoidosis), and
* Cerebral t umours
Treatment
● The unt reat ed mort alit y of Tuberculous meningi-
t is is close t o 100 percent
● Full t reat ment must be st art ed when t he diagno-
sis is suspect ed on clinical grounds, immediat ely
aft er adequat e samples have been t aken for mi-
croscopy, cult ure, and immunodiagnosis.
● ‘Trial’ of chemot herapy is j ust ified when t here is
clinical suspicion of Tuberculous meningit is, par-
t icularly when diagnost ic facilit ies are limit ed
● There is conflict ing evidence regarding t he lengt h
of t reat ment , and t reat ment for 12 mont hs is
probably a conservat ive est imat e of t he t ime re-
quired for bact erial cure
● The combinat ion of I soniazid and Rifampicin for
12 mont hs, wit h Pyrazinamide and St rept omycin
during t he first 2 mont hs wit h init ial adj uvant
st eroids, is an effect ive regimen t hat has been
widely used
● St eroid should be used wit h I V Dexamet hasone
for 1st 7days followed by prednisolone 1mg/ kg
for 1 mont h and t hen t o be t apered over 3-4
weeks. Durat ion of st eroid t herapy may need t o
be ext ended depending on clinical pict ure.
160
Compl i cat i ons of Tuber cul ous Meni ngi t i s
The complicat ions of Tuberculous meningit is are
common, some of which are oft en serious enough t o
cause severe morbidit y and deat h in spit e of act ive
t reat ment wit h ant i-t uberculosis drugs
Nursing care is very import ant during t he acut e
illness, when t here are t he usual problems present ed by
unconscious pat ient s, and during t he prolonged phase
of convalescence and rehabilit at ion
Ant iconvulsant s are oft en needed, especially in
children.
Pr ognosi s
● The prognosis is worst and t he risk of sequelae
highest in t hose admit t ed in coma wit h signs of
brain-st em damage
● I t is severe in t he very young and very old, preg-
nant women, and t hose wit h malnut rit ion or ot h-
er diseases
● The out come of Tuberculous meningit is in HI V-in-
fect ed pat ient s is similar t o t hat in pat ient s wit h-
out HI V infect ion. There are permanent sequelae
in 10 t o 30 percent of survivors
● I nt ellect ual impairment is especially common in
infant s and young children
Long-t er m sequel ae
● As many as 60 percent of pat ient s who have sei-
zures during t he illness will suffer recurrences.
● Upt o 25 percent of survivors will have cranial
nerve deficit s including blindness, deafness, and
squint s
● Some 10 t o 25 per cent of survivors have some
residual weakness aft er hemiparesis or parapare-
sis
● About 10 per cent of pat ient s develop Cerebro-
spinal fluid spinal block at some st age of t he ill-
ness, but t his will recover complet ely in at least
half of t hem.
I mpor t ant not e
A high index of suspicion which helps in early
t reat ment of Tuberculous meningit is is t he cornerst one
in prevent ing t he morbidit y
BCG Vacci nat i on at bi r t h r educes t he r i sk of
i nf ect i on and i s r ecommended f or al l i nf ant s bor n
i n our communi t y.
Ref er ences
● Oxford Text book of Medicine
● Mansons Tropical diseases
● Bradley.S Text book of Neurology
● Park Text book of Prevent ive medicine
Herpes Simplex Encephalitis
Epi demi ol ogy
● I t is t he commonest and gravest form of acut e
encephalit is, account s for 10% of all encephalit is.
● I n unt reat ed cases mort alit y is 70%
● I n t reat ed cases mort alit y is 20%
● Morbidit y in t reat ed and unt reat ed cases is 70%.
Survivors may show permanent neurological se-
quelae.
Causes
Caused by Herpesviruses (HSV–I in 90% of cases).
Also causes herpit ic lesion of oral mucosa. Type 2 virus
causes acut e generalised encephalit is in neonat es
and genit al herpit ic infect ion in t he mot her. Bot h t ype
I and I I cause myelit is. Rarely localized adult t ype
of encephalit is is caused by t ype 2 virus and diffuse
neonat al encephalit is by t ype I .
Mode of t r ansmi ssi on
● Transmit t ed by respirat ory or salivary secret ion.
Upt o 33% of HSV-I encephalit is occurs wit h pri-
mary infect ion.
● Virus spreads from t he olfact ory fibres in t he
nose t o orbit ofront al cort ex and t emporal lobes.
● Mainly due t o react ivat ion and cent ripet al spread
of virus lat ent in t he t rigeminal ganglia from a
prior infect ion.
Symptoms
Fever, headache are consist ent feat ures.
● Onset may be abrupt wit h focal or generalized
seizures, confusion, st upor and coma (or) pro-
t ract ed wit h olfact ory or gust at ory hallucinat ions,
anosmia, t emporal seizures, personalit y change,
bizarre or psychot ic behavior or delirium, aphasia
and hemiparesis.
● St at us epilept icus is rare.
● Memory dist urbances is evident lat er in t he con-
161
valescent st age, as t he pat ient s goes from st upor
t o coma.
● Swelling and herniat ion of one or bot h t emporal
lobes t hrough t he t ent orium may occur leading t o
deep coma and respirat ory arrest during t he first
few days of illness.
Di f f er ent i al di agnosi s
Herpes Simplex Encephalit is must be different i-
at ed from:
● Acut e haemorrhagic leucoencephalit is
● Subdural empyema
● Cerebral abscess
● Cerebral venous t hrombosis
● Sept ic emboli from bact erial endocardit is and
● Mit ochondrial encephalopat hy

I nvesti gati ons
Cer ebr ospi nal f l ui d anal ysi s
● Cerebrospinal fluid is under pressure
● Lymphocyt ic pleocyt osis in t he range of 10 –
1000 WBC/ µl.
● Neut rophils in early st ages
● RBC and xant hocromia are found
● Prot ein cont ent is raised
● Glucose is usually normal
● HSV DNA can be det ect ed in Cerebro-
spinal fluid by PCR t echnique. Has sen-
sit ivit y of > 95% and specificit y
approaching 100% for t he diagnosis of HSV.
False negat ive t est can occur in t he first 48 hours
of febrile illness.
● Fl uor escent ant i body st udy and viral cult ure
of cerebral t issue obt ained by brain biopsy in a few
at ypical cases. Rising t it res of neut ralizing ant i-
bodies can be demonst rat ed but is not diagnost ic.
CT and MRI
● MRI is more sensit ive and is preferred. 40% of
pat ient s wit h HSE and normal CT will show de-
monst rable abnormalit ies in areas of high signal
int ensit y on T2 weight ed images in front o t em-
poral regions.
EEG
● This is abnormal in t he early course of t he dis-
ease. Shows diffuse slowing, focal abnormalit ies
in t emporal regions or Periodic Lat eralizing Epi-
lept iform Discharges ( PLEDS) .
Treatment
● Acyclovir is administ ered int ravenously in t he
dose of 10mg/ kg every 8hours in adult s and
20mg/ kg every 8 hours in neonat es and children.
● Treat ment is cont inued for 14 days.
● Side effect s wit h t herapy are local irrit at ion of
veins and t ransient impairment of renal funct ion
● Treat ment wit h acyclovir reduces mort alit y from
70% of 20%.
● Associat ed brain edema is t reat ed
● Seizures are t reat ed wit h ant iconvulsant s
● Foscarnet is an alt ernat e t herapy for Acyclovir
resist ant st rains or for t hose allergic t o acyclovir.
Pr ognosi s
● Bot h mort alit y and morbidit y is governed by t he
pat ient ’s age and st at e of consciousness at t he
t ime of inst it ut ion of acyclovir t herapy. I f t he pa-
t ient is unconscious t he out come is poor.
● I f t reat ment is began wit h in 4 days of illness in
a conscious pat ient , t he survival rat e is > 90%.
Sequel ae
● I ncludes
* Korasakoff ’s amnesia
* Global dement ia
* Seizures and
* Aphasia
I mpor t ant Not e
Primary prevent ion
The large reservoir of persons wit h asympt omat ic
HSV–I and HSV–I I infect ion indicat es t hat t he sum of
effort s t o cont rol HSV disease t hrough suppressive
ant iviral chemot herapy and educat ional programme
will be limit ed. Cont rol of HSV infect ion is at t ained by
vaccinat ion. Several vaccines are under invest igat ion.
162
Japanese Encephalitis
Japanese encephalit is (JE) is caused by Flavivirus, an
Arbovirus (art hropod-borne virus). They are t ransmit t ed
by culex mosquit oes.
Epi demi ol ogi cal aspect s
● Japanese encephalit is is numerically one of
t he most import ant causes of viral encephalit is
worldwide, wit h an est imat ed 50,000 cases and
15,000 deat hs annually. I t is a zoonot ic disease,
i.e. infect ing mainly animals and incident ally man.
● Maj orit y of cases (about 85%) occur among chil-
dren less t han 15 years of age and 10% of cases
occur among t hose over 60 years of age.
● I ncidence in I ndia: JE was first recognized in I n-
dia in 1955 in Tamilnadu. Half of t he populat ion
in Sout h I ndia has neut ralizing ant ibodies t o t he
virus. JE virus infect s several ext rahuman host s
such as animals and birds.
● Available evidence indicat es t hat t he basic cycles
of t ransmission are:
Pig → Mosquit o → Pig
The Ardeid bird → Mosquit o → Ardeid bird
Causes
● The disease is t ransmit t ed t o man by t he bit e of
infect ed mosquit oes. Man is an incident al dead-
end host . Man t o man t ransmission has not been
recorded so far.
● I nfect ed pigs do not manifest any sympt oms of
illness and are t hus considered as ‘amplifiers’ of
t he virus and infect t he mosquit oes.
● Culicine mosquit oes act as vect ors in t he t rans-
mission of t he viruses. Culex t rit aeniorhynchus is
t he most import ant vect or in Sout h I ndia.
● All t hose bit t en by infect ed mosquit oes do not
manifest t he disease. The rat io of overt infec-
t ion t o inapparent infect ion varies from 1: 300
t o 1: 1000. Thus cases of encephalit is represent
only t he t ip of t he iceberg compared t o t he large
number of inapparent infect ions.
Vi r ol ogy
I n common wit h all flaviviruses, Japanese
encephalit is virus has a small (50 nm) lipoprot ein
envelope surrounding a nucleocapsid comprising of
core prot ein and 11 kb single st randed RNA (3800 kD).
At least five genot ypes of Japanese encephalit is virus
occur in Asia, which relat e roughly t o t he geographical
area of isolat ion.
Symptoms
I ncubat i on Per i od
● 5 t o 15 days. Course of t he disease in man may
be divided int o t hree st ages:
* Pr odr omal st age
» onset is acut e wit h fever, headache and
malaise
» Durat ion is 1 t o 6 days.
* Acut e encephal i t i c st age
» Fever > 38
o
C
» Nuchal rigidit y
» Focal CNS signs
» Convulsions and
» Alt ered sensorium progressing t o coma.
* Lat e st age and sequal ae.
* Pat ient s wit h Japanese encephalit is t ypically
present aft er a few days of non-specific febrile
illness, which may include coryza, diarrhoea,
and rigors. This is followed by headache,
vomit ing, and a reduced level of conscious-
ness, oft en heralded by a convulsion.
* I n some pat ient s, part icularly older children
and adult s, abnormal behaviour may be t he
only present ing feat ure, result ing in an init ial
diagnosis of ment al illness.
* A proport ion of pat ient s make a rapid spon-
t aneous recovery (so called abor t i ve en-
cephal i t i s). Ot hers may present wit h asept ic
meningit is and have no encephalopat hic fea-
t ures.
* Convulsions occur oft en in Japanese encepha-
lit is, and have been report ed in upt o 85% of
children and 10% of adult s. Generalized t on-
ic-clonic seizures occur more oft en t han focal
mot or seizures. Mult iple or prolonged seizures
and st at us epilept icus are associat ed wit h a
poor out come.
* The classical descript ion of Japanese en-
cephalit is includes
» A dull flat mask-like facies wit h wide un-
blinking eyes
163
» Tremor
» Generalised hypert onia, and cogwheel ri-
gidit y
» These feat ures were report ed in 20% t o
40% of I ndian children
» Ophist hot onus and rigidit y spasms, part ic-
ularly on st imulat ion, occur in about 15%
of pat ient s and are associat ed wit h a poor
prognosis.
* Changes of respirat ory pat t ern, flexor and
ext ensor post uring, and abnormalit ies of t he
pupillary and occulocephalic reflexes are poor
prognost ic signs and may reflect encephalit is
in t he brain st em
* However in some pat ient s a clear rost rocaudal
progression of brainst em signs, an associat ion
wit h high Cerebrospinal fluid opening pres-
sures, and a reversal of signs on aggressive
management of raised int racranial pressure
suggest s t ranst ent orial herniat ion.
* Recent ly a subgroup of pat ient s infect ed wit h
Japanese encephalit is virus who present ed
wit h a poliomyelit is-like acut e flaccid paralysis
has been ident ified.
Pr ognosi s
● Case fat alit y rat e varies bet ween 20 t o 40 per-
cent . Around half of t he survivors have severe
neurological sequelae. About 30% of survivors
have frank mot or deficit s. These include a mix-
t ure of upper and lower mot or neuron weakness,
and cerebellar and ext rapyramidal signs.
● Fixed flexion deformit ies of t he arms, and hy-
perext ension of t he legs wit h “ equine feet ” are
common. Twent y percent of pat ient s have severe
cognit ive and language impairment (most wit h
mot or impairment also), and 20% have furt her
convulsions. A higher rat e of sequelae is report ed
for children t han adult s.
Di f f er ent i al Di agnosi s
The different ial diagnosis of Japanese encephalit is
is broad and includes ot her viral encephalit ides
(arboviruses, herpes

viruses, ent eroviruses, and
post infect ious and post vaccinat ion

encephalomyelit is),
ot her CNS infect ions (bact erial and fungal

meningit is,
t uberculosis, cerebral malaria, lept ospirosis, t et anus,

abscesses), ot her infect ious diseases wit h CNS
manifest at ions

(t yphoid encephalopat hy, febrile
convulsions), and non-infect ious

diseases (t umours,
cerebrovascular accident s, Reye’s syndrome,

t oxic and
alcoholic encephalopat hies, and epilepsy).
A peripheral neut rophil leukocyt osis is seen in
most pat ient s, and hyponat raemia may occur as a
consequence of inappropriat e ant idiuret ic hormone
secret ion (SI ADH).
Cer ebr ospi nal f l ui d Anal ysi s
The Cerebrospinal fluid opening pressure

is increased
in about 50% of pat ient s. High pressures (> 250 mm)

are associat ed wit h a poor out come. Typically t here is a
moderat e Cerebrospinal fluid pleocyt osis of

10-100 cells/
mm
3
, wit h predominant lymphocyt es, mildly increased
prot ein (50-200

mg %), and a normal glucose rat io.
I magi ng
● I n about 50% of pat ient s CT shows bilat eral non-
enhancing low densit y areas in one or more of
t he t halamus, basal ganglia, midbrain, pons, and
medulla.
● MRI is more sensit ive, t ypically demonst rat ing
more ext ensive lesions (t ypically high signal in-
t ensit y on T2 weight ed images) of t he t halamus,
cerebral hemispheres, and cerebellum.
● I maging st udies may be useful in dist inguishing
Japanese encephalit is from herpes simplex en-
cephalit is, where t he changes are charact erist i-
cally front ot emporal.
EEG
● Various elect ro-encephalographic abnormalit ies
have been report ed in Japanese encephalit is
including t het a and delt a coma, burst suppres-
sion, epilept iform act ivit y, and occasionally alpha
coma.
● Diffuse slowing may be useful in dist inguishing
Japanese encephalit is from herpes simplex virus,
in which changes are charact erist ically front o-
t emporal.
Treatment
● Treat ment for Japanese encephalit is is support-
ive, and involves cont rolling convulsions and
raised int racranial pressure when t hey occur.
● Careful nursing care and physiot herapy are need-
ed t o reduce t he risk of pressure sores, malnut ri-
t ion, and cont ract ures.
164
● Aspirat ion pneumonia is a common occurrence in
pat ient s wit h a reduced gag reflex
● There is current ly no specific t reat ment for Japa-
nese encephalit is.
Pr event i on and Cont r ol
● Broadly speaking, measures t o cont rol Japanese
encephalit is include t hose which int erfere wit h
t he enzoot ic cycle of t he virus,

and t hose which
prevent disease in humans.
● Measures t o cont rol

breeding of Culex mosqui-
t oes, such as t he applicat ion of larvicides

t o rice
fields, and insect icide spraying have proved inef-
fect ual.

● Avoiding culex bit es by minimising out door ex-
posure

at dusk and dawn, wearing clot hing t hat
leaves a minimum of exposed

skin, using insect
repellent s cont aining at least 30% DEET (N,N-
diet hyl-3

met hlybenzamide) and sleeping under
bed net s are some solut ions.
Vacci nat i on
● Vaccinat ion of populat ion at risk is recommended.
● A killed mouse brain vaccine is available.
● For primary immunizat ion, 2 doses of 1ml each
(0.5ml for children less t han 3 years) should be
given subcut aneously at an int erval of 7-14 days.
● A boost er is given before 1 year for full prot ec-
t ion.
● Revaccinat ion is given aft er 3 years.
● The vaccine is best used in t he int er-epidemic
period.
Neuro-Cysticercosis
I CD Code : B69.0 G99.8
Def i ni tion
Neuro-cyst icercosis is a parasit ic infect ion of t he
cent ral nervous syst em. Larval forms of t he pork
t apeworm Taenia solium causes t his disease.
Epi demi ol ogy
Neuro-cyst icercosis is highly endemic in Lat in
America, Mexico, East ern Europe, Asia, Africa,
and Spain.
Race
Neuro-cyst icercosis t ends t o be diagnosed more
frequent ly in Hispanics.
Sex
No sexual predilect ion exist s.
Age
Report s of cyst icercosis are unlikely in children
less t han 2 years of age. The disease is recog-
nized in children older t han 7 years.
Et i ol ogy
● The pork t apeworm T. solium can cause t wo
dist inct forms of infect ion in human: adult t ape-
worms in t he int est ine or larval forms in t he t is-
sues (cyst icercosis).
● Humans are t he only definit ive host s for T. solium;
pigs are t he usual int ermediat e host s, alt hough
ot her animals may harbor t he larval forms.
● By ingest ing undercooked pork cont aining cyst-
icerci, humans acquire infect ions t hat lead t o in-
t est inal t apeworms.
● I nfect ions t hat cause human cyst icercosis follow
t he ingest ion of T. solium eggs, usually from close
cont act wit h a t apeworm carrier.
● Aut oinfect ion may occur if an individual wit h an
egg - producing t apeworm ingest s eggs derived
from his or her own feces.
Cl i ni cal mani f est at i ons
● I n cyst icercosis, t he clinical manifest at ions are
variable. Cyst icerci can be found anywhere in
t he body but are most commonly det ect ed in t he
brain, cerebrospinal fluid (Cerebrospinal fluid),
skelet al muscle, subcut aneous t issue, or eye.
● The clinical present aion of cyst icercosis depends
on t he number and locat ion of cyst icerci as well
as t he ext ent of associat ed inflammat ory re-
sponses or scarring.
● Neurologic manifest at ions are t he most common.
Seizures are associat ed wt ih inflammat ion sur-
ronding cyst icerci and accompanying inflamma-
t ion or by Cerebrospinal fluid out flow obst ruct ion
from arachnoidit is.
● Signs of increased int racranial pressure, at axia,
or confusion, are oft en evident . pat ient s wit h
hydrocephalus may develop papilloedema or dis-
165
play alt ered ment al st at us.
● When cyst icerci develop at t he base of t he brain
or in t he subarachnoid space, t hey may cause
chronic meningit is or arachnoidit is, communicat-
ing hydrocephalus, or st roke.
Di agnost i c cr i t er i a f or human cyst i cer cosi s
Absol ut e cr i t er i a
● Demonst raion of cyst icerci by hist ologic or mi-
croscopic examinat ion of biopsy mat erial
● Visualizat ion of t he parasit e in t he eye by fun-
duscopy
● Neuro-radiologic demonst rat ion of cyst ic le-
sions cont aininig a charact erist ic scolex
Maj or cr i t er i a
● Neuro-radiologic lesions suggest ive of neuro-
cyst icercosis
● Demonst rat ion of ant ibodies t o cyst icerci in se-
rum by enzyme-linked immuno-elect rot ransfer
blot
● Resolut ion of int racranial cyst ic lesions spon-
t aneously or aft er t herapy wit h Albendazole or
Praziquant el alone.
Mi nor cr i t er i a
● Lesions compat ible wit h neuro-cyst icercosis de-
t ect ed by neuro-imaging st udies
● Clinical manifest at ions suggest ive of neuro-
cyst icercosis
● Demonst rat ion of ant ibodies t o cyst icerci or cyc-
t icercal ant igen in cerebrospinal fluid by ELI SA
● Evidence of Cyst icercosis out side t he cent ral
nervous syst em (e.g., cigar-shaped soft t issue
calcificat ions)
Epi demi ol ogi c cr i t er i a
● Residence in a cyst icercosis-endemic area
● Frequent t ravel t o a cyst icercosis-endemic area
● Household cont act wit h an individual infect ed
wit h Taenia solium
Di agnosi s
Diagnosis is confirmed by eit her one absolut e
crit erion or a combinat ion t o t wo maj or crit eria, one
minor crit erion, and one epidemiologic crit erion.
Di f f er ent i al di agnosi s
● Amoebic Meningoencephalit is
● Cyt omegalovirus I nfect ion
● Lyme Disease
● Schist osomiasis
● Toxocariasis
● Toxoplasmosis
● Trichinosis
● Tuberculosis
● Sarcoidosis
● Hydat id disease
● Tuberous sclerosis
● Von Hippel-Lindau disease
● Ast rocyt oma, Craniopharyngioma, and Medul-
loblast oma may be suspect ed
I nvesti gati ons
Radi ol ogi cal Exami nat i on
* Comput ed Tomography (CT) Scan shows t he
cyst and granuloma st ages of neurocyst icer-
cosis.
* Lesions may be locat ed in t he cort ex or at t he
gray-whit e j unct ion and present as punct at e
hyperdense lesions wit h ring enhancement .
* CT scanning also det ect s edema around t he
cyst , associat ed wit h t he deat h of t he organ-
ism.
* Magnet ic resonance imaging (MRI ) is t he best
imaging t est overall for t he diagnosis. Use
of cont rast shows larval deat h, visible as en-
hancement of t he cyst wall, which indicat es
t hat t he cyst has changed int o a granuloma.
I n addit ion, MRI shows vasogenic edema
around t he cyst .
* Soft t issue radiography can be performed t o
look for ext raneural cyst s.
El ect r o-encephal ogr aphy ( EEG)
* May be essent ial in children wit h int ract able
seizures. Periodic lat eralized epilept iform dis-
charges (PLEDs) may be present .
Labor at or y Test s
* St ool Examinat ion for ova and parasit es. Ob-
t ain 3 consecut ive daily st ool specimens. The
presence of ova may be t he sole diagnost ic
confirmat ion in children.
Cer ebr ospi nal f l ui d Exami nat i on
* Cerebrospinal fluid shows lymphocyt ic pleo-
166
cyt osis (occasionally eosinophilic), decreased
glucose and increased prot ein.
Ser ol ogy
* Enzyme-linked immunot ransfer blot (EI TB)
assay of t he pat ient ’s serum for cyst icercal an-
t ibodies can confirm t he diagnosis. Enzyme-
linked immunosorbent assay (ELI SA) can be
used on serum and Cerebrospinal fluid.
Br ai n bi opsy
* Brain biopsy can be performed in cases where
t he diagnosis remains quest ionable and t he
lesion has not resolved.
Treatment
● Consult a neurologist for management of sei-
zures, increased int racranial pressure, and any
ot her neurologic sequelae of t his disease.
● Consult an infect ious disease specialist for help
wit h a quest ionable diagnosis, eradicat ion of t he
organism, and public healt h issues
● Consult an opht halmologist t o examine t he child
for any signs of sub-ret inal cyst s.
Ant i -convul sant s t o st op sei zur es
Car bamazepi ne
● Adult dose
* I nit ial dose: 200 mg PO bid; increase dose at
weekly int ervals (by 200 mg/ day) unt il opt i-
mal response is achieved
* Usual dose: 800-1200 mg/ day PO divided t ds/
qid.
● Pediat ric dose
* 10-20 mg/ kg/ d PO divided bid/ t id
* I ncrease weekly t o achieve opt imal clinical re-
sponse, administ ered t ds/ qid.
Not e: Unsaf e i n pr egnancy
Adver se dr ug r eact i ons
Adverse drug react ions include dizziness, drowsiness,
and abdominal pain; rarely, rash, agranulocyt osis,
aplast ic anemia, and St evens-Johnson react ion.
Phenyt oi n
● Adult dose: 300 mg PO
● Pediat ric dose: 4-8 mg/ kg/ day PO divided bid/
t id (or) bd/ t ds
● Cont raindicat ions
* Arrhyt hmia.
● Unsafe in pregnancy
● Adverse react ions
* Gingival hyperplasia, nausea, and vomit ing;
rarely, St evens-Johnson syndrome, nyst ag-
mus, slurred speech, and at axia.
Ant i -hel mi nt hi cs
Treat ment wit h ant i-helmint hic drugs can result in
complet e resolut ion or significant regression in 80-90%
of pat ient s.
● A single dose of Praziquant el (5-10 mg/ kg) can
be administ ered t o individuals found t o have T
solium t apeworms in t heir st ool.
● Albendazole - Adult dose 400 mg PO bid
for 14 days wit h meals. (Drug of choice)
Pediat ric dose - 15 mg/ kg/ d PO divided bid for 14
days wit h meals.
I mpor t ant
To avoid inflammat ory response in t he CNS, t he
pat ient must be st art ed on ant iconvulsant s and high-
dose glucocort icoids.
Adverse effect s: Headache, nausea, dizziness,
vomit ing, alopecia, rash, fever, and pancyt openia.
Sur gi cal Car e
Reserve neurosurgical int ervent ion for cases of
cyst s t hat have failed t o resolve wit h ant i-helmint hic
t reat ment and are causing severe neurologic sequelae.
Surgery may be indicat ed for cases of int ravent ricular
cyst s t hat are resist ant t o medical management .
Shunt ing may be indicat ed for hydrocephalus.
Di et
Avoid reinfect ion. No ot her specific diet is necessary.
Pat i ent educat i on
● Educat e pat ient s and t heir families regarding pre-
vent ion
● Emphasize improvement in sanit at ion, separat ion
of pigs from humans, and food preparat ion hy-
giene in endemic areas.
When t o admi t and r ef er
Arrange t ransfer of t he pat ient t o higher cent res if
167
neurologic or neurosurgical care is necessary. I npat ient
care is necessary for t he following clinical st at es:
● Children who need ant i-helmint hic t herapy for ac-
t ive or mult iple cyst s require t o be hospit alized
for t he first 72 hours of t herapy due t o t he inher-
ent risk of anaphylact ic react ion
● Signs of increased int racranial pressure or appar-
ent need for cort icost eroid t reat ment
● I nt ract able seizures
● Hydrocephalus, requiring a shunt procedure.
Fol l ow - up
Pat ient s who have single non-viable lesions do not
require ant i-helmint hic t reat ment and can be managed
safely on an out pat ient basis.
Arrange neurologic follow-up care t o manage
seizures and any sequelae Perform a follow-up MRI in
3-6 mont hs or sooner if sympt oms worsen or recur.
I f a child who was admit t ed for ant i-helmint hic
t reat ment is doing well aft er 72 hours and follow-up
care is assured, t he child can be discharged t o finish
t herapy at home.
Compl i cat i ons
Hydrocephalus, int ract able seizure disorder,
hemiparesis, mot or and speech delay, blindness have
been report ed.
Pr ognosi s
I n cases wit h single lesions, prognosis is excellent .
I n t hose wit h mult iple lesions, especially ext ra-
parenchymal, prognosis can be poor. Treat ment wit h
ant i-helmint hics result s in complet e resolut ion or
significant regression in 80-90% of pat ient s. Most
children wit h calcified single lesions do not require
ant i-helmint hic t reat ment . Seizures cont rol is effect ive
in most children wit h Carbamazepine and t hey can be
weaned from t heir ant i-convulsant s wit hin 1-2 years.
The maj orit y of children remain free of seizures.
Bi bl i ogr aphy
Raj shekhar V, Joshi DD, Doanh NQ, van De N, Xi-
aonong Z. Taenia solium t aeniosis/ cyst icercosis in
Asia: Epidemiology, impact and issues. Act a Trop.
2003; 87: 53–60.
Del Brut t o OH, Raj shekhar V, Whit e AC, et al. Pro-
posed diagnost ic crit eria for neurocyst icercosis.
Neurology. 2001; 57: 177–183.
Vertigo
Def i ni tion
Vert igo is defined as t he ‘hallucinat ion’ of movement ,
eit her of self (subj ect ive) or t he environment
(obj ect ive). Usually t he pat ient uses various t erms (eg.)
bouncing, oscillat ing, st aggering, swimming, t wist ing
rolling, spinning, rocking, light-headedness, imbalance,
float ing, faint ing, falling
For t he most part t hey are benign but always t here
is t he possibilit y t hat t hey signal t he presence of an
import ant neurological disorder.
Gener al Consi der at i ons
Spat ial orient at ion is largely aut omat ic but complex.
Cont inued sensory monit oring assesses t he posit ion
of t he body in space, in relat ion t o t he surrounding
environment . The 5 sensory modalit ies const ant ly
sample posit ion and mot ion: vision, vest ibular sensat ion,
propriocept ion, t ouch and pressure, and hearing.
Normally t he brain int egrat es t he input from each of
t hese sensory modalit ies giving a comprehensive image
of posit ion and mot ion in space. This process enables
us t o maint ain balance, move about , and int eract wit h
ot her obj ect s
When t he orient ing image is unreliable, we become
uncert ain of posit ion and t he result is a sensat ion of
spinning or vert igo.
Cl i ni cal Aspect s
When a pat ient present s wit h t his t ype of dizziness,
t he clinician must next det ermine whet her t he sympt om
is cent ral (brain) or peripheral (inner ear, 8t h cranial
nerve) in origin.
Causes
Per i pher al causes of ver t i go
● Peripheral vest ibulopat hy
* I ncludes labyrint hit is
* Vest ibular neuronit is, and
* Acut e and recurrent peripheral vest ibulopat hy
● Benign posit ional vert igo
* I ncludes benign posit ional nyst agmus
* Benign paroxysmal vert igo
● Post-t raumat ic vert igo
● Vest ibulot oxic, drug-induced vert igo
● Meniere’s disease
168
● Ot her focal peripheral diseases
* I ncludes local bact erial infect ion
* Degenerat ion of hair cells
* Genet ic anomalies of labyrint h
* Cupulolit hiasis, t umor of eight h nerve
* Ot osclerosis
* Fist ula of labyrint h, and
* Rarely focal ischemia
Cent r al neur ol ogi cal causes of ver t i go
● Brainst em ischemia and infarct ion
● Demyelinat ing disease:
* Mult iple sclerosis
* Post infect ious demyelinat ion
* Remot e effect of carcinoma
● Cerebello-pont ine angle t umor
* Acoust ic neuroma
* Meningioma
* Cholest eat oma
* Met ast at ic t umors
● Cranial neuropat hy
● Focal involvement of eight h nerve or in associa-
t ion wit h syst emic disorders
● I nt rinsic brainst em lesions (t umor, art eriovenous
malformat ion)
● Ot her post erior fossa lesions (primarily ot her in-
t rinsic or ext ra – axial masses of t he post erior
fossa, such as hemat oma, met ast at ic t umor, and
cerebellar infarct ion)
● Seizure disorders (rare)
● Heridofamilial disorders such as spinocerebellar
degenerat ion
Syst emi c causes of ver t i go
● Drugs
* Ant iconvulsant s
* Hypnot ics
* Ant ihypert ensive
* Alcohol
* Analgesics
* Tranquilizers
● Hypot ension, pre-syncope (including primary
cardiac causes and post ural hypot ension from a
wide variet y of causes)
● I nfect ious diseases
* Syphilis
* Viral and ot her bact erial meningit is
* Syst emic infect ion
● Endocrine diseases
* Diabet es mellit us
* Hypot hyroidism
● Vasculit is
* Collagen vascular disease
* Giant cell art erit is, and
* Drug–induced vasculit is
● Ot her syst emic condit ions
* Hemat ological disorders
» Polycyt hemia, and
» Dysprot einemia
* Sarcoidosis
* Granulomat ous diseases and
* Syst emic t oxins
169
Charact erist ics of peripheral versus cent ral posit ional
vert igo
Sympt om or sign Peripheral Cent ral
Lat ency (t ime t o
onset of
Vert igo or
nyst agmus)
0-40 sec (mean
7.8* )
No lat ency;
begins
I mmediat ely
Durat ion < 1 min Sympt oms
may persist
(signs and
sympt oms
of single
Episode)
Fat iguabilit y
(habit uat ion)
Yes No
(Lessening signs
and
sympt oms wit h
repet it ion
of provocat ive
manoeuvre)
Nyst agmus
direct ion
Direct ion: fixed
t orsional, Up,
upper pole of
eyes t oward
ground
Direct ion
changing,
variable
I nt ensit y of signs
and sympt oms
Severe vert igo,
marked
nyst agmus,
nausea
Usually mild
vert igo,
less int ense
nyst agmus,
rare nausea
Reproducibilit y I nconsist ent More
consist ent
Peripheral Vestibulopathy
Def i ni tion
Peripheral vest ibulopat hy has been described
as vest ibular neuronit is, labyrit hit is, or viral neuro-
labyrint hit is.
Vest ibular neuronit is, st rict ly speaking, is
charact erized by single or recurrent sudden episodes
of t rue vert igo last ing from hours t o days and is oft en
associat ed init ially wit h vomit ing.
When t he condit ion is associat ed wit h hearing loss,
t he ent ire labyrint h is assumed t o be involved, and t he
t erm labyrint hit is is used.
Symptoms
I n t he acut e phase, most pat ient s present wit h
sudden severe vert igo, nausea, and vomit ing wit hout
any hearing dist urbance or facial weakness. The acut e
sympt oms usually resolve in a few days t o a week but
may recur in weeks or mont hs.
Causes
● Epidemic and seasonal out breaks of acut e vert igo
have suggest ed an infect ious origin caused by vi-
ral disease, but t his remains largely unproved.
● Viral labyrint hit is can also be part of a syst emic
viral infect ion, such as mumps, measles, infec-
t ious mononucleosis, or upper respirat ory t ract
viral infect ions
● I solat ed viral infect ions of t he labyrint h are also
believed t o cause t he sudden onset of hearing
loss, vert igo, or bot h, in children and adult s.
Otitic Herpes Zoster
Def i ni t i on
Ot it ic herpes zost er is an infect ion charact erized by
pain in t he ear, followed in 1-10 days by a vesicular
erupt ion in t he ext ernal ear, when t he sevent h and
eight h nerves are affect ed, t here is a combinat ion of
facial weakness, hearing loss, and vert igo known as t he
Ramsay-Hunt syndr ome. A dysest het ic area of skin
may precede, by many days, t he appearance of t he skin
erupt ion.
170
Beningn Paroxysmal Positional Vertigo
Def i ni tion
Benign paroxysmal posit ional (or “ posit ioning” )
vert igo (Blood pressurePV) is a sympt om complex
suggest ing benign peripheral (end-organ) disease. I t is
a maj or cause of vert igo.
Symptoms
Hist orical fact ors t hat should lead t o t he consid-
erat ion of Blood pressurePV include t he follow-
ing:
● Sympt oms associat ed wit h cert ain head posi-
t ions,
● Episodic rot at ional vert igo of brief durat ion,
● Ant ecedent episode of severe rot ary vert igo wit h
or wit hout nausea and vomit ing, associat ed wit h
an upper respirat ory t ract infect ion t hat suggest s
prior viral neuro-labyrint hit is
● Hist ory of head t rauma before at t acks of vert igo,
● Most severe sympt omat ology early in t he day,
wit h lessening sympt oms as t he day progress
● Relat ive absence of spont aneous sympt oms wit h-
out head movement or posit ion change.
The signs and sympt oms of benign posit ional vert igo
are t ransient and rarely last longer t han 40 seconds.
They usually occur when a cert ain posit ion is assumed,
such as lying down or t urning in bed. Depending on
whet her t he sympt om (vert igo) or sign (nyst agmus) is
being emphasized, t his condit ion can be called benign
paroxysmal posit ional nyst agmus or Blood pressurePV.
I nvesti gati ons
Physical examinat ion findings include
● Vert ical rot ary benign posit ional paroxysmal nys-
t agmus produced by provocat ive maneuvers.
● Lat ency t o onset of sympt oms once precipit at ion
head posit ion is achieved,
● Short-durat ion nyst agmus (3-30 seconds), and
● Adapt at ion of nyst agmus and sympt oms (i.e.,
disappearance wit h repeat ed maneuvers). The
findings of t he t ypical nyst agmus on assumpt ion
of cert ain head posit ions are considered t he most
import ant physical finding in making t he diagno-
sis of Blood pressurePV.
● I n benign paroxysmal posit ional vert igo, t he nys-
t agmus fast phase is horizont al-rot ary direct ed
t oward t he lower ear. The nyst agmus fast phase
is upward t oward t he forehead when gaze is di-
rect ed t o t he upper ear
● Wit h t he eyes in t he cent ral orbit al posit ion, t he
nyst agmus fast phase is vert ical upward and ro-
t ary t oward t he lower ear.
Meniere’s Disease
Def i ni tion
Meniere’s disease is charact erized by at t acks of severe
vert igo and vomit ing, t innit us, fluct uat ing hearing loss,
ill-described aural sensat ions of fullness and pressure
and spont aneous recovery in hours t o days.
This is followed by severe vert igo which reaches
peak int ensit y wit hin minut es and slowly subsides over
hours, wit h a persist ent sense of dis-equilibrat ion for
days aft er an acut e episode.
Consciousness is not lost in such episodes, alt hough
of t he accompanying vert igo, nausea.
Causes
● The most consist ent pat hological finding in
Meniere’s disease is an i ncr ease i n t he vol ume
of t he endol ymphat i c f l ui d and dist ension of
t he canals, hence t he t erm endolymphat ic hy-
drops.
● Alt hough some specific causes, such as bact erial,
viral, and syphilit ic infect ions, may lead t o t he
same pat hological changes and sympt oms, most
cases are idiopat hic
Symptoms
According t o t he guidelines from AAO-HNS Commit t ee
of hearing and equilibrium t he maj or sympt oms are
described as follows:
● Vert igo
* Recurrent , well-defined episodes of spinning
or rot at ion
* Durat ion ranging from 20 min t o 24 h
* Nyst agmus associat ed wit h at t acks
* Nausea and vomit ing during vert igo spells are
common
* No neurologic sympt oms wit h vert igo
● Deafness
* Hearing deficit s fluct uat e
171
* Sensorineural hearing loss
* Hearing loss progressive, usually unilat eral
● Tinnit us
* Variable, oft en low pit ched and louder during
at t acks
* Usually unilat eral on t he affect ed side
* Subj ect ive
Vestibular Neuronitis
Def i ni tion
This t erm is based on t heir clinical findings which
suggest t hat t he syndrome is caused by an isolat ed
lesion of t he vest ibular nerve and it s cent ral connect ions.
Vest ibular neuronit is is diagnosed using t hree clinical
diagnost ic crit eria:
● Vert igo: usually sudden onset
● An absence of cochlear sympt oms or signs (deaf-
ness and t innit us)
● An absence of associat ed neurological sympt oms
and signs.
Ver t i go i n mi gr ai ne
Vert igo has been found t o occur significant ly more
frequent ly in pat ient s wit h migraine t han in cont rols and
a high prevalence of migraine has been found in vert igo
sufferers.
Basi l ar mi gr ai ne
* Basilar migraine consist s of aura and head-
ache. The aura should include at least t wo
of t he following: vert igo, t innit us, decreased
hearing, at axia, dysart hria, double vision,
hemi field visual sympt oms (bot h eyes and
bot h fields), bilat eral paraest hesia, bilat eral
hemiparesis, decreased level of conscious-
ness.
Def i ni t e mi gr ai nous ver t i go
* Episodic vest ibular sympt oms of at least mod-
erat e severit y
* At least t wo of t he following migrainous symp-
t oms during at least t wo vert iginous at t acks:
» migrainous headache
» phot ophobia,
» phonophobia
» visual or ot her aura.
● At t acks of migraine (out side episodes of vert igo)
according t o HI S migrainous
● Some cent ral and/ or peripheral vest ibular abnor-
malit ies may be found in vert igo-free periods.
● Ot her causes ruled out by hist ory, physical ex-
aminat ion and ot her appropriat e invest igat ions.
Pr obabl e mi gr ai nous ver t i go
Def i ni tion
● Episodic vest ibular sympt oms of at least moder-
at e severit y (rot at ional vert igo, ot her illusory self
or obj ect mot ion, posit ional vert igo, head mot ion
int olerance)
● At least one of t he following, in relat ion t o at least
one vert iginous at t ack
* Migrainous headache
* Phot ophobia
* Phonophobia
* Migraine-specific t riggers e.g. specific foods,
sleep irregularit ies, hormone changes
● Response t o migraine prophylact ic drugs
● Migraine (out side vert iginous at t acks) according
t o t he crit eria of t he I HS
● Some cent ral and/ or peripheral vest ibular abnor-
malit ies may be found in vert igo-free periods
● Ot her causes ruled out by hist ory, physical ex-
aminat ion and ot her appropriat e invest igat ions
Beni gn r ecur r ent ver t i go
Def i ni tion
● Episodic vert igo, occasionally wit h t innit us but
wit hout hearing loss
● May be accompanied by nausea/ vomit ing and
at axia
● Nyst agmus may be observed during t he episode
● Durat ion: minut es t o hours, usually less t han
one hour, or hours t o days
● Episodes of migrainous headaches out side ver-
t iginous episodes, and/ or posit ive family hist ory
of migraine
● Normal audiomet ric findings, or no asymmet ry if
t here is an incident al hearing loss
172
● Different ial diagnosis: vest ibular hydrops, ot her
episodic vest ibular disorders, epilepsy
Ver t i go i n Cer ebr ovascul ar di sease
● Several mechanisms can cause vert igo and diz-
ziness in persons wit h cerebrovascular disease.
● Vert igo can occur wit h cerebrovascular disease
t hat involves t he vert ebrobasilar circulat ion,
which supplies t he labyrint h, t he lat eral pon-
t omedullary region t hat cont ains t he vest ibular
nuclei, and t he cerebellum.
● I n vert ebrobasilar art ery (VBA) insufficiency, ver-
t igo is sudden in onset , last s only minut es, is as-
sociat ed wit h nausea and vomit ing, and is usually
accompanied by a range of neurologic deficit s
(eg, ext remit y weakness, numbness, in coordina-
t ion, and dysart hria, diplopia, field defect s, t in-
nit us, hearing loss, loss of consciousness, drop
at t acks).
● I solat ed vert igo wit hout addit ional sympt oms can
be t he present ing manifest at ion of vert ebrobasi-
lar ischemia.
Symptoms
● Sympt oms and signs of post erior fossa cerebrov-
ascular disease include vert igo, t innit us, and
at axia. Sympt oms may be t ransient , permanent ,
recurrent , or isolat ed.
● St roke syndromes t hat involve t he post erior cir-
culat ion vary depending on t he involved t errit ory.
Wallenbergh syndrome (ie, lat eral medullary syn-
drome) appears wit h vert igo, nausea, vomit ing,
imbalance, ipsilat eral facial numbness and weak-
ness, diplopia, dysphagia, and dysphonia.
● I nfarct ion of t he dorsolat eral pont o-medullary
region result s in labyrint hine inj ury (ie, severe
vert igo, nausea, vomit ing, hearing loss) in addi-
t ion t o t he signs and sympt oms of Wallenbergh
syndrome.
● Cerebellar infarct ion also occurs wit h severe ver-
t igo, nausea, vomit ing, and at axia. When cere-
bellar infarct ion occurs wit hout any ot her asso-
ciat ed neurologic or audio logic sympt oms, t he
present at ion may be at t ribut ed t o viral neuronit is
(VN). Such cases of pseudo-VN usually occur af-
t er infarct ion of t he nodulus and uvula, t errit ory
supplied by t he medial branch of t he post erior in-
ferior cerebellar art ery (mPI CA). Cerebellar signs
t hat affect t he ext remit ies can be minimal or ab-
sent in mPI CA infarct ion of t he vest ibulocerebel-
lum. Basilar art ery syndrome result s from infarc-
t ion of t he pons.
● Sympt oms include
* Vert igo
* Hearing loss
* At axia
* Opht halmoplegia
* Blindness and regional sensory losses
* Cerebellopont ine angle (CPA) t umors t ypically
result in disequilibrium or unst eadiness rat her
t han a sensat ion of vert igo. However, sudden
change in t umor size wit h hemorrhage or dis-
rupt ion of regional blood flow t o t he labyrint h
may precipit at e vert igo
* Tumors in t he Cerebellopont ine angle are
most likely t o be vest ibular schwannomas
I nvesti gati ons
All t he pat ient s are t o be subj ect ed t o a t horough
hist ory, clinical examinat ion and various bed side t est s
such as
● The Head t hrust t est
● Dynamic visual acuit y
● Head shaking t est
● Dix Hall pick’s t est
● Fukuda’s t est and Calorie t est
● CT and MRI brain
● X-ray neck
● Blood sugar
● Lipid profile
● Carot id vert ebral doppler.
The Head Thr ust t est
● Met hod
* The pat ient s’s head is held firmly on each side
and t he pat ient is asked t o fixat e on any one
point – say t he examiner’s nose. The head is
moved slowly from side t o side t o see if t he
eyes are remaining fixed on one point (t he ex-
aminer’s nose).
* Once t he examiner is sat isfied t hat t he pa-
t ient is following t he inst ruct ions, t he head is
173
rapidly brought back int o t he midline. I f t he
vest ibulo-ocular reflex is normal, t he eyes do
not move at all.
* I f t here is vest ibular imbalance, t he vest ibulo
ocular reflex on t he affect ed side is hypoact ive
and t he eyes move wit h t he head. When t he
head is brought back t o t he midline, t here is a
re-fixat ion saccade.
* The examiner carefully looks for t his re-fixa-
t ion movement of t he eyes. This saccadic re-
fixat ion only occurs aft er rot at ion of t he head
t o t he affect ed side and persist s for a very
long t ime.
* The Head Thrust t est is very reliable for uni-
lat eral vest ibular hypo funct ion.
Dynami c vi sual acui t y
● Met hod
* Ask t he pat ient t o read t he smallest line pos-
sible on a Snellen’s eye chart wit h best cor-
rect ed vision. Repeat t he visual acuit y (VA)
while passively shaking t he pat ient ’s head at
2Hz. Record t he number of lines “ lost ” during
t he head shakes.
* I f t he VOR is normal, t he eyes remain fixed
on t he t arget line and t he visual acuit y does
not change. I f t he VOR is hypoact ive, t he eyes
move wit h t he head and are no longer fixed
on t he t arget line, result ing in visual degrada-
t ion.
* Loss of t hree or more lines from st at ic VA indi-
cat es vest ibular dysfunct ion and is a good t est
for vest ibular hypofunct ion due t o ot ot oxicit y
or age.
The head shaki ng t est
The pat ient s head is pit ched down 30’ and oscillat ed
at 2 Hz for 20 seconds. An abnormal t est is elicit at ion
of j erk nyst agmus. Post head shake nyst agmus is
considered pat hologic of vest ibular imbalance. I n most
cases a peripheral vert igo is ident ified wit h t he fast
phase beat ing t owards t he unaffect ed (st ronger) ear.
The Di ck-Hal l pi ke t est
I s a manoeuvre which is specifically posit ive if a
pat ient has benign paroxysmal posit ional vert igo (Blood
pressurePV). I t is int ended t o st imulat e t he vert ical semi
circular canals.
The ant erior and cont ralat eral post erior semi circular
canals are approximat ely parallel in a plane orient at ed
45’ from t he sagit t al plane. Wit h t he head t urned 45’ t o
one side, moving pat ient from sit t ing t o supine result s
in rot at ion in t he plane of t he canal pair, ie. in t he
horizont al plane.
I n t he normal pat ient , nyst agmus occurs during
t he manoeuvre but not aft er it . I n Blood pressurePV, a
change of posit ion causes movement of t he endolymph
elicit ing vert igo. The nyst agmus st art s at a lat ency of
4-10 seconds and last s upt o 30 seconds.
I nvolvement of t he post erior semicircular canals
result s in up-beat ing nyst agmus wit h a rot ary
component , t he upper pole of t he eye beat ing t owards
t he lower ear. Blood pressurePV result s from debris
moving freely in t he vert ical semi circular canals, usually
t he post erior.
Fukuda t est ( St eppi ng t est of Under ber ger )
Ask t he pat ient t o march in place wit h eyes closed
and arms out st ret ched- normally less t han 15 degrees
or so of rot at ion is displayed Asymmet ry of labyrint hine
funct ion is manifest ed as excessive rot at ion away from
t he diseased side.
Cal or i e t est
● The pat ient ’s head is ideally t ilt ed forward 30 de-
grees from t he horizont al, each audit ory canal is
irrigated for 30 seconds, first with water at 30˚
C, and then at 44˚ C with a pause of at least 5
minut es bet ween each irrigat ion.
● I n normal persons cold wat er induces a slight
t onic deviat ion of t he eyes t o t he side being ir-
rigat ed, followed aft er a lat ent period of 20 sec-
onds by nyst agmus t o t he opposit e side (direct ion
of fast phase). Warm wat er induces nyst agmus t o
t he irrigat ed side.
Nyst agmus
● The presence of spont aneous or induced nyst ag-
mus is of crucial import ance in making a diagno-
sis of peripheral or cent ral causes of imbalance.
● Spont aneous nyst agmus of a peripheral origin is
usually due t o lesions eit her of t he labyrint h or
eight h cranial nerve.
● The charact erist ics of nyst agmus of a peripheral
origin are as follows
* Mixed–horizont al plus rot at ional or t ort ional.
* Presence of fixat ion suppression – if t here is
174
a gaze evoked nyst amus while t he pat ient is
st aring at a blank wall, asking t he pat ient t o
fixat e on your finger, suppresses t he nyst ag-
mus i.e. t he nyst agmus is so-t o-say “ fat igu-
able”.
* The nyst agmus is int ense, i.e. it int ensifies
(increases in amplit ude) in t he direct ion of t he
fast phase,
* I t is direct ion fixed i.e. it does not change di-
rect ion wit h gaze. Usually in an irrit at ive le-
sion, it is in t he direct ion of t he affect ed ear
and beat s t owards t he unaffect ed ear if t he
lesion is dest ruct ive.
● Spont aneous nyst agmus of cent ral origin is usu-
ally due t o lesions of t he brainst em, cerebellum
or rarely cert ain areas of t he cerebrum.
● The charact erist ics of nyst agmus of cent ral origin
are quit e t he opposit e of peripheral nyst agmus.
Thus t he charact erist ics of cent ral nyst agmus are:
● Pure – purely horizont al, vert ical or t orsional
● Absence of fixat ion-suppression – it is “ non-fa-
t iguable” when one fixat es over t he examiner’s
finger
● Less int ense – does not int ensify in amplit ude
in t he direct ion of fast gaze
● Direct ion changing wit h gaze - left beat ing nys-
t agmus wit h left gaze
Nyst agmus is dampened by convergence, t herefore,
do not hold t he finger very close t o t he eyes – hold
it at least 14 inches away. Primary posit ion nyst agmus
is suppressed by fixat ion. The manoeuvres t o suppress
fixat ion are t o ask t he pat ient t o st are at a t ot ally blank
wall, t he hand held opht halmoscope met hod.
Treatment
Meni er e’s Di sease
● During an acut e at t ack of Meniere’s disease, rest
in bed is t he most effect ive t reat ment , since t he
pat ient can usually find a posit ion in which ver-
t igo is minimal.
● The ant i-hist aminic agent s
* Cyclizine
* Meclizine or t ransdermal scopolamine are use-
ful in t he more prot ract ed cases.
* Promet hazine is an effect ive vest ibular sup-
pressant , as is t ri-met hobenzamide given in
200-mg supposit ories, which also suppresses
nausea and vomit ing.
● For many years a low-salt diet in combinat ion
wit h ammonium chloride and diuret ics have been
used in t he t reat ment of Meniere’s disease, but
t he value of t his regimen has never been est ab-
lished.
● The same is t rue for dehydrat ing agent s such as
oral glycerol and t he more recent ly popular cal-
cium channel blockers.
● Mild sedat ive drugs may help t he anxious pat ient
bet ween at t acks.
Vest i bul ar Neur oni t i s
During t he acut e st age, ant ihist amine drugs,
Phenergan, Clonazepam and Scopolamine may be
helpful in reducing t he sympt oms. Vest ibular exercises
are recommended.
Medi cal t her apy f or ver t i go
Ant i hi st ami nes
● Meclizine 25-50mg 3 t imes / day
● Cyclizine 50mg 2 t imes / day
● Dimenhydrinat e 50mg 2 t imes / day
● Promet hazine 25-50mg / day
Ant i -chol i ner gi cs
● Scopolamine t ablet s 0.45-0.50 mg 2 t imes/ day
● Scopolamine Transdermal pat ch 1/ day for 3 days
Sympat homi met i cs
● Ephedrine 25 mg/ day
Ant i -emet i cs
● Tri-met hobenzamide 250mg 2 t imes / day
PO/ 200-mg supposit ory
● Promet hazine 25-50mg / day
● Prochlorperazine 5-10mg 3 t imes / day PO/ 25-
mg supposit ory
Tr anqui l i zer s
● Diazepam 5-10mg 3 t imes / day
● Oxazepam 10-60mg / day
175
● Haloperidol 0.5-5mg 2 t imes / day
Sur gi cal Tr eat ment
Surgical t reat ment of chronic peripheral vest ibular
dysfunct ion is primarily dest ruct ive. I n pat ient s wit h
severe Meniere’s disease for whom medical t herapy
has been ineffect ive and who have severe recurrent
disabling at t acks, a labyrint hect omy may be performed.
Unfort unat ely, Meniere’s disease may become
bilat eral, event ually result ing in t he need for
labyrint hect omy or vest ibular nerve sect ion on t he
cont ralat eral side.
A medical labyrint hect omy may be performed by
t he use of Aminoglycoside drugs, which are part icularly
dest ruct ive t o t he peripheral vest ibular hair cells.
Surgical or medical labyrint hect omy usually is a last
resort for pat ient s who have clearly defined, severe
at t acks of peripheral vest ibulopat hy, presumably from
Meniere’s disease.
Ref er ences
● Allan H. Ropper, Robert H. Brown, Deafness, Diz-
ziness and Diseases of equilibrium, Adams and
Vict or’s Principles of neurology, 8
t h
edit ion,
pp1117-1126.
● Todd Troost , Lisa.C Arguello, Neuroot ology, Wal-
t er G. Bradley’s Neurology in clinical pract ice, 4
t h

edit ion, pp746-748.
● Art icle from E medicine (www.emedicine.com.)
on Vert igo from int ernet .
177
Nephrology
Chapter 8
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
● Acut e Nephrit ic Syndrome
● Chronic Kidney Disease
● Nephrot ic Syndrome
● Acut e Renal Failure
● Hyponat remia
● Hypernat remia
● Hypokalemia
● Hyperkalemia
179
Acute Nephritic syndrome
Def i ni tion
Acut e post-infect ious glomerulonephrit is following
st rept ococcal pharyngit is or skin infect ion is a
prot ot ypical lesion of Nephrit ic syndrome.
Cl i ni cal f eat ur es
Acut e Nephrit ic syndrome is charact erized by t he
following clinical feat ures
● Hemat uria
● Prot einuria
● Hypert ension
● Oliguria
● Edema
● Decreased GFR
● RBC cast s or dysmorphic RBCs in urine.
Causes
I t is a spect rum of diseases wit h various et iologies
wit h a common sit e of inj ury t he glomerulus. The
common causes are:
Post-infectious diseases:
Post-st rept ococcal glomerulonephrit is
Non-st rept ococcal glomerulonephrit is
I nfect ive endocardit is
Pneumcoccal infect ions
Shunt nephrit is
Meningococcemia
Multisystem diseases
SLE
Vasculit is
Henoch-schonlein purpura
Goodpast eur’s syndrome
Primary Glomerular diseases
I gA Nephropat hy
Membranoproliferat ive glomerulonephrit is
Symptoms
● Puffiness of face
● Pit t ing bilat eral pedal edema
● Cola coloured urine
● Dyspnoea, if pulmonary edema occurs
● Hypert ension
● Hypert ensive encephalopat hy
* Seizures,
* Alt ered sensorium
There is usually a lat ent period of 10 t o 14 days for
occurrence of sympt oms following a respirat ory t ract
infect ion. This lat ent period is about 3 weeks following
a skin infect ion.
I nvesti gati ons
● Urine microscopic examinat ion - dysmorphic RBC’s
or RBC cast s
● Blood urea and serum creat inine levels
● Complement levels: Transient decline in C 3 lev-
els which become normal in 8 weeks
● I nvest igat ions for confirming st rept ococcal infec-
t ion are:
* Test s for serological confirmat ion of post
st rept ococcal glomerulonephrit is: ASO t it re,
Ant i DNA ase - B
* Posit ive t hroat cult ure for bet a hemolyt ic
st rept ococci
Treatment
● Bed rest
● Fluid rest rict ion according t o volume st at us
● Salt rest rict ion
● Diuret ics for cont rol of volume overload st at us:
loop diuret ics are preferred. I nt ravenous rout e if
pulmonary edema is present .
● Cont rol of hypert ension wit h ant ihypert ensive
drugs
● Management of renal failure - may rarely require
dialyt ic support
● Renal biopsy is indicat ed, if feat ures are not sug-
gest ive of post st rept ococcal glomerulonephrit is.
Prognosis:
Epidemic forms of disease in children have a
uniformly favorable short and long t erm prognosis.
Sporadic cases, especially in adult s may have more
serious long t erm consequences. Following resolut ion
of sympt oms, microscopic hemat uria can persist for as
long as a year.
180
Chronic kidney disease
Epidemiology
Chronic kidney disease (CKD) is a maj or public healt h
problem wit h rising incidence and prevalence. The
disease may progress t o end-st age renal disease, which
is associat ed wit h significant morbidit y and mort alit y.
The incidence of CKD in t he general populat ion is
est imat ed t o be 100 t o 250 per million people in I ndia.
CKD is a disease which in most inst ances is silent
unt il lat e st ages. Therefore it is import ant t o ident ify
t hose at risk and screen t hem and t o init iat e appropriat e
measures t o st op t he progression of disease.
Causes
● Diabet es Mellit us
● Hypert ension
● Glomerular diseases
● Congenit al and heredit ary diseases like Polycyst ic
Kidney disease and Vescico uret eric reflux.
I nvesti gati ons
Scr eeni ng f or CKD
I dent ify people at high risk
● Obesit y
● Smokers
● Diabet es
● Hypert ensives
● Family hist ory of renal disease
How t o scr een at r i sk i ndi vi dual s?
● Measure blood pressure
● Urine for prot einuria, hemat uria and ot her sedi-
ment s
● Est imat e Serum creat inine. Screen t hem at least
yearly.
Di agnosi s
Eit her one of t he following est ablishes t he diag-
nosis:
● Kidney damage for more t han 3 mont hs as de-
fined st ruct ural or funct ional abnormalit ies of t he
kidney wit h or wit hout decreased GFR
● Decrease in GFR t o < 60ml/ min for more t han 3
mont hs.
GFR is calculat ed by t he formula: GFR = (140-
age) x (Wt in kg) x (0.85 if female) / (72 x Cr
in mg/ dl)
St agi ng
Chronic Kidney disease has been divided int o five
st ages.
St age Descript ion GFR
(ml/ 1.73m2/
min)
St age I
St age I I
St age I I I
St age I V
St age V
Kidney damage wit h
normal or GFR
Kidney damage wit h
mild GFR
Moderat e in GFR
Severe in GFR
End st age renal disease
> 90
60 - 89
30 - 59
15 - 29
< 15
● GFR (Glomerular filt rat ion rat e)
Treatment
St ep 1:
Look f or cl ues wi t h r espect t o et i ol ogy
● Hist ory of hypert ension or diabet es mellit us.
● Sympt oms relat ed t o lower urinary t ract , recent
infect ions
● Feat ures of connect ive t issue disease
● Past medical records suggest ive of prot einuria
● Pregnancy relat ed problems
● Past renal evaluat ion
● Family hist ory of heredit ary kidney disease like
ADPKD/ Alport s syndrome.
St ep 2:
Reversible factors in CKD
● Obst ruct ive nephropat hy
● Urinary t ract infect ions
● Ext ra renal infect ions
● Nephrot oxic drugs
● Hypovolemia
● Congest ive cardiac failure
● Pericardial t amponade
● Hypokalemia / hyperuricemia
181
St ep 3:
Modifiable Risk Factors
● Cont rol of blood pressure :
* I n pat ient s wit h Prot einuria > 1 g / day, BP
t arget is < 125 / 75 mm Hg
* I f prot einuria < 1 g / day, BP t arget is < 135/
85 mm Hg
● Drugs used t o cont rol Hypert ension :
* ACE inhibit ors
* Diuret ics
* Calcium Channel blockers
● Glycemic cont rol : Target HbA1C levels of < 6.5
● Cont rol of Prot einuria : Done by using ACE inhibi-
t ors
● Cont rol of hyperlipidemia
* Tot al cholest erol < 200 mg/ dl , LDL Choles-
t erol < 100 mg / dl is t he t arget
* Use of HMG CoA reduct ase inhibit ors - st at ins
● Obesit y: Aim for ideal body mass index of < 25
● Cessat ion of smoking
STEP 4:
Pr event and t r eat compl i cat i ons
● Malnut rit ion:
* Diet ary prot ein int ake of 0.6 g / kg body
weight / day
* Diet ary calorie int ake of 30 - 35 kcals / kg /
day
● Cardiovascular disease
* I t is t he commonest cause of mort alit y in CKD
pat ient s.
* Risk for I HD increases by 30% for every in-
crease in serum creat inine by 0.23 mg/ dl.
* At least yearly screening for cardiovascular
disease should be done.
● Anaemia:
* Target hemoglobin of 11 g / dl is desirable in
CKD pat ient s. They need iron and eryt hropoi-
et in inj ect ions
● Renal ost eodyst rophy:
* Target calcium - 8.8 t o 9.7 mg / dl
* Phosphorous - 3.5 t o 5.5 mg / dl
* Calcium - Phosphorous product < 55 mg
2
/ dl
● This is achieved by:
* Use of calcium or non-calcium cont aining
phosphat e binders
* Phosphorus rest rict ion-avoidance of dairy
product s, meat , colas.
* Use of calcit riol
St ep 5 :
Pr epar e f or Renal r epl acement t her apy
● Early referral t o Nephrologist
● Vaccinat ion:
* Hepat it is B vaccine 40 micro grams 3 doses
- 0, 1 , and 2nd mont h followed by boost er
dose at 6 t h mont h .
● Early creat ion of art erio-venous fist ula when t he
GFR is < 25 ml/ min or Serum Creat inine > 4.0
meq/ l
Nephrotic syndrome
Def i ni t i on
● Prot eniuria more t han 3.5 gm/ day in adult s
● Prot einuria more t han 40mg/ m
2
/ hr in children
● Associat ed feat ures:
* Hypoalbuminemia
* Hyperlipidemia
* Edema
Causes
Di seases conf i ned t o ki dney:
* Minimal change disease
* Membranous nephropat hy
* Focal segment al glomerulosclerosis
* Membranoproliferat ive GN
* Mesangioproliferat ive GN
Syst emi c di seases:
* Diabet es mellit us
* SLE
* Amyloidosis
* Henoch-schonlein purpura
* Preeclampsia
Her edi t ar y di seases
* Congenit al nephrot ic syndrome
* Alport s syndrome
182
Compl i cat i ons of Nephr ot i c syndr ome
● I ncreased predisposit ion t o infect ions
● Thrombot ic t endencies
● Hyperlipidemia
● Hypocalcemia
● I ron resist ant hypochromic anemia
I nvesti gati ons
● Urine analysis: Dipst ick t est for prot einuria,
● Urine microscopic examinat ion for deposit s
● 24 hrs urinary prot ein: more t han 3.5 gm/ day es-
t ablishes t he diagnosis
● Renal funct ion t est s: Blood urea, serum creat i-
nine – Usually normal in isolat ed nephrot ic syn-
drome
● USG abdomen
Gui del i nes f or r ef er r al
Refer to a tertiary care center if there is a in-
dication for renal biopsy
I ndicat ions for Renal Biopsy in Nephrot ic Syndrome
● Age > 10 yrs
● Micro - hemat uria in urine analysis
● No response t o st eroid t herapy in adequat e
doses for a period of 4 weeks
● Associat ed renal failure
● Low C 3 levels
● ANA posit ive
● Evidence of syst emic disease
Treatment
● St eriods:
* I n children less t han 10 yrs, wit hout hema-
t uria, wit hout renal failure, st art empirical
st eroids viz.Prednisolone 2 mg/ kg/ day for 4
weeks, t aper over next 4 weeks
● HMG CoA reduct ase inhibit ors for hyperlipidemia
● Diuret ic t herapy:
* High dose int ravenous loop diuret ics
● Diet :
* Prot ein 0.8 g / kg / day + 1 g prot ein per gm
lost in urine,35 kcals / kg / day carbohydrat es
● ACE inhibit ors t o reduce prot einuria
● Treat ment of infect ions.
* The commonest cause of deat h in nephrot ic
syndrome is infect ion.
* Hence t reat infect ion early and aggressively.
* Refer for severe uncont rollable infect ions.
Acute Renal Failure (ARF)
Def i ni tion
Acut e renal failure is defined as a rapid decline in
renal funct ion, reflect ed by GFR over hours t o days as
evidenced by raising creat inine values
● ARF can be classified int o oliguric vs nonoliguric.
(Urine out put < 500 ml/ day is oliguria)
● ARF complicat es upt o 5% of hospit al admissions
and 30% of I CU admissions
Cl assi f i cat i on:
1. Pr e-r enal - 70%
* Hypovolemia - diarrhoea , persist ant vomit-
ing, burns, haemorrhage.
* Low cardiac out put- CCF
* Syst emic Vasodilat at ion – Sepsis, Hepat o-re-
nal syndrome
* Drugs - NSAI D’s
* Management of Pre-renal Failure :
» Volume replacement - 0.9 % saline , ringer
lact at e
2. Renal - 25%
● Can occur due t o disease process in glomeruli /
t ubules / int erst it ium / vasculat ure.
* Acut e t ubul ar necr osi s can occur due t o
* I schemic kidney inj ury - can occur wit h any
cause of pre-renal failure if prolonged
* Nephrot oxic drugs (commonly used)
» NSAI D ‘s
» Aminoglycosides
» Cis-plat in
» Amphot ericin-B
» Acyclovir
3. Post -r enal 5 %
* Prost at ic hyperplasia wit h obst ruct ion
* Renal st one disease
* Carcinoma of cervix
183
* Malignancies of urinary t ract
Eval uat i on of Renal f ai l ur e:
● Exclude Pre-renal and post renal.
● A ult rasound-KUB rapidly rules out t he easily cor-
rect able post renal causes
Pr e-r enal
● Usually occurs wit h volume deplet ion and by defi-
nit ion renal parenchyma is not damaged
● Urine is charact erized by low volume, low sodium
(< 20 mmol/ l) and high osmolalit y.
● Treat ment should be direct ed t owards t he un-
derlying cause.
Renal
Assess for signs and sympt oms of uraemia
Symptoms
● Anorexia
● Fat igue
● Ment al st at us changes
● Nausea / Vomit ing
● Prurit is
● Short ness of breat h
Si gns:
● Ast erixis
● Myoclonus
● Pericardial rub
● Pedal edema
● Pulmonary rales
● Raised JVP
● Seizures.
Look for clues for et iology of renal failure
CLUES ETI OLOGY
Sinusit is,Hemopt ysis Pulmonary renal syndromes,
Vasculit is
Diarrhoea,Vomit ing,
Hypot ension
Pre-renal hypovolemia
Back Pain Mult iple Myeloma
Trauma,Prolonged
immobilit y
Rhabdomyolysis
Skin rash Vasculit is,AI N
Liver disease Hepat orenal syndrome
Prost at e sympt oms BPH
Const it uonal
sympt oms
Vasculit is,
Malignancy,
I nfect ion
Recent surgery I schemia, At heroembolism,
Cont rast .
Medicat ion ACEI ’s,
ARB’s,
NSAI D’s,
Ant ibiot ics
Flank Pain Obst ruct ion, Pyelonephrit is
Bl ood I nvest i gat i ons
● Urea
● Creat inine
● Serum elect rolyt es
● Serum calcium
● Serum PO4
● Serum albumin
Ur i ne Anal ysi s
● Urinary pat t ern
● Pre-renal: small amount , bland few hyaline cast s.
● Post-renal: few hyaline cast s.
● ATN: Prot einuria usually small amount s,WBC’s,
epit helial cells, muddy brown appearance.
● Calculat e FeNa ( f r act i onal excr et i on of so-
di um)
● Urine Na x Serum Creat inine / Serum Na x
Urine Creat inine x100
< 1 – Pre-renal; > 2 – Renal
I ndi cat i ons For Di al ysi s :
● Hyperkalemia
● Met abolic Acidosis
● Volume Overload
184
● Encephalopat hy
● Pericardit is
Lab t est s consist ent wit h ARF (50% increase in
creat inine above baseline or 50% decrease in
baseline GFR
PRE-RENAL
Feat ures:
BUN t o Cr > 20: 1
FeNa < 1
Urine Sp Gr > 1020
Hyaline cast s
No e/ o obst ruct ion
No e/ o int rarenal cause
Treat ment :
Hydrat e
Eliminat e t oxins
Treat underlying cause
RENAL
Feat ur es:
BUN t o Cr > 10: 1 t o 20: 1
FeNa > 2
Urine Sp.Gr 1.010 t o 1.020
Tubular or granular cast s in urine
Tr eat ment :
Eliminat e t oxins
Nephrology consult at ion
POST-RENAL
Feat ur es
USG : Hydronephrosis
Serum and urine t est similar t o renal cause
Tr eat ment :
CT, KUB
Relieve obst ruct ion
Urology Consult at ion
Hyponatremia
Serum sodium reflect s t he rat io of sodium t o t hat
of wat er.
Hyponat remia is defined as Serum sodium < 135
meq/ l
The appr oach t o a pat i ent wi t h hyponat r emi a:
● First st ep is t o rule out pseudohyponat remia
which can occur in condit ions like hypert riglyceri-
demia, para-prot einemia.
● Lab met hods involving direct pot ent iomet ry does
not have t his problem.
● Once pseudohyponat remia is ruled out , assess
volume st at us and follow t he algorit hm.
Tr eat ment of Hyponat r emi a
Sympt omat ology and durat ion of hyponat remia
det ermine t he t reat ment approach.
● Let hargy
● Headache
● Nausea
● At axia
● Psychosis
● Seizures and coma can be manifest at ions of hy-
ponat remia
Not e:
Neurological damage ( osmot ic demyelinat ion) can
occur if
● Acut e sympt omat ic hyponat remia is left unt reat-
ed
● Chronic sympt omat ic hyponat remia is correct ed
t oo rapidly
185
Approach to Hyponatremia
Drugs like Thiazide,
Haloperidol etc.
operatively.
Hypernatremia
I t is defined as Serum Na > 145 m.mol/ l
Thirst and urinary concent rat ing mechanisms are
t he import ant defenses against hypernat remia. Hence
it is a rare finding in a conscious pat ient .
Al gor i t hm t o hyper nat r emi a t her apy:
St ep 1:
* Correct ECF volume st at us
* I sot onic saline if hypovolemic
* Diuret ics if hypervolemic
St ep 2:
Calculat e free wat er deficit :
Tot al body wat er x [ Na/ 140 - 1 ] or
0.6 x body weight (kg) x [ Na/ 140 - 1 ] .
Acut e hypernat remia can be rapidly correct ed. I f
t he hypernat remia is chronic, correct one half us-
ing ½ NS ( cont ains 500 ml free wat er per lit er )
in first 24 hours.
Furt her correct ion is done in subsequent 24
hours.
Hypokalemia
● Defined as serum pot assium < 3.5 meq/ l.
● I t can present wit h muscular sympt oms like flac-
cid paralysis, cardiovascular problems like ven-
t ricular arrhyt hmias and renal involvement like
polyuria.
Emer gency Tr ea t ment
● Urgent t reat ment is required in rare sit uat ions
like periodic paralysis, vent ricular ect opics or in
t he set t ing of myocardial infarct ion.
● Parent eral t herapy is risky, requires cent ral line
and ECG monit oring.
● I t is not indicat ed if t he pot assium is > 3.0. Oral
pot assium chloride 15 ml t ds is usually sufficient
if t here are no cardiovascular or neurological
emergencies.
186
↑ PRA
1. Cushings syndrome
2. Malignant hypertension
Rule out
1. Pseudo hypokalemia
(Leukocytosis > 1,00,000)
2. Redistribution - insulin,
Theophylline, catecholamines,
Thyrotoxicosis, periodic,
paralysis
Algorithm to Hypokalemia
Metabolic aalkalosis
Metabolic acidosis
1. Diarrhea
2. Renal tubular acidosis
3. DKA
True hypokalemia
Saline unresponsive
(U.cl > 10 meq/l)
Saline responsive
(U.cl < 10 meq/l)
1. Vomiting
2. Diuretics
3. Post hypercapnia
Hypertension
Normal blood pressure
1. Barters syndrome
2. Gitelan’s syndrome
3. Hypomagnesemia
↓ PRA
1. Liddle syndrome
2. Primary hyper aldosteronism
3. Apparent mineralo corticoid excess
187
Hyperkalemia
● Hyperkalemia is defined by serum pot assium >
5.5meq/ l.
● I t can be fat al by it s effect s on conduct ion sys-
t em.
● As serum pot assium increases ECG becomes pro-
gressively abnormal viz.
* Tent ing of T waves
* Prolonged PR and QRS int erval
* Flat t ened P waves, sine wave and asyst ole.
● Muscle paralysis can also be a feat ure of hyper-
kalemia.
Emer gency t r eat ment of hyper kal emi a
● Administ er inj .calcium gluconat e 10 ml of 10%
solut ion over 10 min. effect last s for 30-60 mins.
Repeat hourly
● I nfuse 25% dext rose 100 ml + 10 unit s of regular
insulin. The effect last s for 4- 6 hours
● Salbut amol nebulisat ion 10 mg ( 2- 8 t imes t he
normal dose).
● Note: All t hree st eps are t o be combined. All
t hese can buy t ime before pat ient reaches t he
t ert iary care cent er for dialysis.
Rule out Pseudo hyperkalemia
Thrombocytosis
Leucocytosis
Tourniquet
Exercising the limb
Algorithm to Hyperkalemia
Hyperkalemia
Redistribution
Severe acdiosis
Beta blockers
True Hyperkalemia
Mostly due to ↓ GFR
Take emergency measures and refer to
tertiary care centres
189
Endocrinology
Chapter 9
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
1. Diabet es Mellit us
* I nt roduct ion
* Classificat ion
* Approach t o a newly diagnosed Diabet ic
* Treat ment
» Oral Hypoglycaemic Agent s (OHA)
» I nsulin Therapy
» Medical Nut rit ion t herapy (MNT)
2. Gest at ional Diabet es mellit us
3. Complicat ions of DM
* Hypoglycemia
* DKA
* Diabet es and infect ions
* HHNKC
4. Microvascular Complicat ions
* Diabet ic Foot
* Diabet ic Ret inopat hy
* Diabet ic Neuropat hy
* Diabet ic Nephropat hy
5. Macrovascular Complicat ions
* DM and CAD
6. Prognosis of Diabet es mellit us
7. Hypot hyroidism
8. Hypert hyroidism
9. Hypocalcemia
10. Hypercalcemia
191
Diabetes Mellitus
I nt r oduct i on
Diabet es is world-wide in dist ribut ion and t he
incidence of bot h t ype 1 and t ype 2 diabet es is rising.
This global pandemic principally involves t ype 2 diabet es
and is associat ed wit h several cont ribut ory fact ors
including increased lon-gevit y,Obesit y,unsat isfact ory
diet ,sedent ary lifest yle, and increasing urbanisat ion.
Moreover t ype 2 diabet es is also commencing at an
earlier age in many populat ions, and in some et hnic
groups,such as Hispanic and Afro-Americans ,is now
being observed in children and adolescent s.I ndia ,a
fast developing nat ion is invariably set t o become t he
diabet ic capit al of t he World .
Def i ni tion
Diabet es Mellit us is a pan met abolic disorder
charact erised by chronic hyperglycemia wit h
dist urbances of carbohydrat e, fat and prot ein
met abolism due t o defect s in insulin secret ion or insulin
act ion or bot h.
Symptoms
● Polyuria -frequent passage of urine wit h in-
creased noct urnal frequency.
● Polydypsia - increased t hirst
● Polyphagia - abnormal excessive appet it e
● Weight loss
Associ at ed sympt oms and si gns :
● Giddiness or Dizziness
● Prurit is vulvae or Vaginal candidiasis
● Delayed wound healing
● Burning sensat ion of feet
● Ext reme fat iguabilit y
● Can present wit h acut e or chronic complicat ions
of Diabet es mellit us
Cl assi f i cat i on of Di abet es mel l i t us:
1. Type 1 Diabet es mellit us – B cell dest ruct ion; ab-
solut e insulin deficiency
2. Type 2 Diabet es mellit us – I nsulin Resist ance /
Relat ive I nsulin deficiency
3. Ot her Specific Types:
* Genet ic defect s of B cell funct ion – Mat urit y
Onset Diabet es in Young (MODY)
* Genet ic defect s of insulin act ion.
* Diseases of exocrine pancreas –
» Trauma
» Pancreat it is
» Pancreat ect omy
» Cyst ic fibrosis
» Fibrocalculous Pancreat opat hy
» Haemochromot osis.
* Endocrinopat hies.
* Drug induced or chemical induced –
* Pent amidine,
* Nicot inic acid,
* Glucocort icoids,
* Diazoxide,
* Thiazide diuret ics.
* I nfect ions et c.,
4. Gest at ional Diabet es mellit us (GDM)
Onset / Recognit ion of glucose int olerance in
pregnancy
192
APPROACH TO A NEWLY DIAGNOSED DIABETIC
Ketone
yes
Refer Text
Diet, lifestyle
changes, exercise
Obese Nonobese
Insulin
Sensitizers
Good Control
Combination
Insulin
Conventional
insulin
Insulin analogue
Short acting
Long acting
Intermediate acting
Mixed (more PHYSIOLOGICAl)
Absoluter indication:
T1Dm
DKA
HHS
GDM
Relative Indicator:
Newly diagnosed T2DM with
symptoms with Hyperglycemia
Poor control with OHA
Hepatic disease
Renal disease
Intercurrent illness
Allergy to OHA
Continue
Continue
Insulin
Secretogogues
Control
Continue
Yes
Yes
Yes
No
193
I nvesti gati ons
Di agnosi s of Di abet es mel l i t us: ( at l east one)
● Sympt oms of Diabet es mellit us and Random
Blood Sugar > 200 mg% ( mg / dl )
● Fast ing blood sugar > 126 mg % on more t han
one occasion
● 2 hours Plasma glucose > 200 mg % during oral
glucose t olerance t est wit h glucose – 75g Glu-
cose (or) 1.75gm / kg glucose in children.
Diagnostic values
Diabet es
Mellit us
Fast ing blood sugar > 126 mg %
Post-prandial blood sugar > 200mg%
I mpaired
Fast ing
Glucose
Fast ing blood sugar> 100 – 125 mg %
I mpaired
Glucose
Tolerance
Post-prandial blood sugar> 140 – 200
mg%
Treatment
Type 1 Di abet es mel l i t us:
● St rict meal plan
* Carbohydrat e: 50 - 60%
* Prot ein: 10 – 20%
* Fat : 30% (I f pat ient is dyslipidemic, fat should
be 15%)
* Caloric int ake: 30Kcal / kg
● Physical exercise
● Only insulin
Type 2 Di abet es mel l i t us:
● St rict meal plan
● Physical exercise
● Oral hypoglycemic agent s
● I nsulin
Oral hypoglycemic agents
Cl assi f i cat i on:
1. Sulphonyl ureas
2. B-iguanides
3. Sulphonylureas
» Glibenclamide
» Glipizide
4. Biguanides
* Met formin
DRUG DOSE
mg / day
t 1/ 2 SI DE EFFECTS
I nsulin secret ogogue (sulfonylureas)
Glibenclamide 1.25-20 10
hours
Hypoglycemia,
weight gain.
Glipizide 2.5-25 2-4
hours
Glimepride 1-8 9
hours
I nsulin sensit izer (Biguanides)
Met formin 500-
2000mg
1.5
- 4.9
hours
Nausea,
Vomit ing, GI
dist urbances.
Newer Drugs ( Thiazolidinediones)
Pioglit azone 15-45mg 16-24
hours
Anaemia,
weight gain,
fluid ret ent ion,
elevat ed liver
funct ion t est s.
Cont r ai ndi cat i ons f or sul phonyl ur ea t her apy
1. I nsulin dependent diabet es mellit us (I DDM)
2. Pregnancy
3. Pat ient s wit h severe infect ions
4. Allergic react ions
5. Significant liver and kidney disease
6. Pat ient s undergoing surgery
Bi -guani des
Mechanism of act ion of Bi-guanides
* I ncreases insulin sensit ivit y
* I ncreases peripheral glucose upt ake
* Decreases hepat ic gluconeogenesis
* I nhibit ion of glucose absorpt ion in int est ines
Cont r a-i ndi cat i ons t o Bi -guani de t her apy:
1. Renal failure when creat ine clearance < 40 ml /
min
2. Art eriography or int ravenous urography – as in-
t ravenous iodinat ed product s may precipit at e lac-
t ic acidosis on pat ient s wit h bi-guanides
3. Advanced liver cell failure
194
4. Alcoholism
5. Cardiac diseases
6. Diabet es wit h significant acut e and lat e complica-
t ions
7. Pregnancy
8. Old age > 70 years
Consi der i nsul i n as i ni t i al t her apy i n pat i ent s
wi t h:
● Fast ing plasma glucose > 250-300 mg/ dl since
more rapid glycemic cont rol will reduce glucose
t oxicit y t o islet cells, improve insulin secret ion
and possibly make oral hypoglycemic agent s
more effect ive.
● Lean pat ient s or t hose wit h severe weight loss.
● Underlying renal or hepat ic disease.
● Hospit alized or acut ely ill pat ient s.
● I f response t o oral hypoglycemics is not ade-
quat e. Consider insulin as init ial t herapy.
Start with intermediate acting insulin (NPH) or a long acting
insulin (NPH) or a long acting insulin Glargine or Detemir
10 units at bed time or 0.2 units per kg/weight
If HbA1C > 6.5% and Post prandial glucose values
are high > 200 mg/dl
Algorithm to Insulin Therapy
195
Target,if not achieved to add thiozolidinedione
Tab Pioglitazone 15-30 mg /day.
If still inadequate control, then add glucosidase
inhibitor Tab Acarbose 25-50 mg with meals
or consider insulin at this stage
HbAıC
HbAıC
HbAıC,
Algorithm for treatment of patients of Type 2 diabetes
120 mg/dl–180 mg/dl.
mg/dl.
PA view
196
Medical Nutrition Therapy (MNT)
A non-pharmacological mode of management of
diabet es. Medical Nut rit ion t herapy is individualized
and should be a t ailor made regimen. I t is used as a
compliment for an oral glucose lowering agent / insulin
t herapy.
Ener gy Recommendat i ons:
● This depends on body weight and physical act iv-
it y.
* 20 kcal/ kg I deal body weight – Sedent ary
worker
* 30 kcal/ kg I deal body weight – Moderat e
worker
* 40 kcal/ kg I deal body weight – For heavy
worker
I n obese peopl e
● Reduce 500 kcal from t he calculat ed energy re-
quirement
For under wei ght
● Add 500 kcal t o t he calculat ed energy require-
ment
* Of t he t ot al kcal, 45-65 % kcal from carbohy-
drat e and 10-25 % kcal from prot eins
Fat r ecommendat i on :
● 500ml / mont h of a blend of oils / individual
● Gingelly oil and any refined veget able oil could
be used (or)
● Rice brand oil and any refined veget able oil
Fi br e r ecommendat i on
● 14gm/ 1000kcal provided.
Fl ui d r ecommendat i on:
● 8 t o 10 glasses / day of wat er except in LVF, CKD,
Cirrhosis et c.
MNT i n Gest at i onal Di abet es Mel l i t us:
● 30 kcal / kg I nst ant Body weight in first t rimest er
● 30 kcal / kg I nst ant Body weight + 300 kcal/ day
in I I nd and I I I rd t rimest er
● Prot ein - 1gm/ kg I nst ant Body weight + 10gm
daily t hroughout pregnancy
● Avoid hypocaloric diet s in obese GDM
● Provide compulsory bed t ime and evening snack
t o avoid accelerat ed st arvat ion and noct urnal hy-
poglycemia
Gest at i onal Di abet es mel l i t us:
● St rict meal plan
● Physical exercise
● I nsulin
Ot her speci f i c t ypes
● St rict meal plan
● Physical exercise
● I nsulin wit h or wit hout Oral hypoglycemic agent s
Gestational Diabetes mellitus
Def i ni tion
Gest at ional diabet es mellit us is defined as
carbohydrat e int olerance of variable severit y wit h onset
or first recognit ion during t he present pregnancy.
Ri sk f or gest at i onal di abet es mel l i t us:
● Age more t han 25 years
● Family hist ory of diabet es mellit us
● Hist ory of unexplained fet al loss
● Hist ory of baby being large for gest at ional age
● Hist ory of congenit ally malformed infant
● Mat ernal obesit y
● Hist ory of Polycyst ic ovarian disease
● Polyhydramnios
● Pre-eclampsia
● Unexplained int raut erine deat h
Met hods of scr eeni ng;
● Spot t est : Fast ing < 90 mg% [ normal 2 hr post-
prandial < 120 mg% random < 105 mg% values]
ADA recommends
197
One step approach Two step approach
100 gm OGTT Glucose challenge test
oral glucose tolerance
test with 50 gm of glucose
1 hr value > 130mg %
oral glucose tolerance
test with 100 gm of glucose
Methods of screening
Di agnost i c Cr i t er i a:
Car pent ar Coust an ( wi t h 100 gm)
F - 95 mg %
1 hr - 180 mg %
2 hr - 155 mg %
3 hr - 140 mg %
WHO cr i t er i a ( wi t h 75 gm of gl ucose )
F - 95 mg %
1 hr - 180 mg %
2 hr - 155 mg %
I f any t wo values equals or crosses normal value,
it is t ermed as Gest at i onal Di abet es mel l i t us.
I mpor t ant Not e
OGTT value should never be t reat ed.
Treatment
1. Medical Nut rit ion Therapy [ refer MNT]
2. I nsulin is essent ial if MNT fails t o achieve eugly-
cemia
Tar get Gl ycemi c Level
Fast ing glusose – 90 mg %
2 hr post prandial – 120 mg %
Mean glucose – 105 mg %
Moni t or i ng Gl ycemi c Cont r ol
● Blood glucose fast ing and post prandial every
t hree days t ill glycemia is achieved; t hen every
fort night ly, t hroughout first and second t rimest er.
● Every week in t hird t rimest er.
● Glycemic profile monit oring once in 1
st
and 2
nd

t rimest er and t hen every mont h in last t rimest er.
Complications of Diabetes mellitus
Acut e compl i cat i ons:
● Hypoglycemia
● Diabet ic Ket o Acidosis (DKA)
● Diabet es and infect ions
● Hyperosmolar Hyperglycemic St at e (HHKNC)
Chr oni c compl i cat i ons:
Follow t he flow chart below
Microvascular Macrovascular
Neuropathy
Nephropathy
Retinopathy
Coronary Artery Disease (CAD)
Chronic complications
Hypogl ycemi a
.
Def i ni tion
Hypoglycemia is a clinical emergency occurring
in diabet es charact erized by eit her aut onomic or
neuroglycopenic sympt oms (or) biochemically random
blood sugar < 70mg, due t o ant idiabet ic agent , food
and act ivit y mismat ch.
Symptoms
198
Aut onomic sympt oms
● Tremor
● Palpit at ion
● Sweat ing
● Sensat ion of hunger
Neuroglycopenic sympt oms
● Head ache
● Fat igue
● I rrit abilit y
● Dist urbed vision
● Ment al confusion
● Personalit y changes
● Convulsion,night mares
● Coma
Hypoglycemic sympt oms in children
● Rest lessness, rolling (or) frequent falling from
t he bed
● Sudden changes in behavior
● I rrit abilit y
● Crying.
Treatment
● Draw blood sample immediat ely
● Dext rose supplement at ion
* Conscious: Oral Glucose, Sugar, Fruit Juice
* Unconscious: 50% Dext rose 100ml I V St at .
Followed by 10% Dext rose t hen by 5% DNS
Maint enance (or) I nj . Glucagon 1mg im if not
accessible t o int ravenous rout e
● Pat ient st ill remains unconscious
* To rule out cerebral edema
* I f present I V mannit ol + I nj . Dexamet hasone
8mg I V
● St op t he ant idiabet ic agent s for 3 days in Type 2
Diabet ic mellit us pat ient s and recheck blood sug-
ars. I n Type 1 Diabet ic mellit us pat ient s recheck
blood sugars aft er 6 hrs and adj ust insulin dose
accordingly.
● I dent ify t he cause of hypoglycemia
● I f recurrent hypoglycemia, rule out
* Renal funct ion disorder
* Liver funct ion disorder
● Repeat blood sugar value aft er hypoglycemia cor-
rect ion and monit or blood sugars
Referral:
I f t he pat ient remains unconscious even aft er
dext rose administ rat ion refer t he pat ient immediat ely
t o higher cent re for furt her evaluat ion.
I mpor t ant Not e
Pat i ent Educat i on:
● Educat e pat ient and his family members about
low blood sugars and sympt oms
● Never miss a meal aft er insulin / Oral hypoglyc-
emic agent s
● Be caut ious of unaccust omed physical act ivit y
● To carry diabet ic ident it y card
● Always carry simple sugar (biscuit s and t offee) t o
avoid low sugars.
Diabetic Ketoacidosis (DKA)
Symptoms
Suspect DKA in a diabet ic pat ient when he has
● Alt ered sensorium
● Unexplained abdominal pain
● Nausea
● Vomit ing
● Breat hlessness
● I ncreased respirat ory rat e ( Kussmaul’s breat h-
ing )
● Signs of dehydrat ion.
● Thirst
● Polyuria
I nvesti gati ons
● Blood glucose [ usually > 250 mg %]
● Blood Urea [ may or may not be ↑]
● Serum Creat inine [ may or may not be ↑]
● Serum elect rocyt e [ Na ↑ or ↓, K ↑ or ↓]
● Serum Bicarbonat e < 10 mmol / l
● Urine sugar [ posit ive]
● Urine Acet one [ posit ive]
● Chest X-ray
199
● ECG
● Ult rasonogram abdomen / KUB
Treatment
Rehydrat ion wit h normal saline
Hours Volume
1
st
half hour – 1 hour 1 L
2
nd
hr 1 L
3rd hr 500 ml-1L
4
t h
hr 500 ml-1L
5
t h
hr 500 ml-1L
Tot al 1
st
- 5
t h
hr 3.5-5 L
6
t h
– 12
t h
hr 250-500 ml/ hr
NS for first 4 hrs Consider half NS t hereaft er
May need t o adj ust t ype and rat e of fluid adminis-
t rat ion in t he elderly and in pat ient s wit h cardiac
and renal compromise
I nsul i n i nf usi on
St art regular insulin infusion at 5 unit s/ hr and t i-
t rat e infusion depending on blood sugars.
El ect r ol yt e i mbal ance
● I f pot assium > 5.5, and if pat ient is anuric – no
pot assium infusion
● Avoid rapid correct ion of
* Dehydrat ion
* Hyperglycemia and
* Elect rolyt e imbalance.
Ref er r al :
● Refer t he pat ient t o a higher cent re if:
* Pat ient is comat ose
* Hypot ension requiring ionot ropic support
* Anuric
* Elevat ed renal paramet ers
* Evidence of sept icemia
Diabetes and Infections
Bot h diabet es and it s complicat ions predispose
t o infect ions.
Causes
Cont ribut ing
fact or
Mechanism Effect
Hyperglycemia Alt ers leucocyt e
funct ions
I mpairs
phagocyt osis
Defect ive leukocyt e
adherence
Predisposes
t o infect ion
Neuropat hy Foot t rauma Foot
infect ion
Aut onomic-
neuropat hy
Bladder dysfunct ion
Reduced sweat ing
UTI
I nfect ions
Dry skin
I nf ect i on and Or gani sms
Hyper gl ycemi a ket osi s syndr ome
Secondary infect ions in a diabet ic can aggravat e
hyperglycemia and leading t o ket osis analysis.
Hyperglycemic hyperosmolar non-ketotic
coma (HHNKC)
Def i ni tion
I t is an acut e met abolic complicat ion in middle aged
and elderly diabet ics wit h high morbidit y and mort alit y.
Causes
Precipat ed by
● I nfect ion
● Trauma
● Burns
● I nfarct ion
● Hyper-aliment at ion
● Drugs like
* Thiazide
* Cimet idine
* Phenyt oin and
* Parent ral diuret ics
Symptoms and si gns
● Polyuria
● Polydipsia
● Severe hyperglycemia (Blood sugar > 600 mg%)
● Profound dehydrat ion
● Elevat ed osmolalit y
● Hemianopia, muscle fasciculat ion, seizures
200
● Alt ered sensorium, coma
Treatment
1. Fluid replacement : ½ normal saline at t he rat e of
2 lit re in 1st 2 hours and 1 lit re in anot her 2 hours
2. Low dose insulin.
3. Correct ion of elect rolyt es and hyperosmolalit y
4. Low-dose heparin t o prevent vascular t hrombosis
int ravascular coagulat ion.
I nfect ion Organisms Treat ment
Skin and soft t issue infect ion
Carbuncle
Necrot ising cellulit is
St aphlococcus
St rept ococcus
Gram negat ive
clost ridium
Appropriat e ant ibiot ics
Eye
St ye
Blepharit s ,dacrocyst it is
St rept ococcus Appropriat e ant ibiot ics
Dent al sepsis
Gingivit is Pyorrhea
Anaerobes Appropriat e ant ibiot ics
Ear
Malignant Ot it is ext erna
Pseudomonas Ceft riaxone,
Ticarcilin
Nose
Mucor mycosis
Rhinocera
Fungus
Prognosis bad
Lung
Pulmonary TB,
Bact erial pneumonia
Mycobact erium Ant i-t uberculosis t reat ment
Gal l Bl adder
Emphysemat ous cholecyst it is
Clost rit idia Appropriat e ant ibiot ics
UTI
Asympt omat ic bact eriuria
Emphysemat ous pyelonephrit is
Emphysemat ous cyst it is
Balanopost hit is
Vulvo vaginit is
E Coli
Candida
Appropriat e ant ibiot ics
Topical Clot rimazole and oral ant i
fungals if necessary
Distinguishing features between
DKA and HHNKC
Crit eria DKA HHNKC
Age Younger Older
Respirat ion Hypervent ilat ion,
deep
Normal,
shallow
Dehydrat ion Around 10 % Around 25
%
Consciousness Diminished Comat ose
Temperat ure Normal or low May be
raised
Blood glucose > 300 mg/ dl > 600 mg/
dl
Blood urea 42 – 70 mg/ dl 60 – 180
mg/ dl
Sodium 125 – 140
mmol/ l
130 – 155
mmol/ l
Pot t assium 3 – 6.5 mmol/ l 3 – 5
mmol/ l
Bicarbonat e < 14 mmol/ l 16 – 30
mmol/ l
Ket ones + + To + + + 0 t o +
201
Micro- vascular complications
Di abet i c f oot
Causes
Most ly pol ymi cr obi al infect ion
Bact eroids are t he commonest group
Neuropat hy and ischemia lead t o DFS
I nvesti gati ons
1. Blood rout ine and urine rout ine
2. Urine cult ure sensit ivit y
3. Blood cult ure sensit ivit y
Treatment
1. I mpat ient care
2. I nsulin is t he t reat ment of choice except for mild
infect ions
3. Mild infect ions can be managed wit h OGLA
4. Always suspect Tuberculosis since Tuberculosis
and diabet es are concomit ant infect ions
Diabetic retinopathy
1. Definit ion and Classificat ion
2. Screening
3. General recommendat ions
4. Treat ment
Def i ni tion
Diabet ic ret inopat hy is a micro vascular complicat ion
of diabet es affect ing t he vascularit y of t he eye. (Ret ina)
Classifcation of Diabetic retinopathy (DR)
Grade Sympt oms
1. Non Proliferat ive
diabet ic ret inopa-
t hy (NPDR)
a. None
b. Early NPDR
c. Mild NPDR
d. M o d e r a t e
NPDR
e. Severe NPDR
(‘4/ 2/ 1’ rule)
f. Very severe
NPDR
2. Proliferat ive Dia-
bet ic ret inopat hy
(PDR)
* PDR wit hout
high risk chang-
es (HRC)
* PDR wit h HRC
Normal ret ina
Micro Aneurysms (MA)
only
MA (+ )
Ret inal haemorrhages
and / or
Hard exudat es (HE)
(Ext ra macular i.e > 1
DD from fovea)
Mild NPDR (+ )
Haemorrhages and
or Cot t on wool spot s
(> 5) and / or
Venous beading /
looping (or) I RMA* in
one field
Moderat e NPDR (+ )
MA / Hages in 4 (or)
more fields (OR)
Venous beading /
looping in 2 (or) more
fields (OR)
I RMA * in one quad-
rant
Any t wo (or) more of
t he ‘severe’ cat egory
NVE* * or NVD* * *
< 1/ 2 DD
NVE or NVD> ½ DD
Pre-ret inal and / or vit-
reous haemorrhages
* I RMA – I nt ra Ret inal Micro Vascular Abnormalit ies
* * NVE – New Vessel Elsewhere * * * NVD- New Vessel
Disc.
202
Scr eeni ng
Dilated and comprehensive
examination by an
Ophthalmologist
Frequent follow up if DR is progressing
T
1
DM 5 years after onset of DM T
2
DM shortly after the diagnosis of DM
Once in 6 months (follow up)
● DR is a highly specific vascular complicat ion of
bot h T1 DM and T2 DM pat ient s
● The prevalence of ret inopat hy is st rongly relat ed
t o t he durat ion of diabet es.
● DR is t he most frequent cause of blindness in
adult s.
DR and Pr egnancy
● Eye examinat ion: Once in every t rimest er, 6 wks.
aft er delivery, upt o one year
● Pat ient s should be counseled on t he risk of devel-
opment and / or progression of DR.
General Recommendations
Gl ycemi c cont r ol :
● Opt imal glycemic cont rol
* Reduced risk and progression of DR.
● Reduct ion of HbA1c by 1%
* Reduces t he relat ive risk of development of
micro vascular complicat ions by 37%
● Opt imal Blood Pressure Cont rol:
* Reduced risk and progression of DR.
● Diabet ic Nephropat hy is associat ed wit h DR.
Treatment
● Laser Therapy
* Can reduce t he risk of vision loss in pat ient s
wit h high risk changes.
● Prompt referral of pat ient s. wit h any level of mac-
ular oedma, severe NPDR or any PDR
● I ndicat ions for laser t herapy
* Clinically Significant Macular Oedma (CSME)
* Mild (or) Moderat e NPDR
* Severe NPDR / PDR wit h out HRC
* PDR wit h HRC
* NVD (or) NVE wit h Pre ret inal haemorrhage
and / or Vit reous haemorrhage .
Diabetic nephropathy
Def i ni tion
Diabet ic Nephropat hy is defined as progressive
increase in urine albumin, accompanied by rising blood
pressure and declining GFR result ing in end st age renal
disease associat ed wit h ret inopat hy and increased
cardio vascular risk.
Symptoms
● Puffiness of face
● Swelling of legs
● Abdominal dist ent ion
● Reduced urine out put .
Si gns :
● Bilat eral. pedal edema
● Renal angle t enderness
● Abdominal bruit
I nvesti gati ons
Increased Urea
with altered sensorium
Referral to a higher centre
Screening for Diabetic Nephropathy
Three consecutive urine samples
Blood Urea
Serum Creatinine
203
Diabetic Neuropathy
I nt r oduct i on:
Diabet ic Neuropat hy is t he most common compli-
cat ion of Diabet es mellit us.
● I t is a micro-vascular complicat ion
* Endo-neural hypoxia due t o involvement of
micro vascular disease and vasa nervorum
involvement .
* Hyperglycemia plays a dominant role in t he
pat hogenesis of diabet ic Neuropat hy.
Polyneuropat hy
Mononeuropa-
t hy
Aut onomic
neuropat hy
● Sensory
● Proximal
● Truncal
● Mot or
● I solat ed
● Cranial
● Truncal
● Mult iple
● Parasympa-
t het ic
● Sympat het -
ic
Symptoms
1. Burning, shoot ing, st abbing pain of bot h feet
2. “ Pins and needles” sensat ion
3. Absent sensat ion t o several modalit ies
4. Numbness of bot h feet
5. Depressed reflexes
6. Muscle paralysis
Cl i ni cal Feat ur es
Types:
● Large fibre t ype
● Small fibre t ype
Large fbre type
● Unst eady gait
● Absent reflexes
● Reduced vibrat ion / posit ion sense
● Mimics post erior column lesion
Small fbre type
● Pain predominat es
● Variable reflexes
● Variable posit ion / vibrat ion sense
Sympt oms
Di abet i c Aut onomi c Neur opat hy ( AN)

Cardiovascular system
Postural hypotension
Painless MI
Resting tachycardia
Symptoms of
Autonomic Neuropathy
Urogenital
Bladder dysfunction.
Impotence
Retrograde ejaculation
Gastro intestinal tract
Impaired GI motility
Gastric atony
Diarrhoea
Hypoglycemia
Hypoglycemic unawareness
Vasomotor
Loss of skin vasomotor
response
Peripheral vascular changes
Dependent edema
Treatment
1. St rict glycemic cont rol
2. Most of t he following drugs offer only sympt o-
mat ic relief but don’t essent ially reverse t he dis-
ease process
* Tricyclic ant idepressant s
* Ant iconvulsant s
* Ant i-oxidant s
* Topical Capsaicin
* Aldose reduct ase inhibit ors
* Met hylcobalamine
* Pre-gabalin
Ref er r al
Pat ient s wit h severe sensory mot or neuropat hy wit h
aut onomic neuropat hy need referral t o a higher cent re
for furt her evaluat ion.
Macrovascular complications in Diabetes
mellitus
Di abet es mel l i t us and hear t :
I nt r oduct i on :
Heart is involved in many ways in diabet ic pa-
t ient s and t hey are
1. Coronary art ery disease (CAD)
2. Cardiomyopat hy
3. Cardiac aut onomic neuropat hy
4. Heart failure
Cor onar y Ar t er y Di sease ( CAD)
I t is a maj or macrovascular complicat ion seen in
diabet ics. There is a t wo t o four fold increased risk of
CAD in diabet ic pat ient s.
204
Symptoms
● They can present wit h
* Acut e coronary syndromes
* Classical angina
* Silent ischaemia.
● Silent ischaemia and infarct ion are very common
in diabet ics due t o cardiovascular aut onomic neu-
ropat hy.
● At ypical sympt oms such as
* Confusion
* Dyspnoea
* Rest lessness
* Unexplained fat igue
* Sweat ing should alert t he clinician t o rule out
silent infarct ion.
● Diabet es is a risk fact or for cardiogenic shock and
acut e left vent ricular failure in t he set t ing of ACS.
I nvesti gati ons
ECG, ECHO, TMT and advanced invest igat ion if
required.
Treatment
● Admission may be required based on t he clinical
st at us and ECG changes of t he pat ient .
● I t is safe t o swit ch over t o I nsulin t herapy
● Drugs
* Aspirin
* Cardio Select ive bet a blockers
* ACE- I nhibit ors
* St at ins.
Ref er r al :
Pat ient may be st abilised and referred t o a higher
cent re for specialit y care.
Prognosis
I t depends on periodical monit oring and regular
follow up:
● Type I Diabet es mellit us:
* Wit h good glycemic cont rol screen for compli-
cat ions 5 yrs aft er diagnosis
● Type 2 Diabet es mellit us:
* Screen for complicat ions at t he t ime of det ec-
t ion and yearly aft erward.
● Gest at ional Diabet es mellit us:
* Good prognosis for bot h mot her and child if
mot her achieves and maint ains good glycemic
cont rol
● Specific t ypes
* Depends on et iological fact or
Not e:
● All pat ient s should be given chronic follow up
card/ book
● Pat ient who need t o be st art ed on insulin t herapy
should be t aught for insulin inj ect ion t echnique
Hypothyroidism
Causes
Hypot hyroidism may be primary; common causes of
which are aut oimmune, iat rogenic due t o I
131
, ant it hyroid
or lit hium t reat ment and t hyroidect omy, or secondary t o
pit uit ary or hypot halamic disease.
Symptoms
● Coarse dry skin
● Hoarseness of voice
● Facial puffiness, weight gain
● Cardiac enlargement and/ or pericardial effusion,
● Goit er wit h or wit hout prolonged relaxat ion phase
of deep t endon reflexes.
● Myxedema coma is a rare complicat ion of se-
vere hypot hyroidism wit h hypot hermia, hypoven-
t ilat ion, hyponat remia, hypoxia, hypercapnia and
hypot ension.
I nvesti gati ons
● Diagnosis is confirmed by
● Low serum free T
3
and T
4
● serum TSH raised in t hyroid t ypes and low in su-
pra-t hyroid t ypes
● Thyro-peroxidase ( TPO)
* Thyro-peroxidase ant ibodies are seen in 90-
95 % of pat ient s present ing wit h aut oimmune
hypot hyroidism
Treatment
205
● Pharmacological
* Tab. L-Thyroxine 50 – 100mcg/ day
* Dose t o be adj ust ed based on TSH levels
* Goal is normal TSH (lower half of reference
range
* Measure TSH levels aft er about 2 mont hs of
inst it ut ing t herapy
* Adj ust by 12.5 or 25 mcg increment s if TSH
is high; decrement of t he same if TSH is sup-
pressed.
* When full replacement is achieved t hen follow
up measurement at annual int ervals and lat er
by a 2-3 year int erval
* Ensure ongoing compliance.
Speci al t r eat ment consi der at i ons
● A hypot hyroid woman should be eut hyroid prior
t o concept ion and during early pregnancy (effect
on foet al neuronal development )
● Elderly require less Thyroxine (less by upt o 20%)
especially t hose wit h coronary art ery disease,
st art ing dose 12.5mcg/ day wit h similar incre-
ment s every 2- 3 mont hs unt il TSH level is nor-
malized.
● I n hypot hyroidism due t o low TSH (supra-t hyroid
cause is suspect ed) det ailed invest igat ions are
required and pat ient should be referred t o a t ert i-
ary care level
● Asses t he response clinically and by serum TSH
(serum T
3
in suprat hyroid t ype) at 8 weekly in-
t ervals
● Once eut hyroid st at e is rest ored, follow-up at
6-12 mont hly int ervals.
Tr eat ment of Myxedema coma
● Warm blanket s, mechanical vent ilat ion for respi-
rat ory failure.
● Correct ion of met abolic dist urbances and t reat
precipit at ing fact ors.
● Drugs
* L-Thyroxine 500 mcg I V bolus, t hen 50-
100mcg I V daily
* I f int ravenous preparat ion not available, t he
same dose is administ ered t hrough Ryle’s
t ube.
* Once acut e phase is over, maint ain L-Thyrox-
ine as above.
* I nj .Hydrocort isone 100 mg I V st at , 25-50 mg
8 hourly.
● Caut i on: Avoid sedat ives
Pat i ent Educat i on
● L-Thyroxine should be t aken as a single daily
dose, ideally on awakening, at least 30 minit es
before breakfast .
● Fibre and bran product s (e.g., I sapghola husk)
may impair absorpt ion, as also cholest yramine,
cholest ipol, iron sulphat e, sucralfat e, aluminium
hydroxide
● Met abolism of L-Thyroxine is increased by Pheny-
t oin, Rifampicin, and carbamazepine.
● Expl ai n t o t he pat i ent t hat t he t r eat ment i s
l i f e l ong. Do not modify dose or st op t reat ment
wit hout consult at ion.
● Over t reat ment may lead t o decreased bone min-
eral densit y and adverse cardiac complicat ions.
Ref er ences:
1. An updat e on management of hypot hyroidism
and Hypert hyroidism. Arch I nt ern Medicine 2000;
160: 1067 – 1071
2. Disorders of Thyroid Gland. . I n: Harrison’s prin-
ciples of medicine.
Kasper DL, Braunwald E, Fauci AS et al (eds),
16
t h
edit ion, 2005, McGraw-Hill Company I nc.,
New York, pp 2104-2127.
Hyperthyroidism
Causes
Classically occurs in Grave’s disease, which is
charact erized by diffuse goit er, Opt halmopat hy and
Dermopat hy in varying combinat ions. Ot her import ant
causes are Toxic Mult inodular Goit er ( TMN) and t oxic
adenomas.
Symptoms
● Sweat ing
● Tremors
● Wide pulse pressure
● Sinus t achycardia and at rial arrhyt hmias
206
● Worsening of angina or cardiac failure may pre-
dominat e in older pat ient s
● Graves’ disease
* Goit er
* Opt halmopat hy and
* Dermopat hy
I nvesti gati ons
Diagnosis is confirmed by low t o undet ect able serum
TSH and increased Serum free (FT
3
) and free (FT
4
)
Treatment
Phar macol ogi cal
● Adj unct ive t reat ment
* For adrenergic sympt oms such as
sweat ing, t remor and t achycardia.
Tab. Propranalol 40 – 120 mg a day.
● Tab. Propylt hiouracil 100 – 150 mg every 6 – 8 hours or
Tab. Carbimazole 10 – 20 mg every 8 – 12 hours;
● Aft er eut hyroid st at e is achieved in 6 – 8 weeks
once daily dose possible.
● Review wit h serum TSH and FT
3
aft er 3 – 4 weeks
t reat ment has been init iat ed
● Once cont rolled reduce t o t he smallest effect ive
dose or cont inue init ial dose combined wit h L-
Thyroxine
● Drugs are given for an average of 2 years.
Def i ni t i ve t r eat ment i s sur ger y/ abl at i on of
t hyr oi d t i ssue
● Subt ot al t hyroidect omy in younger pat ient s (< 30
years) in whom ant it hyroid t herapy has been un-
successful and in very large goit ers.
● Radioact ive iodine (I
131
):
● Met hod of choice in
* Elderly
* Younger pat ient s who have complet ed family
wit h recurrent t hyrot oxicosis following surgery
or when surgery is refused or cont raindicat ed.
Caut i on
Radioact ive iodine should never be given in
pregnancy. I n woman of childbearing age if radioact ive
iodine is planned, a pregnancy t est should always be
carried out .
Pr egnancy
● I n pregnant woman surgery should not be per-
formed in 1
st
or 3
rd
t rimest ers
● Ant it hyroid drugs are less risky but may induce
hypot hyroidism in t he foet us and should be used
in t he smallest necessary dose t o keep serum
TSH and FT
4
in normal range.
● Propylt hiourcil is preferred – usual maint enance
is 200 mg/ day. I f > 300 mg/ day required during
1
st
t rimest er, Subt ot al t hyroidect omy is indicat ed
in 2
nd
t rimest er
● Propranalol should be avoided as it can cause
foet al growt h ret ardat ion and neonat al respira-
t ory depression.
Opht hal mopat hy
Refer t o opht halmologist .
I nit iat e t herapy in mild cases wit h elevat ion of
head at night , diuret ics t o decrease edema, use of
t int ed sunglasses and 1 % met hyl cellulose eye drops
t o prevent drying and refer pat ient s wit h severe and
progressive exopht halmos t o an opht halmologist .
Toxi c mul t i nodul ar goi t er
● Radioact ive iodine is t he t reat ment of choice.
● Large doses are usually required
● Treat ment wit h ant it hyroid drugs given t ill pat ient
is eut hyroid.
● Propranalol may be useful before and aft er radio-
act ive iodine administ rat ion.
Thyr ot oxi c cr i si s or t hyr oi d st or m
● Refer t o a t ert iary care cent re.
● Life t hreat ening hypert hyroidism wit h fever, vom-
it ing, diarrhoea, j aundice, delirium and coma;
● Usually precipit at ed by acut e illness such as
st roke, infect ion, diabet ic ket oacidosis, t rauma,
pat ient s undergoing surgery or radioact ive iodine
t reat ment in a poorly prepared pat ient :
Treatment
● Tab. Propylt hiourcil 600 mg loading dose, t hen 200
– 300 mg every 6 hours orally or t hrough Ryle’s t ube.
O r
Tab. Carbimazole 15 – 25 mg 6 hourly.
● 1 hour aft er t he 1
st
dose of ant it hy-
207
roid drug, sat urat ed solut ion of Pot as-
sium iodide (SSKI ) 5 drops every 5 hours.
O r
Lugol’s iodine 10 drops 3 t imes a day.
O r
Sodium iodide 1 g I V slowly.
● Tab. Propranalol 40 – 60 mg 4 hourly or 0.5 – 2
mg I V every 4 hours.
● I nj . Dexamet hasone 2 mg I V 6 hourly
● Cont inue iodides and dexamet hasone unt il nor-
mal met abolic st age is achieved and give sup-
port ive t reat ment such as cooling, ant ipyret ics,
ant ibiot ics for infect ion, int ravenous fluids, et c.
● Once eut hyroid st at us is achieved, manage as al-
ready out lined.
Pat i ent educat i on
● I f fever or sore t hroat develops on ant it hyroid
drugs complet e blood count should be done; dis-
cont inue if polymorphs count is < 1500/ mm
3
● I f allergic rash or drug hypersensit ivit y develops,
give ant ihist amines and preferably change t o an-
ot her drug
● I f agr anul ocyt osi s, hepat i t i s, dr ug f ever ,
ar t hr al gi as devel op, pr ef er abl y st op an-
t i t hyr oi d t r eat ment .
● I odide - useful in impending Thyrot oxic crisis
and pat ient s wit h severe cardiac disease; must
be used only aft er following ant it hyroid drugs.
Ref er ences
● An updat e on management of hypot hyroidism
and Hypert hyroidism. Arch I nt ern Medicine 2000;
160: 1067 – 1071
● Disorders of Thyroid Gland. . I n: Harrison’s prin-
ciples of medicine. Kasper DL, Braunwald E, Fauci
AS et al (eds), 16
t h
edit ion, 2005, McGraw-Hill
Company I nc., New York, pp 2104-2127.
Hypocalcemia
Causes
Hypocalcemia may be caused by hypoparat hyroidism,
pseudo hypoparat hyroidism, vit amin D deficiency
st at es, chronic renal failure, mala-bsorpt ion syndrome
and hypomagnesaemia.
Symptoms
● Circumoral parast hesias
● Muscle cramps
● Confusion
● Tet any
● Convulsion
● Posit ive Chovst ek’s and Trousseau’s sign
I nvesti gati ons
● ECG may reveal prolongat ion of QT int erval.
● Tot al serum calcium < 8.5 mg/ dl
● I n hypoalbuminemia, add 1 mg/ dl of calcium t o
t he est imat ed level for every 1 g fall of albumin
below 4 g/ dl (correct ed serum calcium).
Treatment
Sever e sympt omat i c hypocal cemi a
● 20 ml of 10 % calcium gluconat e solut ion over 10
– 15 mins followed by 60 – 80 ml of 10 % solu-
t ion in 1 L of 5 % dist illed wat er (0.5 – 0.25 mg/
kg/ hour element al calcium)
● Caut i on: should not be mixed wit h bicarbonat e
solut ion as it may result in precipit at ion of cal-
cium carbonat e
● I f associat ed wit h hypomagnesaemia
* I nj . Magnesium sulphat e 1 – 2 g I V day 1 fol-
lowed by oral Magnesium oxide 600 – 1200
mg 3 t imes a day t o replenish st ores.
Asympt omat i c Hypocal cemi a/ mai nt enance
t r eat ment
● Treat t he underlying cause if possible. Usually
long-t erm t reat ment is required in condit ions
such as hypoparat hyroidism, pseudohypoparat h-
yroidism and chronic vit amin D deficiency st at es.
Treatment
● Tab. calcium carbonat e (40 % element al calci-
um by weight ) 1 –2 g element al calcium orally
3 t imes a day init ially and subsequent ly maint e-
nance dose of 0.4 – 1.5 g 3 t imes a day
● I n chronic renal failure calcium alone gives in-
adequat e result s. However, correct concomit ant
hyper-phosphat emia before inst it ut ing following
t herapy: Vit amin D 5000 I U/ day for 1 – 2 weeks,
t hen weekly or bimont hly
208
● Calcit riol 1,25 (OH)2D3 0.25 mcg orally daily –
more expensive but less t oxic t han vit amin D for
hyperphosphat emia
● Advise low phosphat e (low cereal) diet and phos-
phat e binding agent s e.g., aluminium hydroxide.
Pat i ent educat i on
● Side effect s of oral calcium carbonat e are dys-
pepsia and const ipat ion.
● Absorpt ion requires gast ric acid and is impaired
in achlorhydria or when acid suppression t herapy
is given.
● Serum calcium should be monit ored frequent ly
(daily in severe hypocalcemia, weekly wit h mod-
erat e hypocalcemia for first mont h) and main-
t ained at 8.0 – 8.6 mg/ dl, and PTH and 24 hour
urinary calcium wit hin 2 – 4 weeks of st art ing
t reat ment .
● Once Serum calcium and urinary calcium is nor-
mal and PTH falls, maint enance t reat ment as de-
scribed wit h reassessment at 3 mont hly int ervals.
Ref er ences
● Diseases of Parat hyroid gland and ot her hyper
and hypo-calcemic disorders. I n: Harrison’s prin-
ciples of medicine Kasper DL, Braunwald E, Fauci
AS et al (eds), 16
t h
edit ion, 2005, McGraw-Hill
Company I nc., New York, pp 2249-2268.
● Calcium I n: The Washingt on Manual of Medical
Therapeut ics, Ahya SN, Flood K. Paranj ot hi S
eds., 30
t h
edit ion, 2001. Philadelphia: Lippincot t ,
Williams and Wilkins, pp-60-66
Hypercalcaemia
Causes
The common causes are hyperparat hyroidism and
malignancy; ot hers include vit amin D act ion, high bone
t urnover or renal failure.
Symptoms
● Fat igue, depression, confusion, anorexia, nau-
sea, vomit ing, const ipat ion, Polyuria,
I nvesti gati ons
● short QT int erval on ECG and occasionally cardiac
arrhyt hmias. Generally sympt oms appear when
serum Ca > 11.5-12.0 mg/ dl; severe hypercal-
cemia > 15 – 18 mg/ dl can result in deat h.
Treatment
Treat ment varies wit h severit y; mild Hyper-calcemia
can be t reat ed wit h rehydrat ion only, while severe
Hyper-calcemia is t reat ed as a medical emergency.
A. Mi l d
3. Rehydrat ion – isot onic saline 2 – 4 L/ day increas-
es calcium excret ion
4. Aft er correct ing dehydrat ion administ er I nj .
Frusemide 20 – 40 m g 2 t imes a day.
5. Monit or elect rolyt es especially pot assium and
magnesium and replace accordingly.
B. Moder at e t o sever e
1. Aggressive preceding approach - isot onic saline
6L Plus I nj . Frusemide upt o 100 mg every 1 t o
2 hours.
2. I nj . Pamidronat e 30 – 90mg I V infusion in 0.9 %
saline over 4 - 24 hours; response last s for weeks.
O r
Tab. Aldronat e Sodium 10 mg orally in t he
morning wit h full glass of wat er at least
30 mins before any food or drink; remain
in upright posit ion for at least 30 mins.
O r
Tab. Zolendronat e 1 – 4 mg I V in few mins.
3. I nj . Calcit onin 2 – 8 U/ kg I V or SC or I M every
6 – 12 ; rapid but mild act ion.
4. Tab. Prednisolone 40 – 100 mg/ day in 4 divided
doses may be useful in ost eolyt ic malignancies,
vit amin D int oxicat ion and sarcoidosis.
5. Tab. Phosphorous (sodium and pot assium phos-
phat e) 1 – 1.5 g/ day in 4 divided doses for sev-
eral days when hypo-phosphat emia is present .
6. Perit oneal dialysis wit h calcium free dialysat e is
useful especially in cases complicat ed by renal
failure.
Definit ive t reat ment , wherever possible, is
parat hyroidect omy in hyperparat hyroidism.
Pat i ent educat i on
● I n pat ient s wit h mild asympt omat ic hyper-cal-
cemia due t o hyperparat hyroidism, advise t o
keep act ive, avoid immobilizat ion, drink adequat e
fluids and avoid t hiazide diuret ics, large doses of
vit amin D or A and calcium supplement s and cal-
209
cium cont aining ant acids.
● Check serum calcium and albumin t wice a year,
renal funct ion and urine calcium once a year and
bone densit y of dist al radius once every 2 years.
Ref er ences:
● Diseases of Parat hyroid gland and ot her Hyper
and hypo-calcemic disorders. I n: Harrison’s prin-
ciples of medicine Kasper DL, Braun wald E, Fauci
AS et al (eds), 16t h edit ion, 2005, Mc Graw-Hill
Company I nc., New York, pp 2249-2268.
● Calcium I n: The Washingt on Manual of Medical
Therapeut ics, Ahya SN, Flood K. Paranj ot hi S
Eds. 30t h edit ion, 2001. Philadelphia: Lippin-cot t ,
Williams and Wilkins, pp-60-62
211
Rheumatology
Chapter 10
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
● Clinical Approach t o Art hrit is
● Rheumat oid Art hrit is
● Spondyloart hropat hies
● Syst emic Lupus Eryt hemat osis
● Vasculit is
● Regional Syndromes
● Juvenile I diopat hic Art hrit is
213
Clinical approach to arthritis
I nt r oduct i on
Art hrit is is defined as inflammat ion of j oint or a
group of condit ions charact erized by t he presence of
some or all of t he cardinal signs of inflammat ion (pain,
t enderness or swelling), syst emic dist urbances (such
as prolonged morning st iffness or fever) and laborat ory
evidence of inflammat ion (raised ESR, elevat ed CRP or
ot her acut e phase react ant s).
St r at i f i cat i on of Pat i ent s:
The pat ient s wit h art hrit is can be st rat ified in t o
cert ain broad groups by
● Durat ion of disease
* Acut e or chronic art hrit is, t he dividing line be-
t ween t he t wo being durat ion of six weeks
● Age of disease onset
* Adult or j uvenile art hrit is, t he lat t er having
disease onset at age less t han 16 years
● Number of j oint s involved
* Monoart hrit is or oligoart hirit is (single j oint )
* Pauciart hirit is (t wo t o four j oint s)
* Polyart hrit is (five or more j oint s)
● Presence of inflammat ion
* I nflammat ory or non-inflammat ory art hrit is
● Presence of bilat eral involvement
* I f polyart hrit is, symmet rical or asymmet rical
Di st i ngui shi ng f eat ur es bet ween var i ous t ypes
of ar t hr i t i s
The condit ions t hat look like art hrit is may act ually be
a manifest at ion of soft t issue rheumat ism. So, it should
be first ruled out before proceeding furt her.
Arthritis and soft tissue rheumatism (STR)
Charact erist ics Art hrit is Soft t issue rheu-
mat ism
Pain Deep,
diffuse and
circumferent ial
Superficial and
sharply localized
Tenderness Circumferent ial
around t he j oint
Localized over t he
affect ed st ruct ure
Pain on act ive
range of
mot ion
Yes Yes
Pain on passive
range of
mot ion
Yes No
Clinical
synovit is or
effusion
Yes No
Crepit us.
inst abilit y,
deformit y
Oft en Yes No
Alt hough most of t he art hrit ic condit ions are
inflammat ory, t here can be except ions. For example, a
hemophilic j oint and a Charcot j oint in diabet ic pat ient s
are non-inflammat ory in nat ure requiring alt oget her a
different line of t reat ment . Ost eoart hrit is can be bot h
non-inflammat ory and inflammat ory.
I nf l ammat or y and non- i nf l ammat or y ar t hr i t i s
Feat ure Infamma-
t ory
art hrit is
Non-
infamma-
t ory
art hrit is
Const it ut ional feat ures
(such as fever, weakness,
fat igue)
Yes (in
cert ain
condit ions)
No
Prolonged early morning
st iffness (> 1hour)
Yes No
Spont aneous disease flares Yes No
I mprovement of j oint
sympt oms on j oint usage
Yes No
Elevat ed ESR, CRP Yes No
Chronic arthritis
214
Mono-ar t i cul ar and pol yar t i cul ar ar t hr i t i s
Even if t he pat ient complains of pain in j ust one j oint ,
it is mandat ory t o examine all t he j oint s t o ensure t hat
ot her j oint s are not involved before proceeding furt her
as mono-art icular art hrit is. The most crit ical diagnosis
t o consider in pat ient s wit h mono-art icular sympt oms is
sept ic art hrit is because bact erial infect ion can dest roy
t he j oint cart ilage wit hin a few days.
Causes f or Mono-ar t hr i t i s
Acut e Subacut e or chronic
Sept ic art hrit is Tuberculosis
Gout (uric acid cryst al
deposit ion)
Ost eoart hrit is
Pseudo gout (calcium
pyrophosphat e cryst al
deposit ion)
Rheumat oid
art hrit is(commonly
polyart icular)
Haemart hrosis Juvenile idiopat hic
art hrit is
React ive art hrit is Malignancy
I schemic necrosis Trauma
Symmet r i cal and asymmet r i cal Pol yar t hr i t i s
I f it is a polyart icular present at ion, it is most useful
t o dist inguish bet ween symmet rical and asymmet rical
j oint involvement . This makes a t remendous difference
in different ial diagnosis. For example, should it be
asymmet rical j oint involvement , chances are t hat t his
would be a case of one of t he seronegat ive spondylo-
art hropat hies. On t he ot her hand, polyart icular
symmet rical present at ion would involve different ial
diagnosis amongst a large number of collagen vascular
disorders including rheumat oid art hrit is.
Causes f or symmet r i cal and asymmet r i cal
pol yar t hr i t i s
Causes for Polyarthritis
Symmet rical Asymmet rical
● R h e u m a t o i d
art hrit is
● A n k y l o s i n g
spondylit is(especially
j uvenile)
● Syst emic lupus
eryt hemat osus
● Scleroderma
● Myosit is
● React ive art hrit is
● Polyart icular gout ● Psoriat ic art hrit is
● Polyart icular sep-
t ic art hrit is (rare-
ly)
● Ent eropat hic art hrit is
● I nf ect i ve- endo-
cardit is
● Endocrine disor-
ders
● Viral art hrit is
● AI DS
● Un d i f f e r e n t i a t e d
spondyl oar t hr opa-
t hies
Concl usi on
A proper hist ory t aking and a det ailed clinical
examinat ion are t he keys t o successful diagnosis. A
simple approach t o t he art hrit ic pat ient as discussed
would help t he primary care physician t o at least
make a t ent at ive clinical diagnosis. The management
of individual condit ions include appropriat e laborat ory
t est s and t reat ment wit h bot h non-pharmacological
measures like physiot herapy and drugs like NSAI DS
and disease modifying agent s. The det ails of t he
t reat ment are described in t he subsequent chapt ers, on
Rheumat oid art hrit is (RA)
215
Rheumatoid Arthritis (RA)
Def i ni tion
Rheumat oid art hrit is is a chronic syst emic
aut oimmune inflammat ory disease wit h long t erm
disabilit y, acut e int ermit t ent morbidit ies and somet imes
wit h premat ure mort alit ies
Di agnosi s
Revised ACR (1988) classifcation criteria
Crit e-
ria
Charact erist ics Durat ion
1 ● Morning st iffness for
more t han 1 hour
Must be
present for
at least six
weeks
2 ● Art hrit is of t hree or
more j oint areas
3 ● Art hrit is of hand j oint s
4 ● Symmet ric art hrit is
5 ● Rheumat oid nodules
6 ● Serum Rheumat oid fac-
t or
7 ● Radiographic changes
“ Pat ient is said t o have Rheumat oid art hrit is if he or
she has four out of seven crit eria”
Compl i cat i ons
I nfect ions Ent rapment neuropat hies
Vasculit is At lant o-axial j oint
subluxat ion
Deformit ies I nt erst it ial lung disease
Tendon and ligament
damage
Amyloidosis
Ost eoporosis Drug t oxicit y
I nvesti gati ons
Hemat ological Bio-chemical I mmunological
Hemoglobin LFT Rheumat oid
Fact or(RF)
TLC, DLC,
Plat elet count
RFT Ant i-cyclic
cit rullinat ed pept ide
(ant i-ccp)
ESR Lipid profile C-react ive prot ein
(CRP)
Rheumat oi d f act or ( RF)
● Posit ivit y indicat es more severe and act ive dis-
ease.
● Early bony erosions are more common
● Posit ive pat ient s may require aggressive t reat-
ment wit h combinat ion of disease modifying ant i
rheumat ic drugs. (DMARDS)
● Absent RF, doesn’t exclude t he diagnosis of Rheu-
mat oid Art hrit is
● I nvest igat ions are done t o assess t he disease ac-
t ivit y and in follow up t o det ect early complica-
t ions as well as t o monit or t he drug side effect s.
● Radiological invest igat ions like plain x-rays, ult ra-
sound and MRI are useful for diagnosis, t o assess
severit y and t o det ect erosions.
● Cardiac and opht halmic workup at base line and
during follow up.
Treatment
Conser vat i ve
Non-Pharmacological Pharmacological
Healt h educat ion NSAI DS
Physiot herapy DMARDS
Occupat ional t herapy I mmunosuppressant s
Support ive devices like
splint s
Cort icost eroids
Rehabilit at ion Biological agent s
Oper at i ve
Open Surgery Closed Procedures
Release of cont ract ures Art hroscopy j oint Lavage
Repair of t endon rupt ure Chemical synovect omy
Joint replacement Radio-synovect omy
Anal gesi c and ant i i nf l ammat or y dr ugs
● Physician must evaluat e t he pat ient s individually
* Diclofenac sodium (25-50mg bid-t id)
* I buprofen (300-800mg bid-qid)
* I ndomet hacin (25mg t id-qid)
Ri sk f act or s f or i ncr eased t oxi ci t y
● Advanced age
216
● Acid pept ic ulcer disease
● Pregnancy
● Cardiac failure
● Ast hma
● Nasal polyposis
DMARDS:
Di sease modi f yi ng ant i -r heumat i c dr ugs t her apy
● Early init iat ion, combinat ion of drugs and regu-
lar monit oring of side effect s are essent ial. The
names of t he DMARDS are furnished below
* Met hot rexat e
* Hydroxychloroquine
* Sulphasalazine
* Leflunomide
* Gold salt
* D.Penicillamine
* Azat hioprine
* Biologicals
Ref er r al :
Severe cases of rheumat oid art hrit is wit h ex-
t raart icular manifest at ions should be referred t o
a higher inst it ut e for furt her work up.
Pr ognosi s:
I t is highly variable.
Pat i ent educat i on
Regular physiot herapy and drugs int ake are es-
sent ial t o preserve t he j oint s.
Spondylo-Arthropathies
I nt r oduct i on
Spondylo-art hropat hies (SpAs) const it ut e a clust er
of int errelat ed and overlapping chronic inflammat ory
rheumat ic diseases t hat include Ankylosing spondylit is
(t he prot o t ype of SpAs) react ive art hrit is (including
Reit er’s syndrome), psoriat ic art hrit is, ent eropat hic
art hrit is and pauci-art icular lat e onset art hrit is, a form
of j uvenile idiopat hic art hrit is. These diseases are not
associat ed wit h rheumat oid fact or
Char act er i st i cs of t he SpAs
● Absence of t he rheumat oid fact or and rheuma-
t oid nodules
● Peripheral art hrit is
● Spinal inflammat ion: I nflammat ory back pain and
sacroiliit is wit h or wit hout spondylit is
● Peripheral ent hesit is
● Familial aggregat ion
● Associat ion wit h HLAB27
Causes for Polyarthritis
217
Ankylosing Spondylitis (AS)
I nt r oduct i on
AS is an HLAB27 associat ed chronic inflammat ory
disease of unknown et iology. I t affect s mainly t he
sacroiliac j oint s and t he axial skelet on, but peripheral
j oint involvement may also be an import ant feat ure.
The disease can be accompanied by ext ra skelet al
manifest at ions such as
● Acut e ant erior uveit is
● Aort ic incompet ence
● Cardiac conduct ion defect s
● Fibrosis of t he upper lobes of t he lungs
● Neurologic involvement and renal (secondary)
amyloidosis
AS is “ primary” or “ idiopat hic” if no associat ed
disorder is present , and “ secondary” if t he disease is
associat ed wit h psoriasis or chronic inflammat ory bowel
disease.
Modi f i ed New yor k 1984 Cr i t er i a f or Ankyl osi ng
spondyl i t i s
● Low back pain of at least 3 mont hs durat ion im-
proved wit h exercise and not relieved by rest .
● Limit at ion of lumbar spine in sagit t al or front al
planes.
● Chest expansion decreased relat ive t o normal
values for age and sex.
● Bilat eral sacroiliit is grade 2 t o 4.
● Unilat eral sacroiliit is grade 3 or 4.
Definit e Ankylosing spondylit is is of
* Unilat eral grade 3 t o 4
* Bilat eral grade 2 t o 4
* Sacroilit is and any clinical crit erion,
Cl i ni cal mani f est i t i ons
Ar t i cul ar
Low back pai n and st i f f ness
The pain is felt deep in t he glut eal region, is dull in
charact er, is difficult t o localize and is insidious in onset .
The but t ock pain may t ypically alt ernat e from side t o
side. The lower lumbar area becomes st iff and painful.
Bot h t he st iffness and pain t end t o be eased by a hot
shower, an exercise program or physical act ivit y.
Chest pai n
The pain accent uat ed by coughing or sneezing which
somet imes is charact erized as “ pleurit ic”. The pain may
be associat ed wit h t enderness over st ernocost al or
cost o-st ernal j unct ions. Reduct ion of chest expansion
is oft en det ect able at an early st age of Ankylosing
spondylit is.
Tender ness
Tender sit es are t he cost o-st ernal j unct ions, spinous
processes, iliac crest s, great er t rochant ers, ischial
t uberosit ies, t ibial t ubercles and heels (Achilles t endinit is
or plant ar fasciit is). These sit es are called ent heses.
Joi nt s
The girdle or “ root ” j oint s (hips and shoulders)
are t he most frequent ly involved ext ra axial j oint s in
Ankylosing spondylit is.
Ext r a-ar t i cul ar
Gener al sympt oms
● Fat igue
● Loss of weight
● Low grade fever
● Occur frequent ly
Psoariatic arthritis
“Sausage middle finger”
Distal inter Phalangeal joint involvement with nail dystrophy
218
Eye di sease
● Acut e ant erior uveit is.
Car di ovascul ar di sease
● Ascending aort it is
● Aort ic valve incompet ence
● Conduct ion abnormalit ies
● Cardiomegaly and
● Pericardit is
Pul monar y di sease
● Slowly progressive fibrosis of t he upper lobes of
t he lungs is a rare and last manifest at ion.
Neur ol ogi c i nvol vement
● Can be caused by fract ure, inst abilit y, compres-
sion or inflammat ion
* At lant o-axial j oint subluxat ion
* At lant o-occipit al subluxat ion
* Upward subluxat ion of t he axis may occur.
* Compressive myelopat hy
* Cauda equina syndrome may also occur.
Renal i nvol vement
● I gA nephropat hy
● Microscopic hemat uria
● Prot einuria may occur
● Amyloidosis is a rare complicat ion
Ost eopor osi s
● Ost eopenia is seen even in early st ages of Anky-
losing spondylit is.
Labor at or y t est s
● An elevat ed ESR or CRP, a mild normochromic
anemia, elevat ions of serum alkaline phosphat ase
and serum I gA are seen.
● X-Rays show changes in sacroiliac, disco-ver-
t ebral, apophyseal, cost overt ebral and cost o-
t ransverse j oint s.
● CT is usually considered superior t o MRI .
Management :
Physi ot her apy
● Hydrot herapy and exercises are useful.
Medi cat i on
● NSAI Ds
* I ndomet hacin
* COX-2 inhibit ors like et oricoxib
Second l i ne dr ugs
● Cort ico- st eroids are effect ive for local int ra ar-
t icular t reat ment
● Sulphasalazine is effect ive in reducing synovit is
in pat ient s wit h peripheral poly art icular involve-
ment but has no result s on axial involvement .
Sur ger y
● Tot al hip replacement can be done for involve-
ment of t he hip j oint .
Ref er r al
● All suspect ed cases should be referred t o higher
inst it ut ions for furt her management .
Nat ur al cour se and pr ognosi s
● I t is highly variable and charact erized by spont a-
neous remissions and exacerbat ions.
Pat i ent educat i on
● Smoking should be avoided.
● Regular physiot herapy
● Follow-up is essent ial for prevent ion of j oint an-
kylosis
Systemic Lupus Erythematosus
I nt r oduct i on
I t is a common aut oimmune mult isyst em
inflammat ory disease wit h diverse clinical and laborat ory
manifest at ions associat ed wit h an unpredict able course
and prognosis. Difficult y in diagnosis, laborat ory
assessment and t reat ment are peculiar feat ures of t his
oft en devast at ing illness.
Epi demi ol ogy
I t is more in females of reproduct ive age group, but
no age is exempt .
I n I ndia, t he female: male rat io is 11: 1.
219
Types Of Lupus
● Discoid lupus eryt hemat osus
● Subacut e cut aneous lupus eryt hemat osus
● Drug induced lupus
Lupus i n speci al si t uat i ons
I n order t o exercise special care for lupus in special
sit uat ions, t he det ails of t he same are provided.
Lupus and pr egnancy
Pat ient s should be allowed t o become pregnant
only when t he disease is in remission for 6 mont hs
bot h clinically and laborat ory wise. Close monit oring is
mandat ory.
Neonat al Lupus
Occurs in newborns of mot hers having ant i Ro (SSA)
and ant i La (SSB) ant ibodies wit h t he mot hers being
sympt omat ic or asympt omat ic. New born int ensive care
is essent ial.
Sympt oms and Si gns
● Unexplained fever
● Art hrit is
● Muscle pain
● Rashes over t he face
● Lymphadenopat hy
● Oral ulcers
● Ext reme fat igue
● Chest pain on deep breat hing-pleurisy
● Unusual loss of hair
● Raynaud’s phenomenon
● Phot osensit ivit y
● Eyelid and leg oedema
● Chest pain
● Anaemia
● Hypert ension
● Headache
● Dizziness
● Confusion
● Depression
● Behavioural changes
● Seizues
● St roke et c.
● At different t imes
* Renal involvement is usually asympt omat ic
except for oedema, hypert ension and ident i-
ficat ion of urinary abnormalit ies.
● Co-morbid st at es
* Accelerat ed at herosclerosis
* Pro-t hrombot ic st at es
* Ost eoporosis
* I nfect ion
Cr i t er i a f or di agnosi s
American College of Rheumat ology (ACR) - in 1999
st ipulat ed t hat at least 4 of t he following 11 condit ions
must be present , serially or simult aneously.
220
whet her it is organ or life t hreat ening or not –
mild, moderat e, severe or wit h miscellaneous
feat ures.
● Treat ment plan has t o be chart ed according t o
t he pat ient ’s age, sex, sympt oms, flare and life
st yle. Pat ient s should be explained about flares
and overall t reat ment .
Dr ugs:
● I buprofen should not be given t o lupus pat ient s
● Exposure t o sun light should be avoided.
● Apart from t reat ment of t he disease (e.g. st eroids
- upt o cyclophosphamide and t hen biologics et c.)
as t he sit uat ion demands, t he following should
also be t reat ed.
● Comorbid st at es: Aspirin for at herosclerosis
prophylaxis is desirable. Ost eoporosis should be
t reat ed.
● I mmuno-prophylaxis
* Vaccinat ions permit t ed include
» Hemophilus
» I nfluenza (HI B)
» Pneumococcal vaccine yearly
Key Message
● Diagnosis can be frust rat ing and primary care
physicians may be t he first t o suspect and have
t o manage in conj unct ion wit h a Rheumat ologist
or Physician.
● Nat ural course is unpredict able wit h remissions
and exacerbat ions.
● Pat ient and family members or care providers
must be informed or educat ed about t he nat ural
course of t he disease, complicat ions, co-morbid
st at us, infect ion, special sit uat ions and long t erm
management .
● Periodic review by a specialist is helpful.
● Referral t o a higher cent re is desirable for con-
firming t he diagnosis, t o assess disease act ivit y
or severit y, for est ablishing or amending t reat-
ment plans and t o improve t he out come.
Ref er ence
● Mary Desmond pinkowish: American College of
Rheumat ology Ad Hoc commit t ee on Syst emic
Lupus Eryt hemat osus Guidelines.
Acr Crit eria For Diagnosis Of Sle
1. Malar rash
2. Discoid rash
3. Oral ulcers
4. Phot osensit ivit y
5. Art hrit is (non-erosive, involving at least t wo pe-
ripheral j oint s and accompanied by t enderness,
swelling, or effusion)
6. Pleurit is or pericardit is
7. Neurologic disorders (seizures or psychosis)
8. Hemat ologic disorder (hemolyt ic anemia, leu-
copenia, lymphopenia, or t hrombocyt openia)
9. Renal disorders (persist ent prot einuria or cel-
lular cast s)
10. Ant i-nuclear ant ibodies (ANA)
11. I mmunologic disorders (abnormal levels of an-
t ibody t o nat ive DNA, ant ibodies t o t he smit h
(SM) nuclear ant igen, or ant iphospholipid an-
t ibodies)
I nvesti gati ons
“ No single t est can est ablish but several laborat ory
t est s help in t he diagnosis”.
Di f f er ent i al di agnosi s:
● I ncludes ot her syst emic connect ive t issue disor-
ders like
* Rheumat oid art hrit is
* Dermat omyosit is
* Polymyosit is
* Vasculit is
* Sj ogren’s syndrome
* Primary ant i-phopholipid ant ibody syndrome
* Fibro-myalgia
* Drug react ions
* HI V
* Hemat ological disorders
Tr eat ment
● Requires a collaborat ive approach comprising
various specialist s
● Pat ient and family educat ion is of vit al impor-
t ance - about remissions, exacerbat ions, mar-
riage, pregnancy et c.
● Treat ment is individualized and depends on
221
Investigation : ANA, Complete haemogarm, Urine analysis
After response, discontine cyclophos phamide;
maintain with mycophenolate or azathioprine
Not life of organ threat Life threatening
No response
Experimental therapy Taper dose of drugs
Response
High dose
glucocorticoids
Mycophenolate
mofetil
Cyclophosphamide
(6 months only)
Diagnostic approach to SLE
Treatment
Some Positive All negative
Not SLE
Not SLE
Quality of life
acceptable
Conservative
management
Conservative
treatment plus
low dose
glucocorticoids
Quality of life
not acceptable
ANA Positive
All tests normal
Symptoms subside
All tests normal
Symptoms persist
Repeat ANA, add
anti-ds DNA, anti-Ro
Deifinte SLE
( > 4 criteria)
Possible SLE
( < 4 criteria)
Deifinte SLE
( > 4 criteria)
Possible SLE
( < 4 criteria)
222
● Guidelines for referral and management of Sys-
t emic lupus eryt hemat osus in adult s. Art hrit is
Rheumd. 1999; 42: 1785-1796.
● A Kumar. A I ndian Guidelines on t he manage-
ment of SLE. J I ndian Rheumat ol Assn 2002: 10:
80-96.
Vasculitis
Def i ni tion
Vasculit is is a clinical condit ion where inflammat ion
of t he blood vessels occurs result ing in eit her necrosis
of t he vessel wall, aneurysmal dilat at ion, narrowing of
t he lumen or occlusion of t he lumen due t o secondary
effect s of inflammat ion - t hrombus, t he final result of
which will be infarct ion of t he t issues if t here are no
adequat e collat erals. I t should be different iat ed from
Vasculopat hies which are non- inflammat ory occlusive
condit ions.
Epi demi ol ogy
● I t is observed in all ages from childhood t o adult-
hood. Takayasu’s art erit is has a highest incidence
in Asia and I ndia.
Et i ol ogy
● The cause may be unknown but is usually due
t o t he result of combinat ion of genet ics, environ-
ment al exposure or infect ion.
When t he cause is not ident ified t hey are called
Primary vasculit is, and classified on t he basis of blood
vessel involvement
Primary Vasculit is
Large ves-
sel
Medium
vessel
I mmune complex medi-
at ed
Takayasu’s
art erit is
Polyart erit is
Nodosa
Goodpast ure’s disease
Giant cell
art erit is
Cut aneous
polyart eri t is
nodosa
Cut aneous
leucocyt oclast ic
vasculit is
Cognan’s
syndrome
Buerger’s
disease
Henoch- schonlein
Purpura
Behcet ’s
disease
Kawasaki’s
disease
Hypo-
complement enemic
urt icarial vasculit is
Primary
angit is of
t he cent ral
nervous
syst em
Essent ial
cryoglobulinemia
Eryt hema elevat um
diut inum
Clinical manifest at ions are varied and t hose common
t o vasculit is of all vessels include
● Fever
● Weight loss
● Malaise
● Art hrit is
● Art hralgias
● Seizures
● Nerve palsies
● Myopat hies
● Hypert ension
● Renal failure
● Wheezing
● Gangrene
● Rashes
● Cerebrovascular accident s and
● Myocardial infarct ion
I nvesti gati ons
Depends on t he t ype of vasculit is. Many t est s are
helpful in t he diagnosis or in evaluat ion of t he act ivit y of
t he disease and in ruling out ot her mimics of vasculit is.
Cases may be referred t o higher cent re for appropriat e
evaluat ion.
A complet e blood count , inflammat ory markers
and individual organ assessment are essent ial. Special
immunological invest igat ions as well as t hose t hat rule
223
out ot her disorders simulat ing vasculit is are required at
higher cent res.
Treatment
Generally accept ed prot ocols for t he different t ype
of vasculit is consist of t he following. However, t he
t reat ment and drugs schedules are individualized.
● Large vessel vasculit is:
* St eroids
* Met hot rexat e
* Azat hioprine
● Medium vessel vasculit is:
* St eroids + Cyclophosphamide for induct ion
* Azat hioprine or Met hot rexat e for remission
● Small vessel vasculit is:
* Treat ment when required wit h init ial st eroid
t herapy and if refract ory and absolut ely nec-
essary, cyt ot oxics
● Kawasaki disease in t he acut e st ages requires in-
t ravenous immunoglobulin and resist ant syst emic
vasculit is require newer t herapies which include
Biologicals.
Emer genci es i n vascul i t i s r equi r i ng speci al i st s
car e i ncl ude
● I mpending visual loss
● I mpending or est ablished gangrene.
● Uncont rolled hypert ension.
● Renal emergencies
● Respirat ory dist ress
● Neurological e.g., Seizures, St roke, Mono-neurit is
mult iplex, Headache
● Acut e abdomen e.g., mesent eric vasculit is and
rupt ured aneurysm
● Myocardial infarct ion
● CCF
● Kawasaki disease
● Takayasu’s art erit is
● Bleeding from any origin
Key Message:
● Vasculit is is an enigmat ic disease wit h remissions
and exacerbat ions.
● Admission: I nst it ut ional management is advis-
able in emergencies.
● Referral:
* Early referral t o t he higher cent re and regular
follow up are mandat ory.
● Out come:
* Prognosis is variable wit h unpredict able com-
plicat ions.
Regional Syndromes
Regional syndromes are charact erized by pain t hat
affect s a single musculoskelet al area (eg: shoulder,
hand or knee). This could be of four main origins:
● Peri-art icular pain
● Joint pain
● Neurogenic pain
● Referred pain
Osteo - Arthritis HIP
1. Joint space narrowing
2. Sub - chondral sclerosis
3. Marginal osteophyte and cysts
224
Di st i nct i ve f eat ur es of r egi onal syndr omes
Pariart icular
pain
Art icular pain Neurogenic pain Referred pain
Enquiry Select ive painful
movement s
All j oint movement s
are painful
Disaest esic.
Aggravat ed by
compression of
nerve or mobilizat ion
of t he spine
Unrelat ed t o
movement “ visceral”
t iming
Pain on mot ion Act ive> passive
select ed mot ions
Act ive ~ passive
several direct ions
Normal. I f root pain,
pain on mot ion of
t he affect ed spine
segment
Normal
Range of mot ion Act ive mot ion can
be limit ed by pain.
passive mot ion: full
Can be limit ed in
act ive and passive
mot ion
Normal Normal
Resist ed mobilizat ion Pain on specific
manoeuvres
No effect No effect No effect
Local palpat ion Pain upon affect ed
st ruct ure
Possible crepit us,
swelling, effusion,
heat , pain along j oint
margin
Normal Normal
Neurological
examinat ion
Normal Normal May be abnormal Normal
Di seases af f ect i ng t he j oi nt s
Hist ory and examinat ion t aken t o decide bet ween
degenerat ive and inflammat ory j oint pain.
Degener at i ve j oi nt di sease
Ost eoart hrit is is t ypically associat ed wit h paint t hat
● I ncreases wit h repeat ed use of t he j oint and
● I s worst at t he end of day
● Pain int ensit y decreases during rest
● I s rarely present at night and
● The pat ient can usually find a pain - free posit ion
Pat ient s can describe t hat pain increases again
aft er rest ing and t his may be accompanied by st iffness
t hat subsides in 2-3 minut es. Early morning st iffness
associat ed wit h degenerat ive art hrit is ceases in a few
minut es (< 10).
I n cont rast t o act ive inflammat ory disease, pain is
worst in t he morning and is relieved by cont inued use
of t he j oint . The pat ient may have pain during t he night ,
not relat ed t o movement in bed and cannot ident ify pain
- rest st iffness may persist for more t han 5 minut es.
Associat ed ext ra - art icular manifest at ions may
accompanay a variet y of inflammat ory art hrit is but
t hey are absent in degenerat ive j oint disease. Then
det ermine
● Which j oint s are affect ed and t heir pat t ern of dis-
t ribut in
● How t he condit ion began and how it developed
over t ime
● The presence or absence of inflammat ory low
back pain
● Accompanyng ext ra - art icular manifest at ions.
Mono-ar t hr i t i s
I t is useful t o separat e acut e ( onset over hours
t o days) from chronic mono-art hrit s.
Acut e mono-ar t hr i t s
The common causes are
● Trauma and Gout , but t his condit ion should be
considered infect ious (sept ic art hrit is) unt ill prov-
en ot herwise.
● Pseudo - gout (calcium pyrophosphat e dihydrat e
disease)
● Post - t raumat ic synovit is
● Palindromic rheumat ism
225
● React ive art hrit is
● Psoriat ic art hrit is and
● Bact erial endocardit is are t he ot her causes
Chr oni c mono-ar t hr i t i s
Mono-art hrit is can have an indolent course, last ing
from weeks t o mont hs. The main possible causes include
● I nfect ion (Brucella, Mycobact erium,)
● Cryst al induced art hrit is and
● Mono-art icular present at ion of oligo or polyart hri-
t is
● Juvenile idiopat hic art hrit is
● React ive art hrit is
● Seronegat ive spondylo-art hropat hy
Different ial diagnosis must include causes such
as ost eoart hrit is and neuropat hic (Charcot ’s)j oint s.
The aet iological diagnosis of chronic mono-art hrit is
usually requires synovial biopsy wit h pat hological and
bact eriological examinat ion.
Chr oni c symmet r i cal addi t i ve per i pher al
pol yar t hr i t i s
This pat t ern describes j oint inflammat ion involving,
simult aneously, five or more j oint s (polyart hrit is), for
more t han six weeks (chronic). small j oint s of t he hands
and feet are predominant ly affect ed, wit h or wit hout
t he wrist and ankle (peripheral), and approximat ely
t he same j oint s are involved on each side of t he body
(symmet rical). There should be no inflammat ory low
back pain.
Causes
● Rheumat oid art hrit is, and t his is t he most com-
mon pat t ern
● Ot her connect ive t issue diseases such as
* Syst emic lupus
* Primary Sj ogren’s syndrome
* Polymyost it is
* Mixed connect ive t issue disease
● Psoriat ic art hrit is can also present wit h t his pat-
t ern
Chr oni c, asymmet r i cal ol i go/ pol yar t hr i t i s
This describes an asymmet rical art hrit is, affect ing
proximal or dist al j oint s. Dact ylit is or involvement of
dist al int erphalangeal j oint s is common.
● Psoriat ic art hrit is is t he most common cause of
t his pat t ern.
● Ankylosing spondylit is (inflammat ory back pain is
expect ed in t his condit ion but may no be obvi-
ous).
● React ive art hrit is
● Art hrit is associat ed wit h inflammat ory bowel dis-
ease.
Pr oxi mal ol i goar t hr i t i s
Pat ient s may present wit h art hrit is involving
predominant ly proximal j oint s. The most common
causes are t he
● Seronegat ive spondylart hropat hies
● Less common causes are
* Behcet ’s disease
* Juvenile idiopat hic art hrit is and
* I ncipient rheumat oid art hrit is
I nf l ammat or y l ow back pai n
This refers t o low back pain t hat persist s or
predominat es at night , does not relieve wit h rest but
rat her wit h movement and is associat ed wit h prolonged
morining st iffness. This is always a significant clue t hat
deserves clarificat ion.
This is a typical mainifest at ion of
● Seronegat ive spondylo-art hropat hies
* Ankylosing spondylit is
* Psoriat ic art hrit is
* React ive art hrit is
* Spondylit is
* I nflammat ory bowel disease
● I t is also a feat ure of Bechcet ’s disease and infec-
t ious or asept ic discit is
Gener al i zed pai n
I n t his syndorme, pain affect s different part s of t he
body diffusely and imprecisely, wit h lit t le or no focus on
j oint s.
Vit amin D deficienc; y and Fibro-myalgia account s for
t he maj orit y of t he cases of generalized pain syndrome.
226
Juvenile Idiopathic Arthritis (JIA)
JI A includes all forms of art hrit is t hat begins before t he age of 16 years, persist s for more t han 6 weeks and is of
unknown cause.
Classifcation of JIA (International League Association For Rheumatology)
Cat egory Definit ion Exclusions
Syst emic onset
JI A
Art hrit is in> 1 j oint wit h, or preceded by, fever of
at least t wo weeks t hat is document ed t o be daily
(“ quot idian” ) for at least 3 days and accompanied by
> 1 of t he following
Psoriasis or a hist ory of psoriasis in
t he pat ient or a first - degree realt ive
Evanescent (non-fixed)eryt hemat ous rash Art hrit is in an HLA-B27+ male
beginning aft er t he 6t h birt hday
Generalized lymph node enlargement AS, Ent hesist is - relat ed art hrit is,
sacroiliet is wit h inflammat ory bowel
disease, React ive art hrit is, or acut e
ant erior uveit is, or h/ o of one of
t hese disorders in a first - degree
relat ive
Hepat omegaly or splenomegaly or bot h Presence of I gMRF on at least 2
occasions at least 3 mont hs apart
Serosit is
Oligoart icular JI A Art hrit is affect ing 1-4 j oint s during t he first 6 mont hs
of disease. Two subcat egories are recognized:
A,B,C,D above, plus
Persist ent oligo-art hirit is affect ing < 4 j oint s
t hroughout t he disease course
Presence of syst emic JI A in t he
pat ient
Ext ended oligo-art hrit is affect ing > 4 j oint s aft er t he
first 6 mont hs of disease
Polyart hrit is (RF
negat ive)
Art hrit is affect ing> 5 j oint s during t he first 6 mont hs of
disease; a t est for RF is negat ive
A, B, C, D, E
Polyart hrit is (RF
Posit ive)
Art hrit is affect ing > 5 j oint s during t he first 6 mont hs
of disease; > 2 t est s for RF at least 3 mont hs of
disease are posit ive
A, B, C, E
Psoriat ic art hrit is Art hrit is and psoriasis, or art hrit is and at least 2 of t he
following:
B, C, D, E
Dact ylit is*
Nail pit t ing and onycholoysis
Psoriasis in a first- degree relat ive
Ent hesit is -
relat ed art hrit is
Art hrit is and ent hesit is, or art hrit is or ent hesit is wit h
at least 2 of t he following
A, D, E
Presence of HLA -B27 ant igen
Onset of art hrit is in a male> 6 yr old
Acut e (Sympt omat ic) ant erior uveit is
Hist ory of ankylosing spondylit is, ent hesit is - relat ed
art hrit is, sacroilit is wit h inflammat ory bowel disease,
Reit er’s syndrome, or acut e ant erior uveit is in a first -
degree relat ive
Undifferent iat ed
art hrit is
Art hrit is t hat fulfills crit eria in no cat egory or in > 2 of
t he above cat egories
227
● Polyart icular onset and polyart icular disease
course
● Ext ended oligo JI A
● Female
● Rheumat oid fact or post ive
● ANA posit ive
● Persist ent early morning st iffness
● Tenosysnovit is
● Subcut aneous nodules
● Rapid involvement of t he small j oint s of t he hands
and feet wit h erosions
● Hip involvement
● Higher mean ESR
● Generalized lymphadenopat hy.
Pr i nci pl es of t her apy
The mangement of JI A benefit s from input
from a large mult idisciplinary t eam including
physiot herapist s, occupat ional t herapist s, podiat rist s
or ort hot ist s, specialist nurses, communit y nursing
t eams, psychologist s, social workers, school liaison
workers, family support groups, general pract it ioners,
opt halmologist s, dent ist is or ort hodont ist s, ort hopaedic
surgeons, and pain management t eams.
Recent changes in t he medical management of
JI A have included increased use of int rart icular and
j udicious use of oral and/ or int ravenous cort icost eroids,
est ablishment of Met hrot rexat e as t he first line disease
modifying ant i - rheumat ic drug (DMARD), and t he
discovery and use of biologic agent s or newer t reat ment s
of resist ant disease. Early, aggressive suppression of
inflammat ion is t he principle underlying t reat ment .
Non - st er oi dal ant i -i nf l ammat or y dr ugs
( NSAI DS)
NSAI DS are used for t he init ial t reat ment of pain,
inflammat ion and st iffness. side effect s are well
recoginised and include gast roint est inal dist urbance,
rash, mood changes, and sleep dist urbance.
Doses used in JI A are higher t han in ot her
indicat ions. Thers is no evidence t o support t he use of
t opical NSAI DS in JI A. There is lit t le evidence base for
differences bet ween NSAI DS and choice is usually made
according t o preferred dosing schedules, availabilit y of
liquid preparat ions, and pat ient preference.
Tabl e acr onyms
RF: rheumat oid fact or
Quot idian fever is defined as a fever t hat rises t o
39oc once a day ret urns t o 37oc bet ween fever
peaks.
Serosist is refers t o pericardit is, pleurit is, or peri-
t onit is, or some combinat ion of t he t hree.
Dact ylit is is swelling of > 1 digit s, usually in an
aysmmet ric dist ribut ion, which ext ends beyond
t he j oint margin.
A minimum of 2 pit s on any or more nails at any
t ime.
Ent hesit is is defined as t enderness at t he inser-
t ion of a t endon, ligament , j oint capsule, or fas-
cial t o bone.
I nflammaroy lumbosacral pain refers t o lum-
bosacral pain at rest wit h morning st iffness t hat
improves on movement .
Management of Juveni l e i di opat hi c ar t hr i t i s
I nvesti gati ons
There is no specific t est for disgnosis of JI A
● Complet e blood count
● Anaemia, raised whit e cell and plat elet count
consist ent , wit h inflammat ion.
● ESR and CRP may be elevat ed
● Rheumat oid fact or (RF) and ant inuclear ant igen
(ANA)
● Aut oant ibodies indicat e poor prognosis in JI A.
● Synovial fluid count s, glucose and cult ure should
be performed if sept ic art hrit is is suspect ed.
● Plain X-rays have a role in excluding t rauma, ma-
lignancy or infect ion, but changes caused by Ju-
venile idiopat hic art hrit is oft en occur lat e in t he
disease course.
● Ult rasound screening of j oint s may be used t o
det ect effusions, especially where clinical assess-
ment is difficult (such as hips), and also t o guide
int ra-art icular t reat ment .
Poor pr ogonst i c i ndi cat or s i n Juveni l e i di opat hi c
ar t hr i t i s ( JLA)
● Act ive syst emic disease at 6 mont hs in Sysemic
Onset JI A (fever, need for cort isocst eroid, and
t hrombocyt osis)
228
Doses of common non - st er oi dal ant i -
i nf l ammat or y dr ugs ( NSAI DS) used f or JI A
● I buprofen: 10mg/ kg t hree or four t imes daily, can
be given up t o 60mg/ kg/ day in syst emic onset
JI A in 6 divided doses
● Naproxen: 5-10mg/ kg t wice daily (suspension
125mg/ 5ml)
● Diclofenac: 1mg/ kg t wice or t hree t imes daily
● I ndomet hacin: 0.5 -1mg/ kg t hree t imes daily
Cor t i cost er oi ds
I nt ra-art icular cort icost eroids if used under proper
asept ic condit ion, are well est ablished for t he t reat ment
of oligoart icualar JI A and as an adj unct in t he t reat ment
of polyart icular JI A.
The preparat ions used are
● Traimcinolone hexacet onide
● Triamcinolone acet onide
● Met hylprednisolone acet at e
Lignocaine Combinit aion for int ra art icular inj ec-
t ion t o be avoided as it can cause anaphylaxis
I nt er mi t t ent pul sed Met hyl pr edni sol one
(30mg/ kg/ day wit h a maximum daily dose of lg,
given on t hree consecut ive days, repeat ed one week
lat er) has been shown t o provide good short t erm
benefit in JI A, achieving rapid cont rol of disease and
allowing for a lower cumulat ive dialy st eroid dosage
t han convent ional oral glucocort icoid t reat ment .
I f long-t erm oral st eroids are required, t hey should
be used at t he minimum does possible t o cont rol
disease. Long act ing st eroids like bet amet hasone,
dexamehasone are not t o be used as t hey cause
prolonged adrenal suppression. St eroid dose is t o be
given in single dose in t he morning.
Doses more t han 1mg/ kg day of prednisolone are
not necessary, in fact can causes more side effect s.
Met hot rexat e has become t he second-line agent
of choice for persist ent , act ive art hrit is because
of it s effect ivenvess and accept able t oxic effect s.
I mprovement in pat ient s is usually seen aft er 6-12
weeks of cont inuous and regular t herapy.
Dose 10mg/ m2 per week.. maximum t herapeut ic
effect wit h parent eral administ rat ion of 15 mg/ m2 per
week along wit h supplement at ion of folic acid 5mg
t wice weekly t o prevent t he occurrence of liver enzyme
abnormalit ies.
The si de-ef f ect pr of i l e
Met hot rexat e is well recognized and drug int erat ions
are rarely significant at doses used. Adverse effect s
occur in up t o 23% of children most commonly nausea,
vomit ing, mout h ulcers, loss of appet it e, alopecia,
t ransient rise in liver enzymes, or leucopenia.
Moni t or i ng Met hot r exat e t oxi ci t y
Complet e blood count s, LFT and creat inine init ially
every mont h for 3 mont h t hen once in every 3 mont h.
Ot her di sease modi f yi ng ant i -r heumat i c dr ugs
● Sulfasalazine can be beneficial for lat e-onset oli-
go JI A, ent hesit is-relat ed or inflammat ory bowel
realat ed art hrit is.
● I t is t o be avoided in Syst emic onset JI A.
● Dose:
* I nit ially 30mg/ kg/ day in divided doses, t hen
increase by 5mg/ kg every week t o maximum
dose of 50mg/ kg/ day in dividied doses.
● Monit oring:
* Tot al blood Count s mont hly for 3 mont hs t hen
every 3rd mont hly t heraft er
Ant i -TNF t r eat ment
Ant it umour necrosis foct or ( TNF) t herapy is
required for many children who have failed t o respond
adequat ely t o Met hot rexat e or have been unable t o
t olerat e Met hot rexat e because of adverse effect s.
Ot her medi cal consi der at i ons i n JI A
● Treat ment of growt h failure
● Treat ment of uveit is - opht almology referral
● Dent al referral
● Vaccinat ions
● Treat ment of varicella cont act if immunosup-
pressed
● Prevent ion of ost eoporosis
● Ort hopaedic referral for j oint replacement
● Psychology and counselling
● Pain management
● Let t ers for school, career advice
● Adolescent care and sexual healt h.
229
Infections
Chapter 11
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
● HI V and AI DS
● Opport unist ic I nfect ions
● Pneumocyst it is Carinii (Jerovici)
● Oesophageal Candidiasis
● Crypt ococcosis
● Toxoplasmosis
● Crypt osporidiosis
● Typhoid
● Lept ospirosis
● Parasit ic I nfect ions
● Amoebiasis
● Giardiasis
● Malaria
● Worm I nfest at ions
● Ascariasis
● Filariasis
● Dengue fever
● Chikungunya
● H1N1 Swine Flu
231
Infections – Bacterial, viral and
opportunistic
HI V and AI DS
HI V infect ion leads t o progressive immunodeficiency
and increased suscept ibilit y t o infect ions, including
TB. The rat e of disease progression is highly variable
bet ween individuals, ranging from 6 mont hs t o more
t han 20 yrs
The median t ime t o develop AI DS aft er t ransmission
is 10 yrs in t he absence of ant i ret roviral t herapy (ART).
Symptoms
● The case definit ion of AI DS is fulfilled if at least 2
maj or signs and at least 1 minor sign are present
where HI V t est ing facilit ies are not available. I n
children if 2 maj or and 2 minor signs are present
(if no ot her causes for immunosuppression)
● Maj or si gns and sympt oms:
* Weight loss (> 10 Kg or > 20 % of original
weight )
* Diarrhoea (> 1 mont h)
* Fever for more t han 1 mont h
● Mi nor si gns:
* Herpes zost er (shingles)
* Prurit ic popular rash
* Kaposi’s sarcoma
* Persist ent generalized lymphadenopat hy
* Oral candidiasis
* Oral hairy leukoplakia
* Persist ent painful genit al ulcerat ion.
* The persist ence of eit her Kaposi’s sarcoma
or crypt ococcal meningit is is sufficient for t he
case definit ion of AI DS
● HI V disease is charact erized by t hree phases
* Acut e primary illness
* Asympt omat ic chronic illness
* Sympt omat ic chronic illness.
● Essent ial laborat ory invest igat ions:
* HI V serology
* CD4+ T lymphocyt es count s (if available)
* Complet e blood count and chemist ry profile
* Pregnancy t est .
● Supplement ary t est s indicat ed by hist ory and
physical examinat ion:
* Chest X-ray
* Urine for rout ine and microscopic examinat ion
* Hepat it is C virus (HCV) and Hepat it is B virus
(HBV) serology (depending on t est availabilit y
and resources)
I mpor t ant not e
I t is most import ant t o confirm t he diagnosis of HI V
infect ion by t est s performed by a t rained t echnician,
preferably in a diagnost ic laborat ory. The t est result s
should include t he t ype of t est performed t o est ablish
t he diagnosis based on WHO guidelines. I n case t here
is any doubt , t he t est should be repeat ed in a st andard/
referral laborat ory.
Treatment
I ni t i at i on of ART i n HI V – i nf ect ed adul t s and
adol escent s
HI V disease st aging is import ant for init iat ing
ant iret roviral (ARV) t herapy. WHO recommends t hat in
resource-limit ed set t ings, in case of HI V infect ed adult s
and adolescent s, st art ARV when t hey have:
● WHO st age I V of HI V disease ( cl i ni cal AI DS) ,
regardless of CD4 count
● WHO st ages I , I I , I I I of HI V disease, wit h a CD4
count below 200/ mm
I f CD4 t est i ng i s avai l abl e
● WHO st age I V disease
● WHO st age I , I I or I I I wit h CD4 count < 200/
mm3
I f CD4 t est i ng i s unavai l abl e
● WHO st age I V disease irrespect ive of CD4 count
● WHO st age I , I I or I I I wit h count < 1200/ mm3.
Though t he t ot al lymphocyt e count correlat es
relat ively poorly wit h CD4 count , in combina-
t ion wit h clinical st aging it is a useful marker of
prognosis and survival
232
WHO Clinical staging of HIV
Disease for adults
Pr i mar y HI V I nf ect i on
● Asympt omat ic
● Acut e ret roviral syndrome
Cl i ni cal st age 1
● Asympt omat ic
● Persist ent generalized lymphadenopat hy (PGL)
Cl i ni cal st age 2
● Moderat e unexplained weight loss (< 10% of pre-
sumed or measured body weight )
● Recurrent respirat ory t ract infect ions
* Sinusit is
* Bronchit is
* Ot it is media
* Pharyngit is
● Herpes zost er
● Angular cheilit is
● Recurrent oral ulcerat ions
● Papular prurit ic erupt ions
● Seborrhoeic dermat it is
● Fungal nail infect ions of fingers
Cl i ni cal st age 3
Condit ions where a presumpt ive diagnosis can be
made on t he basis of clinical signs or simple invest igat ions
● Severe weight loss (> 10% of presumed or meas-
ured body weight )
● Unexplained chronic diarrhoea for longer t han
one mont h
● Unexplained persist ent fever (int ermit t ent or
const ant for longer t han one mont h)
● Oral candidiasis
● Oral hairy leukoplakia
● Current Pulmonary t uberculosis ( TB)
● Severe presumed bact erial infect ions (e.g. pneu-
monia, empyema, pyomyosit is, bone or
● Joint infect ion, meningit is, bact eraemia)
● Acut e necrot izing ulcerat ive st omat it is, gingivit is
or periodont it is
Condit ions where confirmat ory diagnost ic t est ing is
necessary
● Unexplained anaemia (< 8 g/ dl), and or neut ro-
penia (< 500/ mm3) and or
● Thrombocyt openia (< 50 000/ mm3) for more
t han one mont h
Cl i ni cal st age 4
Condit ions where a presumpt ive diagnosis can be
made on t he basis of clinical signs or simple invest igat ions
● HI V wast ing syndrome
● Pneumocyst is pneumonia
● Recurrent severe or radiological bact erial pneu-
monia
● Chronic herpes simplex infect ion (orolabial, geni-
t al or anorect al of more t han one mont h’s dura-
t ion)
● Oesophageal candidiasis
● Ext ra-pulmonary Tuberculosis including Tubercu-
lous lymphadenopat hy
● Kaposi’s sarcoma
● Cent ral nervous syst em (CNS) t oxoplasmosis
● HI V encephalopat hy
Condi t i ons wher e conf i r mat or y di agnost i c
t est i ng i s necessar y:
● Ext ra-pulmonary crypt ococcosis including menin-
git is
● Disseminat ed non-t uberculous mycobact erial in-
fect ion
● Progressive mult i-focal leukoencephalopat hy
(PML)
● Candida of t rachea, bronchi or lungs
● Crypt osporidiosis
● I sosporiasis
● Visceral herpes simplex infect ion
● Cyt omegalovirus (CMV) infect ion (ret init is or of
an organ ot her t han liver, spleen or lymph nodes)
● Any disseminat ed mycosis (e.g. hist oplasmosis,
coccidiomycosis, penicilliosis)
● Recurrent non-t yphoidal salmonella sept icaemia
● Cerebral or B-cell Non-Hodgkin lymphoma
● I nvasive cervical carcinoma
● Visceral leishmaniasis
233
WHO clinical staging of HIV for children
Cl i ni cal St age 1
● Asympt omat ic
● Persist ent Generalised lymphadenopat hy (PGL)
Cl i ni cal St age 2
● Hepat osplenomegaly
● Papular prurit ic erupt ions
● Seborrhoeic dermat it is
● Ext ensive human papilloma virus infect ion
● Ext ensive molluscum cont agiosum
● Fungal nail infect ions
● Recurrent oral ulcerat ions
● Lineal gingival eryt hema (LGE)
● Angular cheilit is
● Parot id enlargement
● Herpes zost er
● Recurrent or chronic recurrent respirat ory t ract
infect ions
* Ot it is media
* Ot orrhoea
* Sinusit is
Cl i ni cal St age 3
Condit ions where a presumpt ive diagnosis can be
made on t he basis of clinical signs or simple invest igat ions
● Moderat e unexplained malnut rit ion not ade-
quat ely responding t o st andard t herapy
● Unexplained persist ent diarrhoea (14 days or
more )
● Unexplained persist ent fever (int ermit t ent or
const ant , for longer t han one mont h)
● Oral candidiasis (out side neonat al period )
● Oral hairy leukoplakia
● Acut e necrot izing ulcerat ive gingivit is / periodon-
t it is
● Pulmonary t uberculosis including t uberculous
lymphadenopat hy
● Severe recurrent presumed bact erial pneumonia
Condi t i ons wher e conf i r mat or y di agnost i c
t est i ng i s necessar y
● Chronic HI V-associat ed lung disease including
brochiect asis
● Lymphoid int erst it ial pneumonit is (LI P)
● Unexplained anaemia (< 8g/ dl)
● Neut ropenia (< 1000/ mm3) and or
● Thrombocyt openia (< 50 000/ mm3) for more
t han one mont h
Cl i ni cal st age 4
Condit ions where a presumpt ive diagnosis can be
made on t he basis of clinical signs or simple invest igat ions
● Unexplained severe wast ing or severe malnut ri-
t ion not adequat ely responding t o st andard t her-
apy
● Pneumocyst is pneumonia
● Recurrent severe presumed bact erial infect ions
(e.g. empyema, pyomyosit is, bone or j oint infec-
t ion, meningit is, but excluding pneumonia)
● Chronic herpes simplex infect ion; (orolabial or
cut aneous of more t han one mont h’s durat ion)
● Ext ra-pulmonary TB
● Kaposi’s sarcoma
● Oesophageal candidiasis
● CNS t oxoplasmosis (out side t he neonat al period)
● HI V encephalopat hy
Condi t i ons wher e conf i r mat or y di agnost i c
t est i ng i s necessar y
● CMV infect ion (CMV ret init is or infect ion of or-
gans ot her t han liver, spleen or lymphnodes on-
set at age one mont h or more)
● Ext ra-pulmonary crypt ococcosis including menin-
git is
● Any disseminat ed endemic mycosis (e.g. ex-
t rapulmonary hist oplasmosis, coccidiomycosis,
penicilliosis)
● Crypt osporidiosis
● I sosporiasis
● Disseminat ed non-t uberculous mycobact eria
infect ion
● Candida of oesophagus, bronchi or lungs
● Visceral herpes simplex infect ion
234
● Acquired HI V associat ed rect al fist ula
● Cerebral or B-cell Non-Hodgkin lymphoma
● Progressive mult ifocal leuko - encephalopat hy
(PML)
● HI V-associat ed cardiomyopat hy or
● HI V-associat ed nephropat hy
Pr i nci pl es and goal s of t her apy of HI V i nf ect i on
● Ongoing HI V infect ion leads t o immune syst em
damage and progression t o AI DS; goal is rest ora-
t ion and/ or preservat ion of immunological func-
t ion
● Plasma HI V RNA levels indicat es t he magnit ude
of HI V replicat ion and t he rat e of CD4+ T cell
dest ruct ion.
● CD4+ T cel l count s i ndi cat e t he cur r ent
l evel of compet ence of t he i mmune syst em.
● Rat es of disease progression differ among indi-
viduals and t reat ment decisions should be indi-
vidualized based upon t he plasma HI V RNA levels
and CD4+ T cell count s
● Maximal suppression of viral replicat ion is t he
goal of t herapy; t hen great er t he suppression t he
less likely t he appearance of drug-resist ant quasi-
species
● The goal of ant i-ret roviral t herapy is reduct ion of
HI V-relat ed morbidit y and mort alit y and improve-
ment in qualit y of life.
● The most effect ive t herapeut ic st rat egies involve
t he simult aneous init iat ion of combinat ions of ef-
fect ive ant i-HI V drugs wit h which t he pat ient has
not been previously t reat ed and t hose t hat are
cross-resist ant wit h ant i-ret roviral agent s t hat t he
pat ient has already received.
● The ant i-ret roviral drugs used in combinat ion
regimens should be used according t o opt imum
schedules and dosages.
● The number of available drugs is limit ed. Any de-
cisions on ant i-ret roviral t herapy have a long t erm
impact on fut ure opt ions for t he pat ient
● Women should receive opt imum ant i-ret roviral
t herapy regardless of t he pregnancy st at us.
● The same principles apply t o children and adult s.
The t reat ment of HI V infect ed children involves
unique pharmacologic, virologic, and immuno-
logic considerat ions.
Recommended regimens for t reat ment of AI DS in
adult s and adolescent s
Fi r st l i ne r egi mens Dose
Zidovudine (ZDV)
Lamivudine (3TC) plus
Efavirenz (EFZ) or
Nevirapine (NVP)
ZDV 300 mg t wice daily
3TC 150 mg t wice daily
EFZ 600 mg once daily
NVP 200 mg once daily
for 14 days, t hen 200 mg
t wice daily
ZDV/ 3TC/ Abacavir
(ABC)
ABC300 mg t wice daily
ZDV/ 3TC/ RTV-
enhanced
PI
a
or Nelfinavir (NFV) NFV 1250 mg t wice daily
I ndinavir (I DV/ r) I DV/ r 800 mg/ 100
mg t wice daily used
Commonly; 800 mg/ 200mg
t o 400mg/ 100 mg
Lopinavir (LPV/ r) LPV/ r 400 mg/ 100 mg
t wice daily
Saquinavir (SQV/ r) SQV/ r 1000 mg/ 100 mg
t wice daily
RTV - enhanced PI = I ndinavir (I DV) / Rit onavir (r),
Lopinavir (LPV), / Rit onavir, Saquinavir (SQV) / Rit onavir.
An RTV - enhanced PI regimen is preferred given t he
pot ency of t hese regimens. NFV can be considered as
an alt ernat ive for t he PI component of t he second - line
t herapy if RTV - enhanced PI is not available or if t here
is a clinical cont raindicat ion t o it s use.
I mpor t ant Not e
Compliance plays an import ant part in ensuring
maximal effect from a given regimen. The simpler
t he regimen, t he easier it is for t he pat ient t o follow. I t
must be explained t o t he pat ient t hat ART requires high
levels of adherence for long-t erm efficacy, most likely
will need t o be t aken life long, and is associat ed wit h
a range of short t erm and long t erm t oxicit ies t hat can
occasionally be life-t hreat ening.
● HI V- DNA PCR or HI V- RNA PCR or immune com-
plex dissociat ed p24 ant igen assays, or HI V cul-
t ure
● I nit iat ion of ARV can also be considered for chil-
dren who have advanced WHO pediat ric st age I I
disease including such as severe recurrent or
persist ent candidiasis out side neonat al period,
weight loss, fevers, recurrent severe bact erial in-
fect ions, irrespect ive of CD4 count .
235
WHO r ecommendat i ons f or i ni t i at i ng Ant i r et r ovi r al t her apy i n i nf ant s and chi l dr en
AGE CD4 count HI V Di agnost i c t est i ng Tr eat ment r ecommendat i on
< 18 mont hs Available Posit ive HI V virologic t est
HI V virologic t est ing not available but
infant HI V seroposit ive or born t o
known HI V-infect ed mot her.
(Not e: HI V Ab t est must be repeat ed at
age of 18 mont hs)
WHO Paediat ric st age I I I b
(I rrespect ive of CD4 cell percent age
WHO Paediat ric st age I / I I disease
wit h CD4 percent age < 20%
> 18 mont hs Available HI V ant ibody seroposit ive WHO Paediat ric st age I I I b disease
WHO Paediat ric st age
I / I I disease wit h
CD4 percent age < 20%
< 18 mont hs Not available Posit ive HI V virologic t est
HI V virologic t est ing not available but
infant HI V Seroposit ive or
Born t o known HI V-infect ed mot her.
WHO Paediat ric st age I I I
Treat ment not recommended
> 18 mont hs Not available HI V ant ibody seroposit ive WHO Paediat ric st age I I I
● The rat e of decline of CD 4 percent age (if meas-
urement available) should be fact ored int o deci-
sion-making.
● Many of t he clinical sympt oms in t he WHO Pae-
diat ric st age I I and I I I disease classificat ion are
not specific for HI V infect ion in resource-limit ing
set t ing; t hus, in t he absence of virologic t est ing
and CD4 cell assay availabilit y, HI V-exposed in-
fant s < 18 mont hs of age should generally not
be considered for ART regardless of sympt oms.
Recommend frst-line antiretroviral regi-
mens for children
Zi dovudi ne ( ZDV)
● ZDC/ 3TC is t he first choice for children as it has
t he highest amount of clinical experience
● Ot her dual NRTI component s can be subst it ut ed
for children, including ZDV/ ddl, d4T/ ddl, and
ddl/ 3TC. ZDV/ d4t should never be used t oget her
due t o proven ant agonism.
Reasons f or changi ng ART
● The reasons for changing ART regimen include
adver se dr ug ef f ect s, i nconveni ent r egi -
mens such as dosing z/ number of pills t hat may
compromise adherence, t r eat ment f ai l ur e, oc-
cur r ence of act i ve t uber cul osi s and pr eg-
nancy.
● Treat ment failure can occur due t o a number of
reasons. These include
* Unsat isfact ory pat ient adherence
* Viral resist ance t o one or more drugs
* I mpaired drug absorpt ion, and
* Alt ered drug pharmacokinet ics.
● The ent ire regimen should be changed from a
first t o a second line combinat ion regimen in case
of t reat ment failure. A si ngl e dr ug shoul d not
be added or changed t o a f ai l i ng r egi men.
● The new second line regimen will need t o use
drugs which ret ain act ivit y against t he pat ient ’s
virus st rain and ideally include at least t hree new
drugs, in order t o increase t he likelihood of t reat-
ment success.
Pr event i on of Par ent t o chi l d t r ansmi ssi on
( PPTCT)
● Primary prevent ion of HI V infect ion among wom-
en of child bearing age
* By giving informat ion, educat ion and counsel-
ling on HI V prevent ion and care t o t he general
populat ion and couples
* Bet t er STI management
* Reduct ion of unsafe t ransfusions
* Condom promot ion: safe sex pract ice, and
encouraging part ner’s involvement in safe sex
236
discussions.
● Prevent ion of unint ended pregnancy in HI V in-
fect ed women- informat ion, educat ion and coun-
selling on HI V prevent ion and care including ap-
proach t o MTCT prevent ion
* I ncreasing t he number of woman who know
t heir HI V sero-st at us
* Counseiling of woman and t heir part ners t o
enable informed choice wit h regard t o pot en-
t ial fut ure pregnancy
* Condom promot ion as a valuable family plan-
ning t ool.
● Women who t est HI V-posit ive in early pregnancy
can make t he decision eit her t o cont inue wit h t he
pregnancy or t o elect for t erminat ion where t his
is legal and safe.
Occupational HIV exposure and
HIV post-exposure prophylaxis (PEP)
PEP involves t he management of healt h care workers
who are possibly exposed t o HI V. The most import ant
management st rat egy is prevent ion of exposure. Nat ure
of exposure and PEP recommendat ion are given below:
Nat ure of exposure and PEP recommendat ions
PEP
r ecommended
PEP
r ecommended
PEP not
war r ant ed
High-risk
exposure
I nt ermediat e-risk
exposure
Low-risk
exposure
Large bore
hollow needle
deep punct ure
Less severe
percut aneous
exposure (e.g.,
solid needle)
Short
exposure (< 1
minut e)
Device in pat ient
art ery or vein
Mucous
membrane
exposure
or non int act
skin: volumes
(e.g., a maj or
blood splash)
prolonged
exposure (> 1
minut e)
Small volume
(e.g. blood
visible on
device
superficial
scrat ch)
Treatment
Management of PEP
● Treat ment of exposure sit e wit h int ermediat e first
aid
* Wash skin wit h soap and wat er
* Rinse eyes wit h eye wash fluid
* Oral exposure- spit out immediat ely and rinse
mout h several t imes.
● Prompt assessment of risk and HI V st at us of ex-
posure source.
● Counselling of healt h care worker
* Pret est counselling for hepat it is B and HI V;
consider for HBV immunoglobulin and HBV
vaccinat ion if not HBV immune; not t o give
blood unt il out come is known; review and
post exposure counselling.
● Giving ART if indicat ed and counsel about adher-
ence and follow up
● I f int ermediat e risk or high risk- commence as
soon as possible (preferably wit hin 72 hours)
* Three drug regimen AZT/ 3TC/ I ndinavir 3
t imes or
* Nelfinavir or
* Third drug can be an NNRTI (EFV is preferred
over NVP)
● Document at ion of t he incident
* Dat e and t ime of exposure
* Det ails of t he event
* Exposure source
* Det ails of PEP given
* Follow up and out come.
Tuberculosis and HIV infection
● Tuberculosis and HI V are closely int erlinked.
● Tuberculosis is a leading cause of HI V relat ed
morbidit y and mort alit y
● HI V is t he most import ant fact or fuelling t he Tu-
berculosis epidemic in populat ions wit h a high
HI V prevalence
● Tuberculosis can occur at any point in t he course
of progression of HI V infect ion
● High levels of MDR-TB in some areas t hreat en
t uberculosis cont rol effort s.
● I n pat ient s wit h HI V-relat ed t uberculosis, t he
priorit y is t o t reat t uberculosis, especially smear-
posit ive Pulmonary t uberculosis. However, pa-
t ient s wit h HI V-relat ed t uberculosis can have
ART and ant i-Tuberculosis t reat ment at t he same
t ime, if managed carefully
237
● Careful evaluat ion is necessary in j udging when
t o st art ART. I n case, e.g., disseminat ed t uber-
culosis and / or CD4 count < 200/ mm
3
, it may be
necessary t o st art ARV concomit ant ly wit h t uber-
culosis t reat ment
● On t he ot her hand, for a pat ient wit h smear posi-
t ive pulmonary t uberculosis as t he first manifes-
t at ion of HI V infect ion, who does not appear t o
be at high risk of dying, it may be safe t o defer
ART unt il t he init ial phase of t uberculosis t reat-
ment has been complet ed and t hen use Et ham-
but ol and isoniazid in t he cont inuat ion phase
● This decreases t he risk of immune reconst it ut ion
syndrome (t emporary exacerbat ion of sympt oms,
signs or radiological manifest at ion of t uberculo-
sis) and avoids t he risk of drug int eract ion be-
t ween rifampicin and prot ease inhibit ors (PI ).
I mpor t ant Not e
Ant i-Tuberculosis drug t reat ment is t he same for HI V
posit ive and HI V negat ive t uberculosis pat ient s, wit h
one except ion: do not gi ve t hi acet azone t o HI V
posi t i ve t uber cul osi s pat i ent s (increased risk of
severe and somet imes fat al skin react ions).
severe and somet imes fat al skin react ions).
Opportunistic infections
Causes
● Tuberculosis
● Pneumocyst is carinii pneumonia
● Esophageal candidiasis
● Crypt ococcosis
● Toxoplasmosis
● Crypt osporidiosis
● Cyt omegalovirus (CMV)
● Mycobact erium Avium Complex (MAC) disease
As t he compromised immune syst em makes t he
individual vulnerable t o a variet y of illnesses, HI V
infect ion may manifest it self in many different forms.
Diagnosis and management of common opport unist ic
infect ions is given below.
Pneumocystis carinii pneumonia (PCP)
Pneumocyst is carinii is a fungus t hat infect s t he lungs
Symptoms
● Sub-acut e onset of sympt oms over a period of
weeks
● Typically fever, dry cough and progressive diffi-
cult y in breat hing, also weight loss, night sweat s
and fat igue.
I nvesti gati ons
● Diagnos is by
* X-ray
* I nduced sput um examinat ion or bronchos-
copy
* CD4 count < 200
*
Treatment
Management of PCP depends on t he degree and
severit y of disease:
● Severe disease—hospit alizat ion, I nt ravenous
TMP / SMX (15 mg/ kg/ day of TMP for 21 days),
supplement al oxygen.
● Pat ient s wit h severe hypoxemia (PaO2 < 70-
mmHg breat hing room air at rest ).,
* Should be given cort ico-st eroids Prednisolone
40 mg t wice daily for 5 days followed by 40
mg once daily for 5 days, followed by 20 mg
once daily for 11days.
● Moderat e disease – an oral agent may be used
and management can proceed on out pat ient
basis,alt hough hospit alizat ion should be consid-
ered.
● Recommended oral regimen: TMP/ SMX (15 mg/
kg/ day of TMP) in divided doses for 21 days.
● Mild disease—Oral TMP/ SMX as above.
Pr event i ve t her apy is indicat ed when CD4+ cell
count s equal or are below (prophylaxis) 200 and / or
sympt omat ic HI V
Al t er nat i ve t her api es
● Dapsone 100 mg once a day for 21 days—pre-
ferred second-line opt ion.
● Clindamycin 450 mg 4 t imes a day + primaquine
15 mg once daily for 21 days.
● At ovaquone 750 mg once a day for 21 days
● Pent amidine (int ravenous) 3-4 mg/ kg/ day for 21
days
238
Toxi ci t i es of t r eat ment
● TMP/ SMX hypersensit ivit y (t ypically fever and
maculopapular rash)
● Nausea and vomit ing
● Bone marrow t oxicit y
● Hepat it is
St oppi ng mai nt enance
● There is some evidence t hat it may be possible
t o st op maint enance t herapy if CD4 count s st ay
above 200 on ant i ret ro t herapy. However t here
is insufficient dat a t o make current recommenda-
t ions.
Oesophageal candi di asi s
Candidiasis is a fungal infect ion t hat frequent ly
occurs in t he mout h and vagina. I t is considered t o
be an opport unist ic infect ion when it occurs in t he
Oesophagus.
Symptoms
● Difficult y in swallowing or ret rost ernal discomfort
● Weight loss is common
● Present at ion - sub acut e over weeks
● CD4 count < 100
● Usually made clinically in presence of oral candi-
dasis and dysphagia.
● Endoscopy is indicat ed only in t hose who fail t o
respond t o a clinical t rial of appropriat e t reat-
ment .
● The diagnosis of esophageal candidiasis should
be reconsidered if oral candidiasis is not present .
● Associat ed fever and oral ulcerat ion are not com-
mon.
Treatment
● Prevent ive t herapy: Not recommended because
current drugs effect ively t reat (prophylaxis) dis-
ease.
● Ant ifungal resist ance may develop and drug-drug
int eract ions may occur
● Drugs
* Flucanazole 100 – 400 mg once a day for 2
weeks is t he t reat ment of choice
● Alt ernat ive t reat ment
* Amphot ericin-B 0.3 – 0.5 mg/ kg/ day.
● Maint enance Therapy
* Fluconazole ( 50 – 100 mg once a day )
● St opping maint enance t herapy
* There is evidence t hat pat ient who achieves
CD4 count s > 100 on ART may cease t reat-
ment
Cryptococcosis
Crypt ococcus is a fungus t hat is inhaled and t hat has
a predilect ion for meninges (brain linings)
Symptoms
● Meningit is
* Headache
* Nausea
* Fever
* Malaise
* Alt ered ment al st at us
* I rrit abilit y and
* Seizures
● Lung involvement may co-exist
* Cough
* Chest pain
* Breat hlessness
● Present at ion
* Sub - acut e wit h progressive sympt oms over
weeks t o mont hs or acut e wit h sympt oms
over days
● CD4 count : < 100
I nvesti gati ons
● Usually by lumbar punct ure t o t est for t he pres-
ence of crypt ococcus or crypt ococcal ant igen in
cerebral spinal fluid. I CP is oft en raised.
● CSF prot ein and glucose are generally normal
and t here may be few whit e blood cells.
Treatment
● Preferred
* Amphot ericin B (0.5 – 0.8 mg/ kg/ day) + Flu-
cyt osine (100 mg/ day) 4 t imes a day) for 2
weeks t hen 8 t o 10 weeks.
239
● Alt ernat ive Treat ment
* Liposomal Amphot ericin
● Maint enance t herapy
* Flucanazole 200 mg once a day
* Pregnant woman should avoid azole drugs
● St opping Maint enance
* Not recommended current ly because of few
available st udies
* Maint enance Therapy
» Cohort st udies suggest t hat maint enance
t herapy can be ceased in pat ient s wit h sus-
t ained CD4 response t o ART (CD4> 200)
for > 3 mont hs.
Toxoplasmosis
Toxoplasmosis is a parasit e t hat has a predilect ion
for t he brain.
Symptoms
● Alt ered ment al st at e (confusion, unusual behav-
ior),
● Headaches
● Fever
● Seizures
● Paralysis
● Coma
● Present at ion : acut e t o sub acut e over days t o
weeks
● CD4 count < 100
I nvesti gati ons
● Typical appearance on CT or MRI scan.Diagnosis
is usually presumpt ive on t he basis of appearance
on scan. May show r i ng shaped cont r ast en-
hanci ng l esi ons.
● I f no response t o empirical ant i-t oxoplasmosis
t herapy aft er 2 weeks t hen consider brain biopsy,
t o rule out CNS lymphoma.
● Prevent ive t herapy is indicat ed when CD4+ cell
count is below 200 (for primary PCP prophylaxis)
● Preferred
* TMP SMX ( 1 double - st rengt h every 12 hours
t hree t imes a week: or
* A single st rengt h or 1 double - st rengt h t ablet
once a day.
● St opping prevent ive t herapy
* CD4+ cell count above 200 for over 3-6
mont hs.
Treatment
● Pyrimet hamine 100 – 200 mg loading dose and
t hen 50 – 75 mg once a day given in combinat ion
wit h sulphadiazine 4 – 6 g/ day, 4 t imes a day or
Clindamycin 2 – 4 g/ day, 4 t imes a day for 6 – 8
weeks durat ion depending upon response
● I f Sulphadiazine is used t hen Folinic acid25 mg
once a day should be given t o prevent haemat o-
logical t oxicit y.
● Cort icost eroids may be used in t he presence of
cerebral edema
Al t er nat i ve t r eat ment
● Pyrimet hamine in combinat ion wit h one of t he
following:
* Azit hromycin 1 – 1.5 mg/ day At ovaquone 3
g/ day
* Dapsone 100 mg/ day
* Clarit hromycin 2 g/ day
Mai nt enance t her apy:
● Pyrimet hamine (25 – 75 mg once a day) + Sul-
phadiazine (500 – 100 mg 4 t imes a day for sev-
eral days wit h Leucoverin)
St oppi ng mai nt enance t her apy:
* Not recommended current ly
Cryptosporidiosis
Crypt osporidiosis is a parasit e t hat infect s gast ro
int est inal t ract
Symptoms
● Chronic diarrhoea wit h frequent wat ery st ools
● Abdominal cramps
● Nausea and Vomit ing
● Fat igue
● Weight loss
● Loss of appet it e
● Fever
● Dehydrat ion
240
● Elect rolyt e imbalance (especially sodium and po-
t assium)
● Present at ion t ime frame: acut e t o chronic pres-
ent at ion over days t o weeks or mont hs in some
cases
● CD4 count < 100
I nvesti gati ons
St ool examinat ion for det ect ion of oocyst s in t he
st ool, on biopsy of small int est ine. A specific request for
examinat ion for crypt osporidiosis is required (specific
lab t echniques are needed)
● Prevent ive t herapy: There are no proven effec-
t ive t herapies. (Prophylaxis)
● There is no good evidence t hat boiling wat er or
t he use of wat er filt ers prevent s t he disease.
Treatment
● There are no proven effect ive t herapies
● Sympt omat ic t reat ment includes Loperamide, co-
deine, and Somat ost at in analogues.
● I mmune recovery induced by ART alone result s in
excellent clinical responses.
● Maint enance Therapy: There are no proven t her-
apies t hat prevent Crypt osporidiosis
I mpor t ant Not e
Drug int eract ions bet ween ARV drugs and drugs
used t o prevent or t reat opport unist ic infect ions:
● Trimet hoprim-sulphamet hoxazole can give addi-
t ive hemat ological t oxicit y when given t oget her
wit h Zidovudine.
● Ant ifungal drugs such as Ket aconazole and Flu-
canazole may inhibit t he met abolism of Prot ease
inhibit ors. This may result in increased serum
levels of Prot ease inhibit ors and increased risk
of t oxicit y.
Ref er ences
● I nfect ion in t he immunocompromised host . I n:
Oxford Text book of Medicine, Warrell DA. Cox
TM, Firt h JD, Benz EJ Jr. (eds), 4
t h
edit ion, 2003,
oxford universit y press,pp 1.864-1.870
● Diagnosis and t reat ment of fungal infect ions.
I n: Harrison’s principles of medicine. Kasper DL,
Braunwald E, Fauci AS et al (eds), 16
t h
edit ion,
McGraw-Hill Company I nc., Newyork, pp 1176
– 1179
● Pneumocyst is carinii infect ions. . I n: Harrison’s
principles of medicine. Kasper DL, Braunwald
E, Fauci AS et al (eds), 16
t h
edit ion, McGraw-Hill
Company I nc., New York, pp 1194 – 1196
● Programme implement at ion Guidelines for a
phased scale up of access t o Ant iret roviral Thera-
py (ART) for people living wit h HI V/ AI DS. Nat ion-
al AI DS Cont rol Organizat ion. Minist ry of Healt h
& Family Welfare, 2004.
● WHO SEARO Training modules on HI V/ AI DS care
and Ant iret roviral t reat ment , 2003.
● TB/ HI V: A clinical Manual WHO Second Edit ion,
2004.
Typhoid or enteric fever
Causes
I t is caused by Salmonella t yphi and Salmonella
parat yphi. Salmonella t yphi causes a variet y of illnesses
including
● Asympt omat ic carrier st at e
● Gast ro-ent erit is
● Ent eric fever
Symptoms
● The onset of fever is t ypically gradual, cont inu-
ous (t emperat ure upt o 40
o
C) wit h const it ut ional
sympt oms such as
* Malaise
* Anorexia
* Let hargy
* Headache
* Const ipat ion or diarrhoea (pea-soup st ools)
which may be associat ed wit h
» Abdominal pain and t enderness
* Hepat omegaly
* Splenomegaly and
* Change in ment at ion
● Usually t he pat ient is sick and has a t oxic appear-
ance wit h a coat ed t ongue and a soft splenom-
egaly.
● Examinat ion may reveal t oxic signs wit h relat ive
bradycardia and mild soft splenomegaly
241
I nvesti gati ons
● Diagnosis is suggest ed by
* Rising t it res of O ant ibodies (widal t est ) and
* Confirmed by isolat ion of organism in blood,
bone marrow, urine or st ool.
● Complicat ions such as
* Hepat it is
* Perit onit is
* Meningit is
* Pneumonit is and
* Myocardit is can occur usually aft er first week.
Treatment
Non-phar macol ogi cal
● Adequat e nut rit ion and hydrat ion should be main-
t ained ensuring adequat e int ake eit her orally or
wit h int ravenous fluids (in severely ill)
● I npat ient t reat ment is recommended if pat ient is
very sick, not accept ing orally wit h inadequat e
urine out put , pat ient has alt ered sensorium/
drowsiness or is having very high pyrexia part icu-
larly in t he second week of illness when t he risk
of complicat ions increases or if t he complicat ions
have already ensued.
Phar macol ogi cal
● Management of fever
● Ant ipyret ics can cause precipit ous fall in t empera-
t ure and even shock in ent eric fever. They should
be used j udiciously. Therefore hydro-t herapy is
preferred for fever.
Speci f i c t her apy
Mult i-drug resist ance is prevalent . Ant ibiot ics are
recommended on t he basis of available cult ure and
sensit ivit y pat t ern or epidemiological dat a.
● Tab. Ciprofloxacin 10 mg/ kg in 2 divided doses
upt o a maximum of 750 mg t wice daily for 10-14
days (for 1 week aft er t he fever subsides).
● Tab. Ofloxacin 200-400 mg daily for 5-7 days.
● I f no r esponse af t er 5 days
* I nj . Ceft riaxone 50-60 mg/ kg/ day I V or I M in
2 divided doses or as a single dose for 7-10
days (preferred in pregnant women pat ient s,
children or pat ient s resist ant t o quinolones)
or Tab. Cefixime 200-400 mg daily as a single
dose or 2 divided doses for 14 days.
● I f t her e i s no r esponse af t er 5 days, al t er -
nat i ve di agnosi s shoul d be consi der ed
* Report t o physician if abdominal sympt oms
worsens or occurrence of bleeding per rect um
or alt erat ion in sensorium and shock (severe
t yphoid wit h high risk of fat alit y)
● Severe t yphoid wit h shock or pat ient s wit h en-
t eric encephalopat hy should be hospit alized and
t reat ed as above plus I nj . Dexamet hasone 3 mg/
kg I V first dose followed by 1 mg/ kg I V every 6
hourly for 8 doses.
● Chr oni c car r i er st at e ( pat ient s who cont inue
t o excret e bacilli in st ool for more t han 1 year)
* Tab. Ciprofloxacin 750 mg t wice a day for 28
days.
Assessment of r esponse t o t her apy
● The t oxic look of t he pat ient decreases and appe-
t it e st art s ret urning in 72-96 hours of t reat ment
and gradually fever subsides, t ouches t he base-
line for increasing durat ion. The fever may t ake
as long as 7 days t o respond.
● Somet imes t he pat ient may apparent ly appear t o
have responded whereas pat ient may be devel-
oping impending shock due t o complicat ions. So
a careful clinical examinat ion has t o be done if
t here is a precipit ous fall in t emperat ure.
Modi f i cat i on or st ep up t her apy i f r equi r ed
● The pat ient should be monit ored for complica-
t ions and usual indicat ions for inpat ient t reat-
ment are
* Myocardit is
» Fall in perfusion and blood pressure
» Arrhyt hmias
* Alt ered sensorium
* Shock
» Tachycardia
» Cold clammy skin
» Diaphoresis
» Hypot ension
* Perforat ion perit onit is
» Acut e pain in abdomen
242
» Guarding, rigidit y
» Hypot ension
» Bilious vomit ing
● I n case t he pat ient worsens in 4-7 days, as dis-
cussed above, a change in ant ibiot ics is suggest-
ed, preferably on t he basis of cult ure and sensi-
t ivit y report , where available.
Pat i ent / Par ent educat i on
● Small frequent feeds should cont inue. Give plent y
of oral fluids and compensat e for increased fluid
loss from t he body due t o high-grade fever.
● The t reat ment should be given t ill t he pat ient
has an afebrile period of 7 days as incomplet e
t reat ment increases t he risk of relapse and emer-
gence of resist ance.
● The caregivers must be informed about t he com-
plicat ions.
● Ciprofloxacin and Ofloxacin are very bit t er and
cause severe nausea and gast rit is. Pat ient s
should be asked t o report any missed dose due
t o vomit ing.
● Three t ypes of vaccines are available for t his dis-
ease. Readers are request ed t o refer st andard
t ext books.
Ref er ences
1. Salmonellosis: Harrison’s principles of I nt ernal
Medicine, Kasper DL et al, 16
t h
edit ion, 2005, Mc-
Graw Hill company, New York, pp 897-902
2. Text book of Paediat ric infect ious diseases. WB
Saunders Co Philadelphia
3. American academy of Paediat ric in: Report of t he
commit t ee on infect ious diseases, 25
t h
edit ion,
2000, Elk Grove Village, I llinois, USA.
4. Salmonella in: Nelson’s t ext book of Paediat ric.
Behrman RE, Kleigman, 17
t h
edit ion, 2004, pp
912-919.
Leptospirosis
Causes
Lept ospirosis is an infect ious disease caused by t he
spirochaet e Lept ospira int errogans.
Symptoms
● Rodent s are t he most import ant reservoirs.
● Lept ospires may ent er t he host t hrough abrasions
in t he skin or t hrough int act mucosa, especially
t he conj unct iva and t he lining of oro- and na-
sopharynx when t hey come in cont act wit h wat er
cont aminat ed wit h lept ospira.
● 90% of sympt omat ic persons have t he relat ively
mild and t he usual anict eric form of Lept ospiro-
sis, wit h or wit h out meningit is.
● Severe Lept ospirosis wit h profound j aundice –
Wei l ’s syndr ome –occurs in 5 t o 10% of pa-
t ient s.
● The most common finding in anict eric Lept ospiro-
sis is
* Fever wit h conj unct ival suffusion
* Less common findings include
* Muscle t enderness
* Lymphadenopat hy
* Pharyngeal inj ect ion
* Rash
* Hepat omegaly and
* Splenomegaly
● Mild j aundice may be present
● Rarely meningit is can occur
● Weil’s syndrome, t he most severe form of Lept-
ospirosis is charact erized by j aundice, renal dys-
funct ion, hemorrhagic diat hesis, and a mort alit y
rat e ranging from 5 t o 15 %.
I nvesti gati ons
Laborat ory support is needed:
● To confirm t he diagnosis
● For epidemiological and public healt h reasons t o
det ermine which serovariant caused t he infect ion,
t he likely source of infect ion and pot ent ial reser-
voir and it s locat ion. The t est s used depends on
t he phase of t he infect ion. During lept ospiremic
phase (< 10days) lept ospires inoculat e in t he
blood and can be isolat ed by blood cult ure and
PCR while in t he immune phase, rising ant ibodies
can be det ect ed by serological t est s.
Cul t ur e
The isolat ion of lept ospirosis by cult ure of blood,
CSF and urine is t he most definit e way of confirming
t he diagnosis of lept ospirosis. Unfort unat ely, cult ure of
243
blood does not cont ribut e t o an early diagnosis as result s
come lat e, weeks or even mont hs aft er inoculat ion of
cult ure medium.
PCR
PCR is promising on bot h sensit ivit y and specificit y
but is complicat ed and expensive. I t s value for rapid
diagnosis is not seen and evaluat ed and not widely
used.
Ser ol ogy:
The serological t est s for diagnosis of lept ospirosis
have been classified as serovar specific t est s and genus
specific t est s.
Serovar specifc tests
1. Microscopic agglut inat ion t est (MAT)
2. Genus specific t est s
Mi cr oscopi c aggl ut i nat i on t est ( MAT)
MAT i s t he gol d st andar d t est f or di agnosi s
of l ept ospi r osi s because of i t s unsur passed
di agnost i c speci f i ci t y. The main advant age is t hat
serovar can be ident ified, which is of epidemiological
import ance.The difficult ies in ut ilizing MAT are due t o
t he following fact ors.
● The ant ibody t it res rise and peak only in second
or t hird week, making it a less sensit ive t est .
● The high t it res of past infect ion persist for a long
t ime (1-5years) and t herefore int erfere wit h t he
diagnosis of current lept ospirosis. Posit ive t it res
may represent a rising t it re of current infect ion or
declining t it re of past infect ion.
● The cut off t it re for diagnosis of current infect ion
depends on whet her t he area is endemic or non-
endemic, for example t he cut off t it re varies from
1/ 80 t o1/ 400.Therefore a second sample is usu-
ally required. ( To demonst rat e 4 fold rising t it re.)
To diagnose current infect ion, seroepidemiologi-
cal st udies are required for det ermining t he cut off
value
● The t est is complicat ed requiring dark field micro-
scopy and cult ures of various live serovars. This
may not be available in small laborat ories.
Genus speci f i c t est s
● The t wo common t est s are t he ELI SA and macro-
scopic slide agglut inat ion t est s (MSAT). The ot her
t est s are lat ex agglut inat ion t est , complement
fixat ion t est and haemagglut inat ion t est s
● The genus specific t est s are t he t est of choice for
t he diagnosis of current infect ion. These t est s are
simple and more sensit ive and become posit ive
earlier t han MAT, only as single ant igen is used,
t he genus specific ant igen
● These t est s det ect genus specific ant ibodies,
which is shared by pat hogenic and saprophyt ic
lept ospira
● These t est become posit ive early in t he disease
(5-6t h day). Det ect i on of speci f i c I gM ant i -
bodi es hel ps i n r api d di agnosi s of cur r ent
i nf ect i on.
ELI SA: These are popular t est s and can be performed
wit h commercial kit s or wit h ant igen preparat ion “ in
house”.
MSAT: The slide agglut inat ion t est is a simple
macroscopic t est in which a drop of t he dense suspension
of lept ospira is mixed wit h drop of serum on a slide is
examined by t he naked eye for agglut inat ion.
Labaratory Criteria For Diagnosis Of
Current Leptospirosis
● Cult ure
* Posit ive
● MAT
* Seroconversion / Four fold rise in t he t it re
* High t it re.
● ELI SA / MSAT
* Posit ive.
Treatment
Chemot her apy:
The aims of chemot herapy are t o eradicat e
lept ospirosis and t o prevent complicat ions. Lept ospirosis
is sensit ive t o most ant ibiot ics.
● Penicillin is t he most effect ive ant ibiot ic when giv-
en early. I n severe illness large doses (6—8mil-
lion unit s per day) of Benzyl penicillin may be
given in divided doses, preferably by I V rout e, for
5-7days. Fever subsides in 24-36 hours.
● Ampicillin 1g I V qid in severe illness or 500-
700mg qid in mild illness.
● Doxycycline 200mg/ day, Amoxycillin 500mg qid
and Eryt hromycin 250mg qid are effect ive.
● Quinolones and Cefot axime are also effect ive
244
against lept ospira. Recent ly t here is evidence t o
suggest t hat ant ibiot ics are useful even in t he
lat e st ages of illness.
Sympt omat i c and suppor t i ve t r eat ment :
● The primary import ance is t he met iculous at t en-
t ion t o fluid and elect rolyt e balance. Hypovolemia
and hypot ension need prompt and specific t reat-
ment wit h int ravenous fluids
● I n pat ient s wit h oliguria, if pre-renal azot emia is
suspect ed, prompt diuresis should be at t empt ed
wit h fluid t herapy
● Pat ient s who have no response t o t herapy should
be managed as est ablished renal failure
● Headache and myalgia are t reat ed wit h analge-
sics. Fever wit h ant i pyret ic
● Rest lessness and anxiet y wit h sedat ives and
anaemia wit h blood t ransfusion.
Per i t oneal di al ysi s has been found t o be a safe,
simple and effect ive procedure for management of
lept ospira renal failure due t o lept ospirosis
I f t here is cont raindicat ion t o perit oneal dialysis,
hemo-dialysis can be done.
Ref er ence
● Harrison’s Text Book of Medicine, 16t h edi-
t ion, Kasper et .al., Mc Graw Hill company inc.
in: pp-988-990.
● Oxford Text Book of Medicine .pp: 478-479.
● Manson Bahr Text Book of Tropical Medicine. Pp:
822-826
Parasitic infections
Intestinal protozoal infections
Amoebiasis and Giardiasis are t he commonest
int est inal prot ozoal infect ions. Pat ient s of Amoebiasis
and Giardiasis present as asympt omat ic carriers.
Amoebi asi s ( I nt est i nal )
Causes
I nfect ion is caused by int est inal prot ozoa- Ent amoeba
hist olyt ica. I nfect ion usually spreads by infect ive cyst s
in st ool, which cont aminat e food and drinking wat er.
Symptoms
● Lower abdominal pain
● Mild diarrhoea develops gradually and may lead
t o full blown dysent ery. 0-12 st ools per day wit h
blood and mucous and lit t le faecal mat t er.
● Caecal involvement may mimic acut e appendici-
t is.
● Chronic form i.e., amoebic colit is, can be confused
wit h inflammat ory bowel disease. Ot her form of
chr oni ci t y may pr esent as amoeboma
● Unt reat ed or incomplet ely t reat ed int est inal in-
fect ion may result in amoebic liver abscess and
involvement of ot her ext ra int est inal sit e.
I nvesti gati ons
● Diagnosis made by demonst rat ion of cyst s and/
or t rophozoit es of Ent amoeba hist olyt ica in t he
st ool.
Treatment
Asympt omat i c cyst passer s
Tab. Diloxanide furoat e 500 mg 8 hourly for 10 days.
Acut e amoebi c dysent er y and chr oni c i nf ect i ons
1. Tab. Met ronidazole 400-800 mg 8 hour-
ly PO for 10 days.I n children 15 mg/
kg divided in t hree doses for 7 days.
( o r )
Tab. Tinidazole (300 mg, 500 mg and 1 g) 2 g
orally as single dose.I n children 50 mg/ kg as a
single dose.
2. Tab. Diloxanide furoat e 500 mg 8 hourly for 10
days.I n children 20 mg/ kg/ day in t hree divided
doses for 10 days.
For t reat ment of amoebic liver abscess see chapt er
on gast roint est inal diseases
Giardiasis
Causes
I nt est inal disease caused by prot ozoal parasit e –
Giardia lamblia. The disease spreads by direct faeco-
oral t ransmission.
Symptoms
● Acut e Giardiasis – alt hough diarrhoea is common,
upper int est inal manifest at ions such as abdomi-
nal pain, bloat ing, belching, flat us, nausea and
vomit ing may predominat e.
● Chronic Giardiasis – hist ory of one or more epi-
245
sodes of acut e diarrhoea, increased flat us, loose
st ools, abdominal dist ension, borborygmi, eruc-
t at ion of foul t ast ing gas and passage of foul
smelling flat us, and weight loss
● Sympt oms could be int ermit t ent , recurring and
gradually debilit at ing; severe disease may result
in malabsorpt ion, weight loss, growt h ret ardat ion
and dehydrat ion.
I nvesti gati ons
● Diagnosis is made by t he demonst rat ion of cyst s
and or t rophozoit es of G.lamblia in t he st ools.
Treatment
● Tab. Tinidazole 2 g as a single dose in adult s.
● I n children 50 mg/ kg as a single dose.
(or)
● Tab. Met ronidazole 400 mg every 8 hours for 7
days in adult s.I n children 15 mg/ kg divided in
t hree doses for 7 days.
Pat i ent educat i on
● These infect ions spread by ingest ion of food or
wat er cont aminat ed wit h cyst s.
● Properly cooked food, use of clean drinking wa-
t er, proper sanit at ion and good personal hygiene-
hand washing wit h soap aft er defecat ion and be-
fore meals may prevent infect ion.
● Avoiding unpeeled fruit s and veget ables may
minimize infect ion.
● Side effect s are usually mild and t ransient and
include nausea, vomit ing, abdominal discom-
fort , met allic t ast e and a disulfiram like react ion,
t herefore, avoid use of alcohol during t reat ment .
Ref er ences
● I nfect ious Diseases: Prot ozoal and Helmint hic.
I n: Current Medical Diagnosis and Treat ment .
Lawrence M Turner Jr, St ephen J McPhee, Maxine
A Papadakis, 38
t h
edit ion, Prent ice Hall I nt erna-
t ional I nc. USA, pp 1353-1417
● Drugs used in t he chemot herapy of Helmint h-
ics. I n: The Pharmacological basis of t herapeu-
t ics. Mart in J Wonsiewich and Pet er MC Curdy, 9
t h

edit ion, 1996, Mc Graw Hill Company I nc., USA,
pp 1009-1026
● Drugs used in t he chemot herapy of Prot ozoal in-
fect ions Trypanosomiasis, Leishmaniasis, Basis of
t herapeut ics. Mart in J Wonsiewich and Pet er MC
Curdy, 9
t h
edit ion, 1996, Mc Graw Hill Company
I nc., USA, pp 987-1008.
● Parasit ic causes of acut e diarrhoea. I n: David-
son’s principles and pract ice of medicine. Haslet t
C Chilvers et al, 19
t h
Edit ion, 2002, Churchill Liv-
ingst one, pp 46
Malaria and National anti-malaria
programme (NAMP)
Causes
● Parasit ic infect ion due t o prot ozoa of genus plas-
modium t ransmit t ed by t he female anopheles
mosquit o. There are four plasmodia species:
* Plasmodium falciparum
* Plasmodium vivax
* Plasmodium malariae
* Plasmodium ovale
Symptoms
● Malaria is an acut e and chronic prot ozoan ill-
ness charact erized by paroxysms of fever, chills,
sweat s, fat igue, anaemia and spleenomegaly.
● Falciparum malaria (severe and complicat ed ma-
laria) is associat ed in varying degrees wit h t he
following clinical signs
* Cerebral malaria
» Ment al clouding
» Coma
» Convulsions
» Delirium, and occasionally localizing signs.
» Hyper pyrexia (> 40.5c)
» Haemolysis
» Oliguria
» Anuria
» Pulmonary edema
» Macroscopic haemoglobinuria.
I nvesti gati ons
Diagnosis is made by presence of prot ozoa in t he
blood in t hick and t hin smear slides. Thick smear for easy
det ect ion of parasit e and t hin smear for ident ificat ion of
species.
246
Not e:
That blood films may be negat ive even in a severe
at t ack because of parasit es in t he deep capillaries.
Treatment
● All fever cases wit hout any ot her obvious causes
should be presumed as malaria cases and ant i-
malarial drug be given preferably aft er t aking
blood smear.
● Chloroquine is t he first line ant imalarial in t he
t reat ment of uncomplicat ed malaria.
● I n high-risk areas pr esumpt i ve t r eat ment 25
mg/ kg of chloroquine base is t o be given over 3
consecut ive days (10 mg/ kg on day 1 and 2, fol-
lowed by 5 mg/ kg on day 3) wit h a single dose of
primaquine 0.75 mg/ kg on t he first day. High risk
area is defined as follows:
* Recorded deat hs due t o malaria (on clinical
diagnosis or microscopic confirmat ion) wit h
P.falciparum infect ion during t he t ransmission
period in an endemic area during any of t he
last 3 years.
* Doubling of slide posit ivit y rat e (SPR) during
t he last 3 years provided t he SPR in second or
t hird year reaches 4% or more, or t he average
SPR of t he last year is 5 % or more.
* P.falciparum is 30% or more provided SPR is
3% or more during any of t he last 3 years.
* An area having a focus of chloroquine resist-
ant . P.falciparum.
● I n t he low risk areas, presumpt ive t reat ment wit h
chloroquine 10 mg/ kg single dose.
● Resist ance should be suspect ed if in spit e of full
t reat ment and no hist ory of vomit ing and diar-
rhoea, pat ient does not respond wit hin 72 hours
parasit ologically. Such pat ient s should be given
alt ernat ive drug i.e., sulfa-pyrimet hamine combi-
nat ion (S-P) and report ed t o concerned dist rict /
st at e malaria officer for monit oring of drug sen-
sit ivit y st at us.
● Sulfadoxime pyrimet hamine is t he second line of
ant imalarial in P.falciparum resist ant t o chloro-
quine. The dose is 25 mg/ kg of sulfadoxime +
1.25 mg/ kg of Pyrimet hamine which is 3 t ablet s
for adult (single dose)
● The dose of primaquine for P.vivax cases is 0.25
mg/ kg daily for 5 days t o prevent relapse and for
P.falciparum 0.75 mg/ kg single dose for game-
t ocyt ocidal act ion. A 14 days primaquine t reat-
ment in P.vivax is NOT recommended in t he pro-
gramme.
● Mefloquine can be given t o chloroquine or ot her
ant imalarial resist ant uncomplicat ed P.falciparum
cases only.
● Resist ance t o chloroquine
* There must be evidence of falciparum posi-
t ive blood slide on t he first and t hird days of
t reat ment .
WHO classifcation of resistance
to Chloroquine
● RI : Tot al disappearance followed by reappear-
ance of t he parasit e.
● RI I : Not iceable fall wit hout disappearance of
t he parasit e.
● RI I I : Parasit e level almost unchanged, indeed
increased
I mpor t ant Not e
Before labeling resist ance verify t hat
* Treat ment has in fact been t aken.
* Correct dose for weight has been prescribed.
* Pat ient has not vomit ed wit hin 30 minut es of
t aking medicat ion.
* There has not been under dosage due t o
confusion in t he expression of dosage as a
chloroquine base and as a chloroquine salt .
Equivalence bet ween salt and base: 130 mg
sulphat e = 150 mg phosphat e or diphosphat e
= 100 mg base.
● I n pregnant woman and infant s, primaquine is
cont raindicat ed. As no dat a is available t o sug-
gest t he safet y of Art emisinin derivat ives in t his
group, t he same cannot be recommended.
● I n severe and complicat ed P.falciparum malaria
cases Quinine iv/ Art emisinin derivat ives (for
adult s and non pregnant women only) is t o be
given irrespect ive of chloroquine resist ance st a-
t us. I n case of non-availabilit y of t he above drugs,
chloroquine 10 mg/ kg in isot onic saline should be
infused over 8 hours followed by 15 mg/ kg in t he
next 24 hours. The t reat ment is t o be cont inued
t ill such t ime Quinine / Art emisinin derivat ives be-
come available.
247
● The use of Art emisinin derivat ives is t o be rest rict-
ed and inj ect ions may be used for t he t reat ment
of severe and complicat ed P.falciparum malaria in
adult s and non-pregnant women only. However
oral forms of t hese derivat ives may be used for
falciparum malaria resist ant t o bot h chloroquine
and sulfa-pyrimet hamine combinat ion.
Treatment
Pat ient s wit h uncomplicat ed malaria can be managed
at a primary level but pat ient s wit h complicat ed malaria
should be admit t ed and managed in a hospit al where
facilit ies for det ailed invest igat ion and blood t ransfusion
exist .
● Presumpt ive t reat ment in uncomplicat ed malaria
* Low r i sk ar ea: wit h chloroquine 10 mg/ kg
single dose (maximum dose is 600 mg) t o all
suspect ed cases.
Hi gh-r i sk ar ea
Day 1
Chloroquine
(600 mg adult )
10 mg/ kg
Primaquine
(45 mg adult )
0.75 mg/ kg
Day 2 Chloroquine
(600 mg adult )
10 mg/ kg
Day 3 Chloroquine
(300 mg adult )
5 mg/ kg
● Conf i r med cases of Mal ar i a
* Tab. Chloroquine as in presumpt ive t reat ment
in “ high risk area”
* I n P.vivax Tab. Primaquine 0.25 mg/ kg/ day for
5 days.
* I n P. falciparum Tab. Primaquine 0.75 mg/ kg
as a st at dose
* I n high risk areas where presumpt ive t reat-
ment wit h 500 mg Chloroquine and 45 mg Pri-
maquine has been given chloroquine need not
be administ ered again but primaquine must
be given for 5 days.
● Chloroquine resist ant P. falciparum cases
I n Chloroquine resist ant P. falciparum cases, sec-
ond line t reat ment must be given wit h 25 mg/ kg
of sulfadoxine + 1.25 mg/ kg of pyrimet hamine
which is 3 t ablet s for adult (single dose) followed
by primaquine (45 mg)
● I n severe and complicat ed Malaria cases
* I n severe and complicat ed Malaria cases, ir-
respect ive of chloroquine resist ance st at us of
t he area: I nj . Quinine salt 10 mg/ kg 8 hourly
I V in 5 % dext rose saline is preferred. Pat ient s
should be swit ched over t o oral quinine as
early as possible wit h oral dose 10 mg/ kg 8
hourly not exceeding 2 g in a day in any case.
* Minimum t ot al durat ion for quinine t herapy
should be for 7 days including bot h parent ral
and oral doses. Or I nj ect able form of Art emisi-
nin derivat ives may be used in non-pregnant
adult s and G-6-PD deficiency.
* Any of t he following Art emisinin derivat ives,
dosages as follows:
» I nj . Art emisinin: 10 mg/ kg at 0 and 4 hours
followed by 7 mg/ kg at 24, 36, 48, and 60
hours.
» I nj . Art esunat e: 2.4 mg/ kg I M/ I V followed
by 1.2 mg/ kg aft er 12 hours t hen 1.2 mg/
kg once daily for t ot al durat ion of 5 days.
» I nj . Art emet her: 3.2 mg/ kg st at followed
by 1.6 mg/ kg daily for 3-5 days.
» I nj . Art et her: 150 mg daily I M for 3 days
in adult s only.
Suppor t i ve t r eat ment
Treat ment of fever, hypoglycemia, elect rolyt e
imbalance, hypot ension, renal failure, anaemia, and
convulsions appropriat ely.
Chemopr ophyl axi s i n sel ect i ve cases
● Chemoprophylaxis is recommended for
* Pregnant women in high-risk areas and
* Travellers including service personnel who
t emporarily go on dut y t o highly malarious
areas.
● Chemoprophylaxis is t o be st art ed a week be-
fore arriving t o malarious area for visit ors and for
pregnant women prophylaxis should be init iat ed
from second t rimest er.
Chl or oqui ne sensi t i ve ar ea
● St art wit h a loading dose of Tab. Chloroquine 10
mg/ kg followed by a weekly dose of 5 mg/ kg.
This is t o cont inue t ill 1 mont h aft er delivery in
case of pregnancy and t ravellers t ill one mont h
aft er ret urn from endemic area
● The t erminat ing dose should be 10 mg/ kg along
248
wit h 0.25 mg/ kg of primaquine for 5 days.
● Caut i on: I n pregnancy, primaquine should not
be given
● Chemoprophylaxis wit h chloroquine is not recom-
mended beyond 3 years because of it s cumula-
t ive t oxicit y.
● I n chloroquine resist ant areas chloroquine 5 mg/
kg weekly and pr oguani l 100 mg daily.
Pat i ent educat i on
● To t ake measures t o st op mosquit o breeding and
prot ect ion from mosquit oes.e.g., mosquit o net s,
repellent s, long sleeves, long t rousers.
● Fever wit hout any ot her signs and sympt oms
should be report ed t o nearest healt h facilit y.
● Chloroquine should be given wit h plent y of wa-
t er aft er food and not on an empt y st omach. I f
chloroquine syrup is not available for children,
t he t ablet form should be crushed and given wit h
honey and t hick syrup.
● Wat ch for side effect s of drugs prescribed. Chlo-
roquine may cause nausea, vomit ing, diarrhoea,
mild headache and skin allergy/ rash.
● I f vomit ing occurs wit hin 30 minut es of chloro-
quine int ake repeat t he dose of chloroquine.
● Chl or oqui ne, Pr i maqui ne and Sul pha-py-
r emet hami ne shoul d not be gi ven i n pa-
t i ent s wi t h G-6-PD def i ci ency.
● Pat ient s should be educat ed about cerebral ma-
laria, and should seek medical help immediat ely
on occurrence of t hese sympt oms.
Ref er ence
● Nat ional Ant imalaria Programme (NAMP) drug
policy, Government of I ndia, DGHS, Direct orat e
of Nat ional Ant imalaria Programme. 22-Sham-
nat h Marg, New Delhi.
● Malaria (Plasmodium) in: Nelson’s t ext book
of Paediat rics, Behrman RE, Kleigman RM, HB
(eds), 17
t h
edit ion, 2004, Harcourt Publishers I n-
t ernat ional Company, pp 1139-1143.
Worm infestation
Hookwor m I nf est at i on
The maj orit y of worm infest at ions are asympt omat ic.
Causes
I nfect ion is caused by A.duodenale and N.americanus.
The infect ive larvae penet rat e t hrough skin usually t he
foot and t ravel t hrough subcut aneous t issue t o t he
int est ines. The adult forms live in t he j ej unum and
feed on blood, t hus leading t o chronic blood loss and
anaemia.
Symptoms
● Most of t he affect ed individuals may be asymp-
t omat ic
● Pat ient s usually present wit h sympt oms of anae-
mia (hypochromic microcyt ic)
● Prurit ic maculopapular dermat it is (ground it ch) at
sit e of skin penet rat ion by infect ive larvae.
● Serpigenous t ract s of subcut aneous migrat ion in
previously sensit ized host .
● Mild t ransient pneumonit is because of larvae mi-
grat ion t hrough lungs.
● I nt est inal manifest at ions – epigast ric pain oft en
wit h post-prandial accent uat ion, inflammat ory di-
arrhoea.
● Maj or consequences – progressive iron deficiency
anaemia and hypoprot enemia.
I nvesti gati ons
● Diagnosed by demonst rat ion of ova of
A.duodenale and or N.americanus in t he st ool
and occult blood.
Treatment
● Tab. Mebendazole 100 mg 12 hourly for 3 days in
children above 2 years of age. (Caut ion: cont rain-
dicat ed in children less t han 2 years) or
● Tab. Pyrant el palmoat e (250 mg); syr. (250 mg/ 5
ml) 10 mg/ kg body weight once daily for 3 days.
(Caut ion: not recommended in children below 1
year of age)
● I n children more t han 1 year Susp. Pyrant el pal-
moat e 10 mg/ kg as a single dose. Or Tab. Alben-
dazole 400 mg t o be chewed as a single dose.
● I n children bet ween 1-2 years of age syr. Alben-
dazole 200 mg as a single dose. I n children more
t han 2 years syr. Albendazole 400 mg as a single
dose.
249
Pat i ent educat i on
● Hookworm infest at ion occurs t hrough skin pen-
et rat ion by t he infect ive larvae.
● The disease can be prevent ed by use of boot s
and gloves while working in t he fields.
● The deworming agent s should not be used in
pregnancy, lact at ion and along wit h alcohol.
● Side effect s of t hese drugs are generally mild
which may include nausea, abdominal pain,
headache, dizziness, malaise and skin rash.
Ascariasis (Roundworm infestation)
Causes
Ascariasis is caused by Ascaris lumbricoides, t he
largest nemat ode parasit e of humans reaching upt o 40
cm in lengt h. The worm is locat ed in t he large int est ine.
Symptoms
● Most infect ed individuals have low worm burden
and are asympt omat ic.
● Feat ures of pulmonary involvement because of
larval migrat ion include irrit at ing non-product ive
cough, bronchospasm or pneumonit is and burn-
ing subst ernal discomfort aggravat ed by cough-
ing or deep inspirat ion, dyspnoea, fever, eosi-
nophilic pneumonit is.
● Heavy int est inal infect ion- pain in abdomen, small
bowel obst ruct ion t hat may get complicat ed by
perforat ion, int ussuscept ion or volvulus
● Aberrant migrat ion of a large worm may cause
* Biliary colic
* Cholangit is
* Cholecyst it is
* Pancreat ic and
* Oral expulsion of t he worm.
Treatment
● Tab. Mebendazole 100 mg 12 hourly for 3 days
in children above 2 years of age. (Caut i on: con-
t raindicat ed in children less t han 2 years) or
● Tab. Pyrant el pamoat e 11 mg/ kg as a single
dose. or
● Tab. Albendazole 400 mg as a single dose.
● I n heavy infest at ion, however, a 2-3 day course
is indicat ed. (caut i on: cont raindicat ed in preg-
nancy)
● I n children bet ween 1-2 years of age syr. Alben-
dazole 200 mg as a single dose. I n children more
t han 2 years, syrup. Albendazole 400 mg as a
single dose.
Not e
Nasogast ric suct ion, I V fluids, and inst illat ion of
piperazine t hrough nasogast ric t ube may manage
part ial int est inal obst ruct ion. Complet e obst ruct ion and
ot her surgical complicat ions require surgical referral for
int ervent ion.
Pat i ent educat i on
● I nfect ion occurs by faecal-oral rout e.
● Proper sanit at ion and good personal hygiene-
hand washing wit h soap aft er defecat ion and be-
fore meals may prevent infect ion.
● I nfect ion can be minimized by avoiding unpeeled
fruit s and veget ables and use of clean drinking
wat er.
Ref er ences
● I nfect ious Diseases: Prot ozoal and Helmint hic. in
Current Medical Diagnosis and Treat ment . Law-
rence M Turner Jr, St ephen J McPhee, Maxine A
Papadakis, 38
t h
edit ion, Prent ice Hall I nt ernat ion-
al I nc. USA, pp 1353-1417
● Drugs used in t he chemot herapy of Helmint h-
ics. in t he Pharmacological basis of t herapeut ics.
Mart in J Wonsiewich and Pet er MC Curdy, 9
t h

edit ion, 1996, Mc Graw Hill Company I nc., USA,
pp 1009-1026
● Drugs used in t he chemot herapy of Prot ozoal in-
fect ions Trypanosomiasis, Leishmaniasis, Basis of
t herapeut ics. Mart in J Wonsiewich and Pet er MC
Curdy, 9
t h
edit ion, 1996, Mc Graw Hill Company
I nc., USA, pp 987-1008.
● Helmint hes not associat ed wit h eosinophilia.
I n: Davidson’s principles and pract ice of medi-
cine. Haslet t C Chilvers et al, 19
t h
Edit ion, 2002,
Churchill Livingst one, pp 72-73.
Filariasis
Causes
● Lymphat ic filariasis result s from infect ion of
250
* Wucheriria bankcroft ii
* Brugia malayi
* Brugia t imori
Sympt oms and si gns
● Manifest s in bot h acut e and chronic form wit h or
wit hout fever.
● Adeno-lymphangit is
* Hydrocele
* Elephant iasis
* Chyluria
* I nvolvement of spermat ic cord-Funiculit is,
Lymphocoele, Epi-didymoorchit is
* Tropical Pulmonary Eosinophilia ( TPE)
* Abscesses
* Mono-art icular art hrit is
● Suspect ed when a pat ient present s wit h a
* Sudden onset of fever
* Acut e groin pain wit h swollen t ender lymph
gland and
* Oedemat ous swelling of t he legs.
I nvesti gati ons
● Blood examinat ion
● Thick film: Blood is t aken at t he t ime when peak
concent rat ion of microfilaria is expect ed i.e., be-
t ween 8: 30 PM and 12 mi d ni ght
● Membrane filt er concent rat ion (MFC) met hods
* Most sensit ive met hod for low-densit y micro-
filaremia.
● DEC provocat ion t est
* Microfilaria can be induced t o ent er t he blood
st ream during dayt ime. Di-Et hyl- Carbazine
(DEC) 100 mg orally is given and blood is
drawn aft er 15-20 minut es.
Treatment
Medi cal t r eat ment
● Diet hylcarbazine (DEC) – 6 mg/ kg/ day – in di-
vided doses for 12 days
● Treat ment is repeat ed about every 6 mont hs for
as long as t he person remains microfilaremic or
has sympt oms.
● For Tropical Pulmonary Eosinophilia: 3 week
course of DEC is given.
● Sympt omat ic t reat ment : for t reat ing acut e at-
t acks of filarial fever and lymphadenit is
* Analgesics
* Ant ipyret ics and
* Bed rest
● Management of lymph-edemat ous limbs:
* Elevat ion of affect ed limb.
* Elast ic bandage, st ocking, massage.
* Prevent ion of superficial bact erial/ fungal in-
fect ions.
Sur gi cal t r eat ment
Prior t o any surgical procedure, a course of DEC
is recommended.
Chr oni c hydr ocoel e – Excision and eversion of
sac.
Scr ot al el ephant i asi s – Surgical removal of
grossly elephant oid skin and scrot al t issues wit h
preservat ion of penis and t est icles.
Li mb el ephant i asi s – Lympho-venous proce-
dures followed by removal of excess of subcut a-
neous and fat t y t issue from affect ed ext remit ies
and adequat e post ural drainage and physiot her-
apy.
Fi l ar i al cont r ol i n communi t y
1. Mass t herapy: abandoned now.
2. Select ive t herapy
* Given only t o t hose who are microfilaria posi-
t ive
* Given for bot h filarial cases and human car-
riers
* 6 mg/ kg/ day – 12 doses t o be complet ed in
2 weeks
* Endemic areas – dose is repeat ed every 2
years.
3. DEC medicat ed salt
* 1 t o 4 gram of DEC/ kg of salt for at least 6-9
mont hs.
Vect or cont r ol :
Lar va cont r ol : Organophosphorus larvicides –
* Temephos
251
* Fen-t hion
* Removal of pist ia plant .
Adul t mosqui t o cont r ol : Space spray wit h py-
ret hrum.
Ref er ence
● Oxford Text Book of Medicine. Pp: 787-792.
● Manson Bahr Text Book of Tropical Medicine. Pp:
1321 t o 1368.
● Park’s Text Book of Prevent ive and Social Medi-
cine. Pp: 213-216.

Dengue
Causes
● Dengue is t he most import ant emerging t ropical
viral disease of human beings in t he world t oday.
All four dengue virus (Dengue 1, 2, 3 and 4) in-
fect ions may be asympt omat ic or may lead t o
* Undifferent iat ed fever, dengue fever (DF)
* Dengue hemorrhagic fever (DHF)
» Wit h plasma leakage t hat may lead t o hypo-
volemic shock
* Dengue shock syndrome (DSS).
Symptoms
● Dengue fever is an acut e febrile illness of 2-7
days wit h t wo or more of t he following manifes-
t at ions
* Headache
* Ret ro-orbit al pain
* Myalgia
* Art hralgia
* Rash
* Hemorrhagic manifest at ion (pet echiae and
posit ive t ourniquet t est ) and
* Leucopenia
● Dengue hemorrhagic fever (DHF) if one or more
of t he following are present
* Posit ive t ourniquet t est
* Pet echiae, purpura or ecchymosis
* Bleeding from mucosa
* Haemat emesis, malaena
* Thrombocyt openia (plat elet s 100,000/ mm
3
or
less) and evidence of plasma leakage.
● Dengue shock syndrome (DSS)
* All t he above crit eria of DHF plus signs of cir-
culat ory failure.
Not e:
The t ourniquet t est is performed by inflat ing a blood
pressure cuff t o a mid-way bet ween t he syst olic and
diast olic pressure
Dengue f ever and DHF dur i ng f ebr i l e phase
Non-phar macol ogi cal
● Rest
Phar macol ogi cal
● Tab. Paract emol 500 mg 6 hourly (not more t han
4 t imes in 24 hours)
● ORS in pat ient s wit h dehydrat ion
● Caut i on: No role of ant ibiot ics, st eroids; do not
use aspirin or ibuprofen
I mpor t ant Not e
To report immediat ely if pat ient develops any of
t he following danger signals: severe abdominal pain,
passage of black st ools, bleeding int o t he skin or from
t he nose or gums, sweat ing and cold skin.
Dengue hemor r hagi c f ever : gr ade I ( posi t i ve
t our ni quet t est ) and gr ade I I ( spont aneous
bl eedi ng) and t hr ombocyt openi a < 100,000, Hct
r i se > 20% .
● I mmediat e hospit alizat ion.
● As above in dengue fever.
● Send sample for blood grouping and cross mat ch-
ing.
● I V fluids if pat ient has persist ent vomit ing or Hct
rise > 20 %, cont inue I V fluids for 12-24 hours.
(Caut i on: I V fluid t herapy be-
fore leakage is not recommended)
Monit or vit als and urine out put on an hourly
basis. Based on periodic haemat ocrit , plat elet
count s and vit al signs review and revise t reat-
ment .
DHF gr ade I I I ( wi t h ci r cul at or y f ai l ur e) and
gr ade I V ( pr of ound shock wi t h undet ect abl e
252
bl ood pr essur e and pul se)
I mmedi at el y admi t t he pat i ent i n a hospi t al
wher e t r ai ned per sonnel can manage shock and
wher e bl ood t r ansf usi on f aci l i t i es ar e avai l abl e.
● I f a pat ient had already 1000 ml of I V fluids and
st ill vit als are not st able, t he haemat ocrit should
be repeat ed and (a) if t he haemat ocrit is increas-
ing, I V fluids should be changed t o colloidal solu-
t ion preferably dext ran or (b) if t he haemat ocrit is
decreasing, fresh whole blood t ransfusion 10 ml/
kg/ dose should be given.
● I n case of cont inued or profound shock give col-
loidal fluid following t he init ial fluid bolus (Do not
give I V fluids indiscriminat ely leading t o eit her
fluid overload or under t ransfusion in shock pa-
t ient s).
● I n case of persist ent shock when, aft er init ial flu-
id replacement and resuscit at ion wit h plasma or
plasma expanders, t he haemat ocrit cont inues t o
decline, int ernal bleeding should be suspect ed.
I t may be difficult t o recognize and est imat e t he
degree of int ernal blood loss in t he presence of
haemoconcent rat ion
● Give fresh whole blood in small volumes of 120
ml/ kg at one t ime
● Give plat elet rich plasma t ransfusion in excep-
t ional cases when plat elet count s are below
5000-10000/ mm
3
● Monit or pulse, BP, and t emperat ure every 15-30
minut es
● Aft er blood t ransfusion, cont inue fluid t herapy at
10 ml/ kg/ h and reduce st epwise t o bring it down
t o 3 ml/ kg/ h and maint ain for 24-48 hours.
● During convalescent phase (2-3 days) aft er re-
covery from t he st at e of shock, advise rest , nor-
mal diet
Si gns of r ecover y
* St able pulse, respirat ion and blood pressure
* Normal t emperat ure
* No evidence of bleeding
* Ret urn of appet it e
* No vomit ing
* Good urinary out put
* St able haemat ocrit
* Convalescent confluent pet echial rash.
Cr i t er i a f or di schar gi ng pat i ent s:
● Absence of fever for at least 24 hours wit hout t he
use of ant i pyret ic agent s.
● Ret urn of appet it e.
● Visible clinical improvement .
● Good urine out put .
● Minimum of t hree days aft er recovery from shock.
● No respirat ory dist ress from pleural effusion and
no ascit es.
● Plat elet count of more t han 50,000/ mm
3
.
Pat i ent educat i on
● Since t his disease can rapidly become very se-
rious and lead t o a fat alit y, carefully wat ch for
danger signs and immediat ely report t o a doct or.
Do not wait .
● The compl i cat i ons usual l y appear bet ween
t he t hi r d and f i f t h day of i l l ness.
● Give large amount s of fluid along wit h normal
diet .
● All cont rol effort s should be direct ed against
mosquit oes. Effort s should be int ensified before
t ransmission season and during rainy season.
Ref er ence
● Guidelines for t reat ment of Dengue fever/ DHF in
small hospit als, 1999, WHO Regional office for
Sout h-East Asia, New Delhi.
Chikungunya
Causes
Chikungunya is caused by an alpha virus closely
relat ed t o O’ nyong-nyong virus.
Main vect or-Aedes aegypt i.
Symptoms
● Acut e self-limit ing illness.
● I ncubat ion period – 2 t o 4 days. Bi-phasic dis-
ease.
● Abrupt onset present ing as fever wit h severe
j oint pain.
● Aft er 1 – 4 days, fever subsides; t here will be a
253
afebrile period of 3 days, fever ret urns wit h an
it ching maculopapular rash on t runk and ext en-
sor surfaces of limbs.
● Aft er anot her 3 – 6 days, fever subsides and
t here is complet e recovery.
● Crippling art hropat hy can occur int ermit t ent ly for
upt o 4 mont hs, in some cases even upt o 5 years.
I nvesti gati ons
● Leucopenia.
● I g M ant ibody det ect able by ELI SA – first de-
t ect ed by 48 hours and can be det ect able upt o
6 mont hs.
Treatment
● Sympt omat ic t reat ment wit h ant i-inflammat ory
drugs t o relieve art hralgia.
● Chloroquine phosphat e can be used in refract ory
art hralgia.
● No licensed vaccines or no specific t reat ment
available at present .
● Measures t o reduce Aedes aegypt i populat ion
and avoiding mosquit o bit es.
Ref er ence:
● Oxford Text Book of Medicine .pp: 378-379.
● Manson Bahr Text Book of Tropical Medicine. Pp:
624-626.
SWI NE FLU
H1N1 VI RUS I NFECTI ON
(Syn: Swine infuenza / S-OIV infection / H1N1 - A
virus infect ion)
Def i ni tion
I t is respirat ory disease of pigs affect ing human
beings, caused by t ype A I nfluenza viruses wit h regular
out breaks in pigs. Source of t he virus in swine are avian,
human and swine. All t hree viruses re-assort and form
a new virus which is a mixt ure of all t hree. At present
t here are four t ypes H1N1, H1N2, H3N2 and H3N1. The
present pandemic is by I nfluenza A H1N1 t ype.
Char act er i st i cs of t he I nf l uenza vi r uses
I nfluenza viruses belong t o t he ort homyxoviridae
family, wit h t hree separat e genera A, B, and C based on
ant igenicit y of t he nucleoprot ein (NP) and mat rix (M)
prot ein.
I nfluenza A has subt ypes based on surface ant igens
of Hemagglut inin (H) 16 dist inct subt ypes (H1 t o H16)
and Neuraminidase (N) ant igens 9 dist inct (N1 t o N9)
subt ypes. Only H1, H2, H3, N1, and N2 have been
associat ed wit h epidemics.
Epi demi ol ogy
Epidemics of H1N1 - A begin abrupt ly, peak over a
2 t o 3 week period and generally last for 2–3 mont hs.
There is an increase in t he number of children wit h
febrile respirat ory illnesses followed by increase in rat es
of influenza-like illnesses among adult s. Event ually
t here is a spurt in hospit al admissions for pneumonia,
exacerbat ions of chronic pulmonary disease and
worsening of pre-exist ing congest ive heart failure.
Tr ansmi ssi on of H1N1 vi r us
The infect ious period is one day before and unt il
7 days aft er t he case’s onset of illness. Dat a available
indicat e t hat t his virus is t ransmit t ed in ways similar
t o ot her influenza viruses. When an infect ed person
coughs or sneezes large-part icle respirat ory droplet s
are released. These droplet s being large, generally
t ravel only a short dist ance (< 1 met er).
Droplet s cannot remain suspended in t he air for
long and hence set t le on t he surfaces. Because of t he
above, spread is eit her by a direct cont act bet ween
source and recipient persons or by respirat ory-droplet
cont aminat ed surfaces. All respirat ory secret ions and
bodily fluids (diarrheal st ool) of (H1N1) pat ient s should
be considered pot ent ially infect ious.
Hi gh r i sk popul at i on f or H1N1 vi r us i nf ect i on
Populat ions at high risk are children less t han5 years
old and persons aged above 50 years. Pregnant women,
adult s and children wit h chronic organ dysfunct ion
(pulmonary, cardiovascular, hepat ic, hemat ological,
neurologic, neuromuscular or met abolic disorders) or
immuno suppression (caused by medicat ions or by HI V)
and resident s of nursing homes, ot her chronic-care
facilit ies are also more vulnerable for H1N1 infect ion.
Case Def i ni t i ons:
A confirmed case of H1N1 infect ion is defined as
a person wit h an acut e febrile respirat ory illness wit h
laborat ory confirmed H1N1 infect ion at CDC by one or
more of t he following t est s: Real-t ime RT-PCR, viral
cult ure or four fold increase in H1N1 virus specific
neut ralizing ant ibodies.
A probable case of H1N1 is a defined as a person wit h
acut e respirat ory illness who is posit ive for influenza A
but negat ive t o H1 and H3 by RT-PCR
254
A suspect ed case of S-OI VA (H1N1) is defined a
person wit h an acut e febrile respirat ory illness who has
had close cont act wit h a person who is a swine-origin
influenza confirmed case or t ravelled t o a communit y
in t he Unit ed St at es or int ernat ionally where t here are
one or more confirmed swine-origin influenza cases or
resides in a communit y where t here are one or more
confirmed swine-origin influenza A (H1N1) cases.
Acut e r espi r at or y i l l ness
Defined as recent onset of at least t wo of t he
following: rhinorrhea or nasal congest ion, sore t hroat ,
cough (wit h or wit hout fever or feverishness).
Cl i ni cal Feat ur es of ( H1N1) vi r us i nf ect i on
Sympt oms include fever, headache, cough, sore
t hroat , rhinorrhea, myalgia, fat igue, vomit ing, or
diarrhea. Pat ient s appear flushed and t he skin is hot
and dry. Pharynx is normal despit e a severe sore t hroat .
There may be mild cervical lymphadenopat hy. I llness
generally resolves over 2–5 days and recovery occurs
in 1 week. Cough may persist 1–2 weeks longer and
post-influenzal ast henia may persist for several weeks.
Frank dyspnea, hyperpnoea, cyanosis, diffuse rales
and signs of consolidat ion are indicat ive of pulmonary
complicat ions.
Lit t le is current ly known about t his infect ion in
children since it is difficult t o dist inguish from illnesses
caused by ot her respirat ory pat hogens by sympt oms.
Sympt oms of severe disease may include apnea,
t achypnoea, dyspnoea, cyanosis, dehydrat ion, alt ered
ment al st at us and ext reme irrit abilit y.
Compl i cat i ons of H1N1 i nf ect i ons
The complicat ions are dominant ly respirat ory and
include secondary bact erial pneumonia wit h or wit hout
sepsis, bronchiolit is, st at us ast hmat icus, sinusit is,
ot it is media and croup. Exacerbat ions of underlying
chronic medical condit ions are frequent . Ot her rare
complicat ions are viral pneumonia, myocardit is,
pericardit is, myosit is, rhabdomyolysis, acut e and post-
infect ious encephalopat hy, encephalit is, febrile seizures
and st at us epilept icus.
H1N1 r el at ed Pneumoni as
Usually bact erial pneumonia is common. I t is
charact erized by reappearance of fever, cough,
product ion of purulent sput um wit h physical and
x-ray signs of consolidat ion. Common Organisms are
St r.pneumoniae, St aph. aureus, and H. influenzae.
The pneumonia responds t o ant ibiot ic t herapy when
inst it ut ed prompt ly.
Primary Viral pneumonia is a least common but
most severe complicat ion t hat has a predilect ion for
individuals wit h cardiac disease part icularly t hose wit h
mit ral st enosis. Manifest at ions include persist ent fever,
dyspnoea, and event ual cyanosis. Sput um t hough
scant y can cont ain blood. Diffuse rales may be not ed
in advanced cases wit h X-ray showing diffuse int erst it ial
infilt rat es and/ or ARDS.
Test i ng f or swi ne-or i gi n i nf l uenza A ( H1N1)
vi r us
Upper respirat ory specimens, nasopharyngeal swab
or wash, nasal aspirat e or t racheal aspirat e should be
t est ed by t he st at e public healt h laborat ory. Real t ime
RT-PCR, viral cult ures are t o be performed t o confirm
t he H1N1 infect ion.
Suppor t i ve measur es f or H1N1-A vi r us i nf ect i on
● Bed rest
● Hydrat ion wit h oral or parent eral fluids and nut ri-
t ional support
● Cough suppressant s generally are not indicat ed
but codeine-cont aining compounds may be em-
ployed if t he cough is t roublesome
● Management of t he met abolic consequences of
dehydrat ion and increased met abolic demand.
● Fever management wit h ant ipyret ics like acet a-
minophen 4t h hourly. (‘aspirin’ is cont raindicat ed
in children and t eenagers).
● Cold sponges, ice bags, ice bat hs, ice wat er en-
emas and sprinkling a pat ient wit h wat er is t he
opt imal approach for hyperpyrexia.
Ant i vi r al dr ugs f or S-OI V ( H1N1)
H1N1 - A virus is suscept ible t o neuraminidase
inhibit or ant iviral medicat ions
Zanamivir and Oselt amivir are t he t wo drugs widely
used in t he present epidemic of (H1N1) virus infect ion.
I t is resist ant t o t he adamant ane ant ivirals amant adine
and rimant adine. For oselt amivir-resist ant human A
(H1N1) viruses, eit her zanamivir or combinat ions of
oselt amivir and rimant adine or amant adine provide
adequat e empiric t reat ment . Oselt amivir ( Tamiflu) is
administ ered orally while Zanamivir by inhalat ion.
Ant i vi r al t r eat ment gui del i nes
Treat ment is considered for confirmed, probable or
suspect ed cases of S-OI A infect ion. RT-PCR or viral
255
cult ure t est ing must be done t o confirm S-OI A (H1N1)
infect ion. Priorit y is given for hospit alized pat ient s and
pat ient s at higher risk of complicat ions. Ant ivirals are t o
be st art ed wit hin 48 hours of onset of illness. Reduct ion
in mort alit y or durat ion of hospit alizat ion is not ed even
if ant iviral t herapy is st art ed aft er 48 hours. Durat ion of
t reat ment is five days.
Ant i vi r al Chemopr ophyl axi s f or ( H1N1) vi r us
i nf ect i on
Chemoprophylaxis is recommended for high risk
individuals wit h household cont act s of confirmed case
and healt h care workers or public healt h workers who
were not using personal prot ect ive equipment (PPE).
I t may be considered in high risk individuals wit h
household cont act s and HCW of suspect ed case of
H1N1 and t ravelers t o t he count ries where t he epidemic
is going on.
Post exposure chemoprophylaxis considered for
cont act during t he infect ious period. The durat ion of
chemoprophylaxis post-exposure is 10 days aft er t he
last known exposure t o a confirmed case. Pre-exposure
prot ect ion is given during t he pot ent ial exposure period
and is cont inued for 10 days aft er t he last known
exposure t o a confirmed case.
Adver se ef f ect s
Adverse effect s of Oselat amivir include nausea and
vomit ing which might be less severe if it is t aken wit h
food. Rarely anaphylaxis, Toxic Epidermolysis Necrosis
( TEN), Eryt hema Mult iforme (EMF), St even Johnson’s
syndrome, t ransient neuropsychiat ric event s (self-inj ury
or delirium) have been report ed. Persons receiving
oselt amivir should be monit ored closely for abnormal
behaviour.
Zanamivir is not recommended for t reat ment for
pat ient s wit h underlying airway disease since t hey can
produce cough and sympt oms of bronchit is. Allergic
react ions, including oropharyngeal or facial edema,
nausea, diarrhoea, headache, dizziness may occur.
Occasionally t hey may develop seizures, confusion or
abnormal behaviour.
Ant i vi r al s f or Pr egnant women wi t h H1N1
i nf ect i on
No clinical st udies have been conduct ed t o assess t he
safet y of t hese ant ivirals in pregnancy but no adverse
effect s have been report ed among women or infant s
born. Alt hough pregnancy is not a cont raindicat ion
t o Oselt amivir or Zanamivir t hey are used during
pregnancy, only if t he pot ent ial benefit j ust ifies t he
pot ent ial risk t o t he fet us.
Ant i vi r al dr ugs and dosages Recommended f or
H1N1 i nf l uenza i nf ect i on
OSELTAMI VI R ( TAMI FLU)
Age and
groups
Weight Treat ment
Chemopro-
phylaxis
Adult s
75 mg
caps. t wice
daily
75 mg caps.
Once daily
Children
40 Kg and
above
75 mg
caps. t wice
daily
75 mg caps.
Once daily
25 Kg t o
40 Kg
60mg caps.
t wice daily
60 mg caps.
Once daily
15 Kg
t o24 kg
45 mg
caps. t wice
daily
45 mg caps.
Once daily
Less t han
15 Kg
30 mg
caps. t wice
daily
30 mg caps.
Once daily
ZANAMI VI R
Adult s and children
Two 5 mg
(t ot al
10 mg)
inhalat ion
One 5 mg
inhalat ion
once daily
Gener al Pr ecaut i ons f or heal t h car e per sonnel
● Avoid close cont act wit h t he sick person
● Keep at least 6 feet dist ance from t he pat ient
● Hand hygiene
● Use face prot ect ion (medical or surgical mask /
eye-visor or goggles / face shield )
● Use a gown and clean gloves
Per sonal Pr ot ect i ve Equi pment s ( PPE) whi l e
t r eat i ng suspect ed case
● Fit t est ed disposable N95 respirat or
● Eye prot ect ion (goggles or eye shield)
● Disposable non st erile gloves and gown while
going closer t o t he pat ient s
Pr ecaut i ons whi l e t r eat i ng non suspect ed case
● St andard surgical mask for t he pat ient s
● Respirat ory hygiene
● Using non-st erile glove for cont act wit h t he pa-
t ient , pat ient secret ions or surfaces t hat may
256
have been cont aminat ed
● Hand washing or cleansing wit h alcohol based
disinfect ant aft er cont act
Respi r at or y pr ot ect i on f or heal t h car e per sonnel
● Use face mask or an N95 respirat or t hat fit s snug-
ly on your face
● Wear an N95 respirat or if you help a sick person
wit h respirat ory t reat ment s using a nebulizer or
inhaler
● Avoid re-using disposable facemasks and N95
respirat ors
● Aft er you t ake off a facemask or N95 respirat or,
clean your hands wit h soap and wat er or an alco-
hol-based hand sanit izer
● Hand hygiene
Sur vei l l ance of heal t hcar e per sonnel
● I f sympt oms of infect ion develop, healt h worker
is inst ruct ed not t o report for work
● I f at work already- should cease pat ient care ac-
t ivit ies
● Asympt omat ics who have had unprot ect ed expo-
sure should have chemoprophylaxis
Gui del i nes f or communi t y wi t h conf i r med cases
of H1N1
● I f anyone develops I LI (influenza like illness) t hey
must self isolat e t hemselves
● Period of isolat ion
* 7 days aft er t he sympt oms st art ed or at least
24 hours aft er t he sympt oms resolved
● I f t he person should go int o t he communit y
* Should wear a mask
* Handkerchief or t issues may be used for cov-
ering if mask is not available
● Household members
* Should be given infect ion cont rol inst ruct ion
* Should do met iculous hand washing
* Should remain home at t he earliest sign of in-
fect ion
Per sonal pr ot ect i on wher e t her e i s r i sk of
i nf ect i on
● Covering t he mout h and nose wit h a t issue while
sneezing or coughing
● Throwing t he t issue in t he t rash aft er use
● Washing t he hand wit h soap and wat er espe-
cially aft er sneezing and coughing
● Alcohol based hand cleaners are useful
● Touching of eyes, nose and mout h t o be avoided
● Avoiding close cont act wit h infect ed persons
Pr ecaut i ons f or st af f pr ovi di ng car e t o pat i ent s
● Use a medical or surgical mask
● Emphasize hand hygiene and provide hand hy-
giene facilit ies and supplies.
● Use face prot ect ion (medical or surgical mask
and eye-visor or goggles, face shield) and use a
gown and clean gloves.
● Do not forget hand hygiene aft er PPE removal.
Ref er ences
www.cdc.gov/ h1n1flu/ guidance/
www. who. i nt / csr / di sease/ swi nef l u/ gui dance/
healt h_professionals/ en/ index.ht ml
Harrison’s principles of int ernal medicine CMDT
2009.
257
Geriatrics
Chapter 12
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
● Falls
* I nt roduct ion
* Assessment
* Evaluat ion
* Treat ment
● COMA
* Definit ion
* I nvest igat ions
* Treat ment
● Geriat ric Surgery
* I nt roduct ion
* Geriat ric Case Principals
* Treat ment
* Special Considerat ions
* Keypoint
259
FALLS
I nt r oduct i on
Falls are one of t he maj or problems faced by t he
elderly and it is considered as a “ Geriat ric Giant ”.
Recurrent falls is an import ant cause of morbidit y and
mort alit y in t he elderly and a marker of poor physical
and cognit ive st at us.
The incidence increases as age advances, and is a
leading cause of deat h due t o it s complicat ions. The
morbidit y due t o falls are fract ures, soft t issue inj ury,
rest rict ed mobilit y and psychological t rauma. More
t han 80% of hip fract ures in t he elderly are due t o falls.
These lead t o increased healt h care ut ilizat ion. The
psychological fear may lead t o “ Post Fall Syndrome” a
st at e in which an elderly person rest rict s his mobilit y
or becomes dependent on ot hers t o move, in spit e of
normal neurological st at us.
Def i ni tion
Fall is best defined as a sudden unint ent ional change
in posit ion, causing a subj ect t o land on t he ground
or on lower level not as a result of maj or int rinsic or
ext rinsic hazards. A recurrent fall is defined as t wo or
more fall event s occurring wit hin a period of six mont hs.
About 1/ 3 of t he communit y living elderly fall in a
year. Some st udies indicat e t hat 25-50% of communit y–
dwelling elderly fall at least once annually and half of
t hem have mult iple falling episodes.1 The incidence of
falls is higher in t he inst it ut ionalized elderly, owing t o
t heir poor healt h and higher report ing rat es.
Causes
Basically, t he upright human body is unst able wit h
a very small base of support relat ive t o it s height .
During physical act ivit ies t he balance is maint ained by
complex neuromuscular feedback mechanism. The
cent ral st ruct ures (cort ex, basal ganglia, brain st em and
cerebellum) coordinat e t he sensory input s from visual,
vest ibular and propriocept ive organs and cont rol t he
effect or organs i.e. t he musculoskelet al act ion of lower
limbs, neck and t runk. Aging changes include impairment
of vision and hearing, reduct ion of propriocept ive and
vibrat ory sensat ion, increased sway, alt ered gait and
slower right ing reflexes. These physiological changes
alone do not cause a fall but increase t he liabilit y t o fall.
Most oft en t he cause of a fall is mult ifact orial. I t is due
t o mult iple underlying problems such as physical illness,
cognit ive decline, medicat ions and environment al
hazards. The risk fact ors for falls in elderly 1-5 are
list ed below
Assessment of f al l s:
Scr eeni ng:
Falls and t heir sequalae are pot ent ially prevent able
and hence annual screening for falls is recommended.
For individuals who have experienced one or more falls,
a furt her evaluat ion is recommended.
Assessment includes a complet e det ailed hist ory
regarding t he fall, individual’s fear of falling, t he
presence of acut e or chronic illness and medicat ions.
The pneumonic “ SPLATT” is useful for recalling t he
fall circumst ances.
S Sympt oms t hat occurred immediat ely
prior t o fall or wit h t he fall episode (light
headedness, dizziness, vert igo, palpi-
t at ions, chest pain, dyspnoea, sudden
f ocal neurological deficit , aura, syn-
cope, or urinary / faecal incont inence.
P Previous hist ory of falls
L Locat ion of fall
A Act ivit y at t he t ime of fall
T Timing of fall and lengt h of t ime on
ground
T Trauma or inj ury as a result of fall.
● Assessment of individual’s fear of falling is done
by self efficacy t est s.
● Depression is assessed wit h t he Geriat ric Depres-
sion Scale (GDS).
● Medicat ion hist ory is elicit ed in det ail wit h spe-
cific at t ent ion given t o newly st art ed drugs or for
which t he dose has been increased recent ly.
● Funct ional assessment wit h ADL score is done.
260
RI SK FACTORS FOR FALLS
I nt rinsic Fact ors
1. Old Age / Female sex / Low body mass index
2. Neurological
* Cognit ive impairment
* Post ural inst abilit y
* Parkinsonism
* CVA / Gait disorders
* Peripheral neuropat hy
* Sleep dist urbance
3. Visual impairment
4. Musculoskelet al
* Foot disorders
* Muscle weakness of lower limbs
5. Cardiovascular
* Arrhyt hmias
* Post ural hypot ension
* Cardiac failure
6. Medicat ion
* Polypharmacy
* Sedat ives / hypnot ics
* Diuret ics / Ant idepressant s
7. Acut e I llness
* Acut e pneumonit is / Myocudial infect ion.
8. Met abolic dist urbances
9. Behavioral
* Alcohol int oxicat ion
10. Psychological
* Depression
Ext rinsic Fact ors
1. Ground surface
* Uneven surface
* Slippery Floors
* St eps
2. Light ing
* Poor light ing
* Glare from lamps
3. Furnit ure
* Low lying furnit ure
* Chairs wit hout arms
4. I mproper walking aids and foot wear
Symptoms
This includes assessment of vision, gait and
balance and lower ext remit y j oint funct ion. Det ailed
neurological examinat ion including cognit ive screening
using Mini Ment al St at e Examinat ion (MMSE) is done.
Cardiovascular assessment and evaluat ion of various
int rinsic and ext rinsic fact ors are done.
I nvesti gati ons
I nj urious falls require X-Ray or ot her imaging st udies
depending on t he sit e of inj ury and condit ion of t he
pat ient .
Speci al i zed Assessment
This includes assessment of gait and balance by
various t est s such as t he
* Funct ional Reach (FR) which measures dy-
namic balance
* Berg balance scale- a measure of funct ional
act ivit y
* Timed get up and go t est and
* Performance orient ed mobilit y assessment
which is a measure of balance and gait .
261
Al gor i t hm f or Eval uat i on of Fal l s:
Fall
Injury
Yes No
History
LOC
Vasodep.Syncope
Cardiac Arrhythmia
Postural Hypotension
Epilepsy
Trip / Slip
No
No
Unwell Recurrent
Yes
Yes No Yes
Musculoskeletal
Environmental
Drug - induced
Neurological
Psychiatric
Acute Illness
Treatment
Reassurance
and Follow up
Treatment of injury
Treatment
● Home safet y evaluat ion is done for falls t hat oc-
cur at home, wit h regard t o ext rinsic fact ors.
● Treat ment of t he inj ury and t he associat ed ill-
ness. Aft er t he pat ient is st abilized t he t reat ment
of t he primary cause of fall should be implement-
ed. These include physiot herapy (balance t rain-
ing and muscle st rengt hening exercise) use of
elast ic st ockings for ort host at ic hypot ension and
specific drug t herapy, dose adj ust ment and re-
view of medicat ions.
Fal l pr event i on
1. Fall-relat ed educat ion
2. Environment al assessment and modificat ion
3. Modificat ion of medicat ion regimen
4. Exercise program t o improve st rengt h, balance
and endurance.
* Muscle st rengt hening / resist ance exercise
* Balance t raining
* Aerobic / endurance t raining
* Flexibilit y exercises and
* Tai-chi- an ancient mart ial art form of China.
The slow and direct rhyt hmicit y of movement s
cont ribut e t o development of movement st rat-
egy t o prevent falls in act ual life.
I mpor t ant Not e
Falls occur frequent ly in elderly wit h increased
morbidit y. A number of int rinsic and ext rinsic risk fact ors
are associat ed wit h a fall. Falls are oft en mult ifact orial.
Hence a det ailed evaluat ion is mandat ory, part icularly
in t hose wit h recurrent falls. Falls may be prevent ed by
t arget ed, mult ifacet ed int ervent ions.
Ref er ences :
1. Tinet t i ME, speechley M, Gint er SF : Risk fact ors
for falls among elderly persons living in t he com-
munit y. N Engl J Med 1988; 319 : 1701-7.
2. Nevit t MC, Cummings SR, Kidd s et al: Risk fac-
t ors for recurrent non syncopal falls. JAMA 1989;
261: 2663-68.
3. O’ Loughin JL, Robit aile Y, Boivin JF et al: I nci-
dence of and risk fact ors for falls and inj urious
falls among t he communit y dwelling elderly. Am
J Epidemiol 1993; 137: 342-354.
4. Gragmans WC, Ooms ME, Hofst ee HM et al:
Falls in t he elderly: a prospect ive st udy of risk
fact ors and risk profiles. Am J Epidemiol 1996;
143: 1129-1136.
5. Leipzig RM, Cumming RG, Tinet t i ME: Drugs and
falls in older people : a syst emat ic review and
met a-analysis : I . Psychot ropic drugs. J Am Geri-
at r soc 1999; 47: 30-39.
6. Tideiksaar R : Prevent ing falls : how t o ident i-
fy risk fact ors, reduce complicat ions, Geriat rics
1996; 51(2) : 43-46, 49-53.
7. Tinet t i ME, Richman D, Powell L : Falls ef-
ficacy as a measure of fear of falling.
J Geront ol A 1990; 45: M239-M243.
8. Powell LE, Myers AM : The act ivi-
t ies specific balance confidence scale :
J Geront ol A 1995; 50 : M28 – M34.
9. Anonymous : Guideline for t he prevent ion of falls
in older persons. J. Am Geriat r Soc 2001; 49: 664
– 672.
10. Close J, Ellis M, Hooper R et al: Prevent ion of
falls in t he elderly t rial (PROFET): a randomized
cont rolled t rial. Lancet 1999; 353: 93-97.
262
COMA
Coma is defined as a prolonged period of
uncondciousness and lack of react ion t o st imulus.
Pat ient s in coma can not be aroused.
Sal i ent f eat ur es
Following causes affect t he funct ions of ret icular -
act ivat ing syst em and it s connect ions wit h cerebrrum.
● St ruct ural damage t o brain (haemorrhage, t u-
mors, t rauma, localized infect ions, meningit is,
st roke).
● Met abolic dist urbances (ischaemia, anoxia, urae-
mia, diabet es), respirat opry/ hepat ic/ renal failure,
dyselect rolyt aemia, endocrinopat hies, drugs like
opiat es, barbit urat es, benzodiazepines, ant i-de-
pressant s and cyanide.
● Abnormal elecrical act ivit y - periodic lat eralized
epilept iform discharge (PLED).
Treatment
Nonphar macol ogi cal
● The immediat e goal in acut e coma is t he preven-
t ion of furt her nervous syst em damage.
● Hypot ension, hypoglycaemia, hypercalcmia, hy-
poxia, hypercapnia and hypert hermia should br
correct ed rapidly and assiduously.
● An orophat yngeal airway is adequat e t o keep t he
pharynx open in drowsy pat ient s who are breat h-
ing normally.
● Tracheal int ubat ion is indicat ed if t here is apnoea,
upper airway obt ruct ion, hypovent ilat ion or em-
esis, or if t he pat ient is liable t o aspirat e because
of coma.
● Mechanical vent ilat ion is required if t here is hy-
povent ilat ion or if t here is an int racranial mass
and a need t o induce hypocapnia in order t o law-
er int racranial pressure.
● Est ablish int ravenous access.
Phar macol ogi cal
1. I nj . Glucose (25 or 50%) 50 g I V.
2. I nj . Thiamine 100 mg I V.
3. I f opiat e overdose is suspect ed, give I nj . Naloxone
0.8 mg I V. response is inadequat e, double t he
dose every 15 minut es (for det ails see sect ion on
opioid int oxicat ion).
4. I f benzodiazepine overdose is suspect ed give I nj .
Flumazenil 200 mcg I V slowly. I f no response re-
peat 100-200 mcg aft er 1 minut e. I f required give
maximum does of 1 mg or give as I V infusion of
100-400 mcg/ h if drowsiness recurs.
5. I f focal neurological deficit or signs of herniat ion/
decerebrat ion/ decort icat ion occurs, CT scan, EEG
and neurologic consult at ion is required.
6. I f no clear aet iology and no herniat ion - CSF ex-
eminat ion should be done.
7. I f signs of raised int racranial t ension (papilloede-
ma, convulsions, decerebrat e post ure indicat ing
herniat ion) occurs:
* Avoid giving free fluid (glucose solut ion) in-
t ravenously.
* I nj . Frusemide 40 mg I V t o maint ain adequat e
urine out put of 30-50 ml/ h.
* I nj . Mannit ol 1.0 g/ kg I V over 10 minut es.
* Hypervent ilat e t o bring down PCO2 t o 25
mmHg.
* I nj . Dexamet hasone 20 mg I V st at and 6 mg
4 hourly.
Children and young adult s may have ominous early
clinical findings such as abnormal brainst em reflexes
and yet recover. Met abolic comas have a far bet t er
prognosis t han t raumat ic comas. Glasgow coma scale
empirically has predict ive value in case of brain t rauma
( Table 2.5). For anoxic and met abolic coma, clinical
signs such as papillary and mot or responses aft er 1 day,
3 days and 1 week have been shown t o have predict ive
value. Absence of cort ical waves of t he somat osensory
evoked pot ent ials has also proved a st rong indicat or of
poor out come in coma from any cause.
Gr edi ng of coma
Glasgow coma scale for head inj ury ( Table 2-5)
Glasgow coma scale
263
Eye opening (E) Coma score
Spont aneous 4
To loud voice 3
To pain 2
Nil 1
Best mot or response (M)
Obeys 6
Localizes 5
Wit hdraws (flexion) 4
Abnormal flexion post uring 3
Ext ension post uring 2
Nil 1
Verbal response (v)
Orient ed 5
Confused, disorient ed 4
I nappropriat e words 3
I ncomprehensible sounds 2
Nil 1
Not e: Coma score= E+ M+ V. Pat ient s scoring 3 or 4
have an 85% chance of dying or remaining veget at ive,
while scores above 11 indicat ive only a 5 t o 10%
likelihood of deat h or veget at ive st at e and 85% chance
of moderat e disabilit y or good recovery. I nt ermediat e
scores correlat e wit h proport ional chances of recovery.
Ref er ence
1. Coma. I n: Harrison’s Principles of I nt ernal Medi-
cine. Kasper DL, Braunwald E, Fauci AS et at
(eds), 16t h Edit ion 2005, McGraw Hill Company
I nc., New York, pp 1624-1631.
2. Head I nj ury. I n: Harrison’s Principles of I nt ernal
Medicine. Kasper DL, Braunwald E, Fauci AS et al
(eds), 16t h Edit ion 2005, McGraw Hill Company
I nc., New York, pp 2447-2452.
Geriatric surgery
Longevit y has increased all over t he globe due t o
advances in science and healt h care delivery syst ems,
result ing in an increased elderly populat ion. There is not
only a large number of elderly populat ion in (absolut e
t erm) but t hey also live longer t han ever before t o
cont ract many diseases and problems
As age advances t here is progressive and generalized
det eriorat ion of organ funct ion wit h loss of reserve. The
rule of t hirds st at es t hat 1/ 3 of decline in funct ion is
due t o disease; anot her 1/ 3 due t o disuse and t he rest
due t o ageing. Ageing changes can be minimized and
post poned by balanced diet , exercise, and avoiding
smoking and alcohol
Healt h st at us of t he elderly is generally poor in
addit ion t o t heir physical, ment al, social and financial
problems. They have mult iple medical disorders
like diabet es, hypert ension, ischemic heart disease,
neurological problems and as age advances t hey may
develop cancers of various organs.
Pr i nci pl es of ger i at r i c sur ger y:
● Maximize independent funct ion
● Reduce disabilit ies, suffering and pain
● Enhance qualit y and dignit y of life
Best f or ms of heal t h car e i n t he el der l y:
● Respect elderly pat ient s at all t imes by list ening
t o t heir st at ement s
● Execut e healt h promot ional act ivit ies- good nut ri-
t ion, exercise, social act ivit ies
● I mplement prevent ive measures like st opping
smoking, chewing t obacco and drinking alcohol (
it is never t oo lat e t o st op smoking and drinking)
and t o swit ch over t o a healt hy life st yle
● Screening of common diseases, early det ect ion
and int ervent ion
Ger i at r i c car e pr i nci pl es:
● I mprove qualit y of life, it is more import ant t han
prolonging life
● Honor t he pat ient ’s wishes while invest igat ing
and t reat ing
● I mprove t he general condit ion and nut rit ional
st at us
● I dent ify co - morbid condit ion and correct t hem
before surgery
● Explain t he procedure, possible risks and compli-
cat ions of surgery
● Get det ailed informed consent in writ ing for all
procedures
● I nit iat e t reat ment early
● Consider alt ernat ive modalit ies of t reat ment in-
st ead of high risk surgery
● Modify t he t reat ment regimen considering t he
ageing physiology
● Take up proact ive measures so as t o prevent ia-
264
t rogenic complicat ions
● Assess t he capabilit ies of t he pat ient and t he
family or caregivers as it is essent ial t o make a
good and safe managemnet plan
● Provide cont inued, comprehensive int erdiscipli-
nary t eam care
Hi st or y t aki ng i n el der s:
● Elicit hist ory , including medicat ion review
● Past hist ory, t reat ment t aken, polypharmacy
● Get all old records wherever possible
● Rely on hist ory given by t he relat ive/ care t aker
or by t he referring physician if no hist ory can be
elicit ed from t he pat ient
● Complet ely rely on physical findings, invest iga-
t ions if no hist ory is possible
Physi cal exami nat i on:
● Complet e general and physical examinat ion
● Examine in comfort able surroundings
● I t may be necessary t o post pone t he examinat ion
as per t he pat ient ’s wishes
● Examine t he pat ient in mult iple sit t ings if required
I nvesti gati ons
● Special t est s t o be carried out if any abnormalit y
is suspect ed
● Rout ine and repeat ed invest igat ions should be
avoided
● Cost ly and invasive invest igat ions for diagnosis
need not be done in case of very old and very ill
pat ient s, if no t reat ment is cont em plat ed
Di agnosi s:
● Mult iple pat hological problems wit h mult iple
sympt oms are common in t he and no single diag-
nosis is common for all sympt oms
● General measures are t o be t aken t o keep t he
geriat ric pat ient comfort able and free from pain
when t he diagnosis is delayed or not possible
.
Treatment
● Always aim at complet e cure
● Consider t he general condit ion and co morbid
condit ions
● Always weigh t he benefit of surgery against t he
possible risks and complicat ions
● Consider alt ernat ives t o high risk surgery and
non operat ive managemant
● Always provide general support ive measrues and
t ender loving care when no specific t reat ment of
t he problem is cont emplat ed
Speci al consi der at i ons:
● Preoperat ive:
● Preop assessment and preparat ion
● Det ect and t reat comorbid condit ions- Diabet es,
I HD, Hypert ension
● I mprove respirat ory funct ion, preop physiot her-
apy
● Correct anemia, hypoprot enemia, t reat infect ive
foci
● Preoperat ive counselling
There is generalised det eriorat ion of organ funct ion
and loss of reserve, hence minor degrees of fluct uat ion
in blood volume and BP can t ilt t he balance in t he
elderly
Anaest hesi a:
● Good anaest het ic t echniques likie smoot h induc-
t ion, maint anence and quick reversal wit hout any
cerebral complicat ions
● During anaest hesia, adequat e cerebvral and
coronary blood flow, maint anence of fluid and
elect rolyt e balance , urinary out put and glycemic
cont rol are of paramount import ance in t he eld-
erly
Sur ger y:
● Do t he minimum necessary procedure
● Avoid blood loss/ replace immediet ely
● Avoid hypot ension, hypoxia and hypot hermia
● Neat and fast surgery t o keep anaest hesia t ime
t o t he minimum
Post -oper at i ve car e
I mmedi at e:
● Maint ain vit al signs and blood pressure
● Adequat e oxygenat ion and fluids t o avoid hypo-
t ension, hypoxia and hypot hermia
● Prevent cerebral anoxia and avoid delirium
265
● Adequat e analgesia, early mobilizat ion and physi-
ot herapy t o prevent pulmoray complicat ions
Ear l y post oper at i ve car e:
Avoid prolonged parent eral nut rit ion, use gut
early Prevent respirat ory and wound infect ions Avoid
prolonged bed rest , ambulat e early
I n elderly immobilit y my lead t o:
● Loss of muscle mass
● Decreased t issue sensit ivit y t o insulin
● Ort host at ic hypot ension, t achycardia, decreased
cardiac out put , and decreased st roke volume
● Urinary ret ent ion, urinary t ract infect ion
● Negat ive nit rogen balance
● Depression, sensory deprivat ion
● Deep vein t hrombosis
● Const ipat ion, fecal impact ion
● Decubit us ulcers
Key poi nt s:
● Always t ake t he pat ient ’s / relat ives signat ure in
writ ing when deciding on hospit alizat ion, ordering
cost ly and t roublesome invest igat ions , init iat ing
int ensive and invasive monit oring and t reat ment
● Manage elders j udiciously wit hout pushing t hem
t o financial difficult ies
● Good communicat ion wit h t he pat ient s, family
members, caregivers and t he family physicians
will help t o get t he expressed preferences
● Medical et hics, moral values and legal formalit ies
should be followed st rict ly while t aking manage-
ment decisions
● Reassurance and t ender loving care should be
given life long.
267
Paediatrics
Chapter 13
Standard Treatment Guidelines
Tamil Nadu Health Systems Project
Neonat ol ogy
● Guidelines for management of normal New born
● High risk new born
● Neonat al resuscit at ion
● Management of LBW babies
● Neo nat al seizures
● Jaundice in t he new born
● Respirat ory dist ress in new born
● Bleeding in neonat es
● Hypot hermia in new born
● Neo nat al t ransport
● Surgical problems in neo nat es
Paedi at r i cs
● Alt ered level of consciousness
● Febrile seizures
● Acut e respirat ory infect ion
● Pneumonia
● Bronchiolit is
● Empyema
● Approach t o fever in children
● Malaria
● Dengue
● Typhoid
● UTI
● Lept ospirosis
● Viral hepat it is
● Tuberculosis
● Rheumat ic fever in children
● Nephrot ic syndrome
● Acut e nephrit ic syndrome
● Prot ein energy malnut rit ion
● Anaemia
● Management of scorpion st ing
● Management of snake bit e
● Management of Poisoning in children
269
Guidelines for Management of
Normal Newborn
Pr i or t o del i ver y
Review mat ernal hist ory t o ant icipat e problems
in neonat e.
Check l i st f or New bor n ki t
1. Mucus cat het er (Lee’s) / Bulb sucker
2. Warm t owels
3. Warmer
4. Equipment for resuscit at ion
5. Test t ube for cord blood
6. Disposable syringes and needles
7. Emergency drugs including I nj .vit amin K 25%
dext rose, 10%calcium gluconat e, adrevaline,
naloxone.
At del i ver y
1. Keep t he baby on level wit h mot her. Do not
milk t he cord. Clamp 5 cm away from t he baby,
cut it and t ie wit h double ligat ures. Leave t he
cord uncovered. Collect cord blood for grouping,
Coomb's t est , VDRL, screening t est s if necessary.
2. Resuscit at e, if required. Assess Apgar.
3. Thermo regulat ion. Dry t he baby well wit h a
pre-warmed t owel soon aft er birt h. Wrap in dry,
warm sheet / blanket and place wit h mot her. No
bat h need be given. Head should be dried t hor-
oughly.
4. Clean eyes from medial t o lat eral wit h separat e
moist st erile swabs if necessary.
5. Weigh t he baby, assess gest at ion.
6. For ident ificat ion, t ie wrist t ag.
7. Record t ime and dat e of birt h.
8. Record passage of meconium, urine.
9. Carry out a preliminary examinat ion. Rule out
life-t hreat ening congenit al anomalies.
10. Administ er Vit amin K 1 mg int ramuscularly
11. Put t he baby t o t he breast soon aft er birt h, pref-
erably in t he first half hour.
12. Normal newborns must be kept wit h mot her.
Car e of t he nor mal newbor n
1. Aft er delivery t he baby is placed next t o t he
mot her and leaves t he labour room wit h t he
mot her. Baby should be kept wit h t he mot her in
t he post nat al ward.
2. Feeding
* Exclusive breast milk
3. No pre-lact eal feeds including wat er, glucose wa-
t er or honey.
4. Clot hing
* Soft , whit e, clean clot hes.
5. No pins, hooks or but t ons, only t ies.
6. Easy t o put on at neck and arms.
7. Napkins: cot t on napkins may be used inst ead of
disposable napkins.
8. Care of cord
* Left open t o dry.
9. Baby bat h
* No full wat er bat h should be given immedi-
at ely aft er delivery t o ensure maint enance of
t emperat ure
* Baby can be cleaned wit h oil / warm wat er t o
remove excess of vernix and meconium
* I n a busy, crowded ward it is wiser t o avoid
baby bat hs t o prevent cross infect ion
* At home, baby is safely bat hed on ext ended
legs in t he I ndian way. Oil and powder are not
necessary. A mild soap should be used.
Cl eani ng
Baby should be cleaned everyday and each t ime
when urine or st ools are passed. Bot t om should be
dipped in warm wat er and perineum cleaned from
above and below.
Vi t ami ns
Normal, full-t erm babies do not require vit amin
supplement s.
I mmuni zat i on
Baby should be given BCG, hepat it is B (wherever
given) and t he first dose of oral polio before discharge.
St ool s and ur i ne
The first st ools of t he baby are dark green / black,
st icky and is called meconium. I t is passed in t he first
270
24 hours aft er birt h. Aft er init iat ion of feeds t he colour
slowly changes t o green, yellow (t ransit ional) and finally
yellow. The normal baby who is breast fed can pass upt o
7 - 8 bright yellow, past y st ools or one st ool per day
(past y) or once in t wo t o t hree days.
A baby must pass urine in t he first 48 hours of life
and should pass urine at least 5 - 6 t imes a day. The
frequency can vary upt o 15 - 20 t imes a day.
● Feeding schedule will depend on t he gest at ional
age and clinical st at us of newborn (Given in t he
chapt er on low birt h weight )
● Treat ment will depend on t he individual condit ion
High risk newborn
High risk newborns are required t o be kept in
observat ion areas according t o t he specific indicat ions
as follows
Treatment areas for high risk newborns
Wit h mot her under obser-
vat ion
Observat ion area (nursery) Premat ure unit NI CU
1. I nfant s of elderly /
very young primi-
gravida
2. Rh - ve mot her
3. Mat ernal medicat ion
4. Tubal ligat ion done in
mot her
5. Pre-eclampsia
6. PROM
7. LSCS, vacuum, for-
ceps delivery
8. Meconium st ained
liquor, mild asphyxia
(asympt omat ic in-
fant )
9. I nfant weighing 2-2.5
kg
10. Previous deat h of a
sibling
11. Birt h t rauma
1. I nfant s of mot her
wit h t oxaemia of
pregnancy
2. I nfect ed mot her
3. Mot her wit h post-
part um psychosis
4. I DM
5. Polycyt hemia
6. Birt h t rauma
7. Hyper-bilirubinemia
8. Pre-t erm less t han 37
weeks of gest at ion.
1. Babies weighing less
t han 2 kg.
1. Severe asphyxia
2. Sy m p t o m a t i c
meconium aspira-
t ion
3. Severe respira-
t ory dist ress syn-
drome
4. Life t hreat ening
congenit al anom-
alies.
5. Congenit al infec-
t ions
6. Sept icaemia
7. Seizures
8. Bleeding neonat e
9. Congest ive car-
diac failure
10. Necrot ising-ent e-
rocolit is (NEC)
11. Severe anaemia
12. Po st - o p e r a t i v e
surgical neonat e
271
3
0

s
e
c
o
n
d
s
3
0

s
e
c
o
n
d
s
3
0

s
e
c
o
n
d
s
Eval ute Respi rati on,
Heart rate and Col our
T - Temperat ure
A - Airway
B - Breat hing
C - Circulat ion
D - Drugs
Neonat al resuscit at ion
272
Management of Low Birth Weight
(LBW) babies
I nfant s weighing less t han 2.5 kg.
These babies can be pret erm or small for gest at ional
age. (SGA)
Aet i ol ogy
● Mat ernal
* I nfect ions
* Chronic diseases
* Malnut rit ion
* Trauma
* Drugs
● Obst et ric fact ors
* Toxaemia
* Ant epart um haermorrhage
* Premat ure rupt ure of membranes
● Ut erine fact ors
* St ruct ural abnormalit y - bicornuat e or sept at e
ut erus
* Premat ure rupt ure of membranes
● Fet al fact ors
* Mult iple pregnancies
* Congenit al anomalies
* Chromosomal anomalies
* I nt raut erine infect ions
Management of t er m LBW and Pr e-t er m babi es
LBW ( Pr e-t er m) : Pr obl ems
● Birt h asphyxia
● Hypot hermia
● Feeding difficult ies
● I nfect ions
● Hyper-bilirubinemia
● Respirat ory dist ress syndrome (RDS)
● Ret inopat hy of premat urit y (ROP)
● Apnoeic spells
● I nt ravent ricular hemorrhage (I VH)
● Hypoglycemia
● Met abolic acidosis
LBW ( Smal l f or gest at i onal age) : Pr obl ems
● Birt h asphyxia
● Meconium aspirat ion syndrome
● Hypot hermia
● Hypoglycemia
● I nfect ions
● Polycyt hemia
LBW - I ssues i n del i ver y
● Transfer mot her t o a well - equipped cent re be-
fore delivery.
● Skilled person needed for effect ive resuscit at ion.
● Prevent ion of hypot hermia - t opmost priorit y.
LBW - I ndi cat i ons f or hospi t al i zat i on pr ovi ded
bel ow.
Decision t o choose t he referral hospit al may be
decided by t he t reat ing doct or.
● Birt h weight < 1800 g
● Gest at ion < 34 weeks
● Unable t o feed
● Sick neonat e irrespect ive of birt h weight and ges-
t at ion
Tr eat ment gui del i nes f or LBW babi es
● Prevent ion of Hypot hermia
* Keeping warm at home by skin t o skin cont act
- Kangaroo Mot her Care (KMC).
* Keeping t he baby warm in hospit al - skin t o
skin cont act ; warm room and bed; warmly
wrapped; radiant warmer; incubat or
● Feeding
* Weight < 1200 g; Gest at ion < 30 wks
» St art init ial int ravenous fluids (refer fluid
t herapy guidelines)
» I nt roduce lavage feeds once st able.
» Shift t o paladai / spoon feeds over next
few days. Lat er on breast feeds.
* Weight 1200 - 1800 g; Gest at ion 30-34 wks
» St art init ial gavage feeds.
» Paladai / spoon feeding aft er 1 - 3 days.
Shift t o breast feeds as soon as baby is
able t o suck.
273
» May need int ravenous fluids, if sick.
* Weight > 1800 g; Gest at ion > 34 wks
» Breast feeding
» Paladai / spoon feeding, if sucking not sat-
isfact ory on breast .
» Shift t o breast feeds as soon as possible.
● LBW - Feeding schedule
* Begin at 60 t o 80 ml/ kg/ day; I ncrease by 15
ml / kg/ day; maximum of 180 - 200 ml/ kg/
day. First feed at 2 hours of age, t hen every
2 hourly.
● LBW - Weight pat t ern
* Pre-t erms lose 2 t o 3% weight every day for
1st week wit h a cumulat ive loss of 15-20%.
Weight gain commences by 10-15 days
* Excessive weight loss or inadequat e weight
gain consider: Cold st ress, anaemia, poor in-
t ake, sepsis et c,
● LBW
* Supplement s
» Vit amin : Vit . K 1.0 mg I M at birt h
» Vit A 1000 I U / day and
» Vit D 400 I .U / day from 2 weeks of age.
* I ron oral 2 mg/ kg/ day from 8 weeks of age
* Calcium and phosphorus: 100 mg/ kg/ day
● Danger signals (early det ect ion and referral)
* Let hargy, refusal of feeds.
* Hypot hermia
* Tachypnea, grunt , gasping, apnea
* Seizures, vacant st are
* Abdominal dist ension
* Bleeding
* I ct erus over palms / soles
* Sudden pallor
● LBW babies require dose monit oring and follow
up of
* Growt h monit oring - Head circumference and
weight
* Development al assessment and early st imula-
t ion.
* I nt ravent ricular hemorrhage screening by ul-
t rasound cranium on day 1, 3, 7 and at 4-6
wks.
* Screening t est s for hearing - at discharge
* Ret inopat hy of premat urit y screening at one
mont h of age.
* Screening for ost eopenia of premat urit y
Neonatal Seizures
Seizures are abnormal involunt ary movement s
affect ing part or whole of t he body, occurring due t o an
excessive synchronous elect rical discharge of neurons
wit hin t he CNS.
Point s t o remember
● Neonat al seizures are not easy t o recognize be-
cause of varying clinical pat t erns.
● Seizures oft en result from underlying CNS dys-
funct ion and t hey cause CNS damage.
● I nt ravenous administ rat ion of ant iconvulsant s in
correct doses is essent ial as absorpt ion by ot her
rout es is errat ic.
Aet i ol ogy
● Asphyxia
● I nt racranial haemorrhage.
● Met abolic
* Hypoglycemia
* Hypocalcemia
* Hypomagnesemia
* Hyponat remia
* Hypernat remia
● Meningit is, encephalit is
● Polycyt hemia
● Pyridoxine deficiency
● I nborn errors of met abolism
● Congenit al malformat ions of CNS
● Narcot ic drug wit hdrawal.
Cl i ni cal pr esent at i on
Classical t onic clonic convulsions of older children
are not seen in neonat es. Seizures present as:
● Subt le convulsions
* Abnormal eye movement s - Blinking, flut t er-
ing of eyelids, horizont al deviat ion of eye balls
wit h nyst agmus.
274
* Oro-buccal - lingual movement s - Sucking,
chewing, drooling, lip smacking, et c.,
* Abnormal limb movement s - Swimming, row-
ing, cycling
* Apnoea.
● Focal clonic : Common in mult i-focal disorders,
focal lesions.
● Mult i-focal clonic.
● Generalized t onic spasms : Common in pret erm
babies.
● Myoclonic j erks.
Suggest ed i nvest i gat i ons
● Blood sugar, Dext rost ix
● Serum calcium, magnesium.
● Serum elect rolyt es.
● Haemat ocrit .
● Lumbar punct ure.
● Ult rasonography of cranium
● CT Scan
● Urine and Plasma screening for inborn errors of
met abolism.
● EEG
● Sepsis screening
Not e
Diazepam is not safe in neonat es as it int erferes wit h
vit al funct ion, it s sedat ive effect exceeds 24 hours and
sodium benzoat e, t he preservat ive used increases t he
risk of bilirubin encephalopat hy.
Ot her s
● Hypomagnesemia
* Magnesium sulfat e, 50% solut ion : 0.2 ml/ kg,
I M;
● Refract ory seizures
* Pyridoxine : 50-100 mg/ kg I V (wit h EEG moni-
t oring)
Dur at i on of ant i convul sant t her apy - gui del i nes
i n Neonat al per i od
● Neurological examinat ion normal
* Discont inue t herapy
● Persist ent ly abnormal
* Consider et iology
* Obt ain EEG
* Cont inue phenobarbit one
* Discont inue phenyt oin
* Re-evaluat e in a mont h
One mont h af t er di schar ge
● Neurological examinat ion normal
* Discont inue phenobarbit one aft er 2 weeks
● Persist ent ly abnormal
* Obt ain EEG
* No seizure act ivit y
* Discont inue phenobarbit one over 2 weeks
● Seizure act ivit y persist s
* Cont inue phenobarbit one unt il 3 mont hs of
age and reassess in t he same manner.
275
Guidelines for treatment of Neonatal seizures
Treatment:
10% Dextrose at 2 ml/kg
(200 mg/kg) intravenously
Target blood sugar 70-120 mg/dl.
Then dextrose infusion at 8 mg
/kg/min
Neonate with clinical seizure
Ensure adequate ventilation and perfusion (ABC's)
Dextrostix test
CBG < 45 CBG > 45
10% Ca gluconate 2 ml/kg IV diluted
with equal volume of 10% Dextrose in
case of hypocalcemia (under cardiac monitoring)
Phenobarbitone : 20 mg/kg IV over 15-20 minutes
Actively convulsing
Actively convulsing
Actively convulsing
Actively convulsing
Actively convulsing
Actively convulsing
Actively convulsing
Phenobarbitone 5 mg/kg IV 10 min
Phenobarbitone repeated at 5 mg/kg
doses at 10 min intervals
(Max upto 40 mg/kg totally)
Phenytoin : 15-20 mg/kg IV as loading dose
over 20 minutes (with cardiac monitoring)
Phenytoin may be repeated at 5 mg/kg
dose at 10 min intervals (Max total: 30 mg/kg)
Midazolam : 1 - 4 mcg/kg/min IV infusion or
Clonazepam : 0.01 - 0.03 mg/kg/day I.V. in 2 divided doses
Treatment:
Inj phenytoin 4-8 mg/kg/
day maintenance in two
divided doses along with
phenobarbitone maintenance
Treatment:
Inj phenobarbitone 3-4
mg/kg/day maintenance
in two divided doses
Hypoglycemia
Seizures controlled
Seizures controlled
276
Jaundice In The Newborn
Points to remember
ł Jaundice is common in neonates and is predomi-
nantly of the indirect type.
ł It is important to distinguish between physiologi-
cal and pathological jaundice and establish an
aetiology for the latter.
ł Jaundice is clinically appreciable in newborns
with serum bilirubin values of 7 mg% or more as
compared to 2 mg% in adult and is best appreci-
ated not in the sclera but by blanching the body
skin in good day-light.
ł All newborns should be screened at least twice a
day for jaundice.
ł The most accurate method to assess and moni-
tor jaundice is by estimating bilirubin in serum,
especially in dark babies and babies under pho-
totherapy, where clinical judgement is not to be
relied upon.
ł Babies with asphyxia, acidosis, hypoglycaemia
(sick neonate) and pre-terms run a higher risk
of bilirubin encephalopathy (kernicterus) at lower
levels of bilirubin.
Criteria For Pathological Jaundice
ł Clinical jaundice in first 24 hours of life.
ł Total serum bilirubin increasing by more that 5
mg%/day.
ł Total serum bilirubin more than 12.9 mg% in
full-term.
ł Direct serum bilirubin more than 2 mg%.
ł Clinical jaundice persisting for more than one
week in full-term and for more than 2 weeks in
pre-term infants.
[Look for various causes related to time of ap-
pearance of jaundice after birth and associated
clinical findings]
Evaluation
ł Clinical determination of jaundice by Kramer's
criteria.
ł Jaundice in the newborn presents a cephalocau-
dal pattern of appearance.
Clinical Determination Of Jaundice By
Kramer’s Criteria.
Area of body
Range of serum bilirubin
(mg%))
Head and neck 4 – 8
Upper trunk 5- 12
Lower trunk and thigh 8 – 16
Arms and lower limbs 11 – 18
Palms and soles more than 15 mg
Investigations
Following investigations must be done in each
case of neonatal jaundice.
ł Serum bilirubin direct, indirect.
ł Blood grouping of mother and child ABO and Rh.
ł Direct Coomb's test in infant
ł Hematocrit and peripheral smear for RBC mor-
phology and reticulocyte count.
ł Indirect Coomb’s test in mother if she is Rh nega-
tive
277
Treatment modalities of Hyperbilirubinemia
● Hydrat ion
● Phot ot herapy
● Exchange t ransfusion
● Drugs t o increase conj ugat ion
Hydr at i on
Cont inued and frequent breast feeding - 8 - 10
t imes / day
Phot ot her apy ( Tabl e I and I I )
● Special blue light s t o be used
● 45 cm dist ance bet ween baby and phot ot herapy
unit
● Eyes and genit alia should be covered
● Double surface phot ot herapy is preferred
● Wat ch for side effect s (diarrhoea, skin rash, hy-
per / hypot hermia)
TABLE 1 - Gui del i nes f or phot ot her apy accor di ng
t o AAP
Healt hy, t erm newborn (> 37 weeks)
Age (hours)
Consider Pho-
t ot herapy TSB
(mg/ dl)
Phot ot herapy
TSB (mg/ dl)
< 24
25 – 48 > 12 > 15
49 – 72 > 15 > 18
> 72 > 17 > 20
Not e: TSB-Tot al ser um bi l i r ubi n
TABLE I I – Phot ot her apy i ndi cat i ons
Based on birt h weight and healt h of t he newborn
Birt h weight
(gms)
Healt hy; TSB
(mg/ dl)
Sick; TSB
(mg/ dl)
< 1000 5 - 7 4 - 6
1001 – 1500 7-10 6-8
1501 – 2000 10 - 12 8 - 10
2001 – 2500 12 - 15 10 - 12
TERM
> 2500 15-18 12-15
Poi nt s t o r emember
● Try t o est ablish diagnosis before inst it ut ing pho-
t ot herapy by carrying out necessary invest iga-
t ions.
● Check blue light s funct ioning; life of t hese light s
is 1500 - 2000 h. (approx. 3 mont hs). Keep light s
at a dist ance of 18" from t he baby.
● When blue t ube light s are not available, four pairs
of whit e t ube light s may be used inst ead.
● Change t he posit ion of t he baby aft er every 2 h.
● Babies can be t aken out of phot ot herapy for
breast feeding
● Monit or baby's t emperat ure 2 hourly
● Monit or fluid balance-daily weight and urine out-
put . I ncrease fluids as necessary
● Shield t he eyes in bot h sexes t o prevent ret inal
damage and genit als in males t o prevent mut a-
t ion defect s in adult hood
● Monit or rise or fall of bilirubin every 12 hourly.
● Do not give phot ot herapy for direct hyperbiliru-
binemia.
● Exchange t ransfusion
Choi ce of Bl ood
● I f baby or mot her is Rh - ve use only Rh -ve Blood
● Always cross-mat ch donor’s blood wit h bot h
mot her’s and baby’s blood.
278
* Cord bilirubin more t han or equal t o 4.5
mg% and Hb less t han 11 g%.
* Rat e of rise of bilirubin > 1 mg/ dl despit e
phot ot herapy
* I n LBW babies, indirect bilirubin > (weight
in g)/ 100.
* Exchange earlier at levels of 2 mg% less for
following crit eria:
» Sepsis
» RDS
» Asphyxia
» Acidosis
» Hypoglycemia
Respiratory Distress In Newborn
Presence of t wo or more of t he following indicat es
respirat ory dist ress.
● Respirat ory rat e more t han 60 / min.
● Cyanosis.
● Use of accessory muscles of respirat ion, nasal
flaring, int ercost al, subcost al ret ract ion.
● Expirat ory grunt .
Poi nt s t o r emember
1. Commonest problem in neonat es wit h a wide dif-
ferent ial diagnosis.
2. Caused by respirat ory and non-respirat ory condi-
t ions.
3. Hist ory and clinical examinat ion are useful, but
X-ray chest is a must .
4. Surgical problems should be suspect ed and ruled
out .
5. Respirat ory paramet ers, i.e., clinical and art erial
blood gases (if possible) t o be monit ored regu-
larly.
Aet i ol ogy
Respi r at or y
● Development anomalies: Upper airway obst ruc-
t ion, t racheo - oesophageal fist ula, diaphragmat-
ic hernia, et c.,
● Parenchymal disease: Hyaline membrane dis-
ease, pneumonia, meconium aspirat ion, et c
● Transient Tachypnea of Newborn ( TTN)
Car di ac
Met abol i c
● Such as met abolic acidosis
Neur ol ogi c
● Such as int ravent ricular hemorrhage
Ot her s
● Polycyt hemia
● Sepsis
● Hypot hermia
Di agnost i c appr oach
Time of onset of respirat ory dist ress
At birt h Lat er onset
● Congenit al airway ob-
st ruct ion.
● Development al anoma-
lies of respirat ory t rack
● HMD, Meconium aspira-
t ion.
● Transient t achypnoea
of new born
● Pneumonia
● Air-leak syn-
dromes.
● Br o n c h o p u l -
monary dys-
plasia.
Pr ogr ess
● Early onset , progressive increase
* HMD
* Meconium aspirat ion
* Diaphragmat ic hernia
* Lobar emphysema
● Early onset , lat er improvement
* Transient t achypnoea of new born
Treatment Guidelines of Respiratory
Distress In New Born
Ask
1. Time of onset
2. Age
3. EDD
4. Birt h weight
5. Feeding problems
Assess
279
1. Temperat ure
2. Downe score
3. Capillary Refill Time (CRT)
4. SaO2
5. Gest at ional age
6. Present weight
7. Blood pressure
8. Heart rat e
Downe Scoring
Sign 0 1 2
Respirat ory
rat e
< 60 60 t o 80 > 80 or
apnoea
Cyanosis None I n room air I n 40%
oxygen
Ret ract ions None Mild Mod and
severe
Grunt None Audible wit h
st et hoscope
Audible
wit hout
st et h
Air ent ry Good Delayed or
decreased
Barely
audible
Look f or
● Pat ency (nasal and oesophageal)
● Chest asymmet ry
● Apical impulse
● Scaphoid abdomen
● Hepat omegaly
I nvesti gati ons
● Chest X-Ray (wit h NGT in sit u)
● Sept ic screening ( Tot al and different ial count ,
Band – neut rophil rat io, CRP, micro ESR)
● Blood cult ure
● ABG if feasible
● Serum elect rolyt es
● Renal Funct ion Test s (RFT), Blood glucose
Management of Respi r at or y di st r ess
● Maint ain t emperat ure 36.5o C - 37.5o C
● Posit ioning (Supine posit ion wit h head and neck
in neut ral posit ion)
● Oxygen-according t o Downe’s Score
* 0 t o 3 Oxygen by hood (51 / min)
* 4 t o 7 CPAP wit h Oxygen
* Above 7 I nt ermit t ent Posit ive Pressure Ven-
t ilat ion (I PPV) / Synchronized I nt ermit t ent
Mandat ory Vent ilat ion (SI MV)
● I f glucose is low - Bolus 10% dext rose 2 ml. / kg.
(2 boluses)
● Maint enance fluid I f CRT is more t han 3 sec.:
10 ml/ kg of normal saline, monit or liver size
I f st ill no improvement in CRT, commence ino-
t ropes
* Dopamine 5 t o 10 mcg / kg / min
o r
Dobut amine 10 t o 20 mcg / kg / min
* I f bradycardia inspit e of all t he above
» Adrenaline infusion 0.1 mcg / kg. / min.
● Ant ibiot ics
* Ampicillin at 50 mg. / kg / dose BD if < 7 days
and 50 mg/ kg/ dose TI D if > 7 days
+
* Gent amycin 5 mg/ kg in 2 divided doses
* Cefot axime at 50 mg/ kg/ dose BD if < 7 days
and 50 mg/ kg/ dose TDS if > 7 days (in place
of ampicillin in a very sick neonat e)
● Document ed met abolic acidosis :
Correct t he acidosis, t reat t he underlying cause.
Specific Management : Depending on individual
condit ion
Bleeding In Neonates
Poi nt s t o r emember
1. Coagulat ion fact ors do not cross from mot her t o
fet us.
2. Physiological deficiency of clot t ing fact ors such
as I I , VI I , I X, X result s in prolongat ion of Pro-
t hrombin Time (PT) and Part ial Thromboplast in
Time (PTT).
3. Bleeding is more common and severe in pre-
t erm and LBW infant s due t o accent uat ion of t his
deficiency.
4. All newborns should receive Vit amin K immedi-
at ely aft er birt h.
Common causes
280
1. Hemorrhagic disease of newborn (HDN) due t o
Vit amin K deficiency.
2. Disseminat ed int ravascular coagulat ion (DI C)
3. Thrombocyt openia of any cause.
4. I nherit ed deficiency of clot t ing fact ors.
5. I ncreased capillary fragilit y causing bleeding int o
skin. e.g. breech delivery, t raumat ic delivery.
Appr oach
Mat er nal Hi st or y
Condi t i on
I ncr eased r i sk due
t o
Ant enat al infect ions
TORCH
Thrombocyt openia
Drugs given t o
mot her, i.e. phenyt oin,
phenobarbit one, aspirin,
ant icoagulant s
Early onset HDN
H/ o bleeding in mot her,
e.g. I TP, SLE in mot her
Thrombocyt openia
Det ails of labour:
hypoxia, t rauma, et c.
DI C
Fami l y hi st or y
H/ o Bleeding in previous sibling, or ot her mem-
bers of family.
Pr esent hi st or y
● Day on which bleeding observed.
● Day 1 -Early onset HDN.
* Afibrinogenemia
* Hypofibrinogenemia
* Fact or XI I I deficiency
* DI C.
● Day 2
* Classical HDN
● H/ o administ rat ion of Vit . K at birt h
Physi cal exami nat i on
● First asses t he baby, i.e. sick versus well baby
from it 's appearance, cry and act ivit y.
Sit e of bleeding Likely cause
● GI T
● Mucosa, skin, sub-
cut aneous t issue
● Umbilicus, circum-
cision sit e
● Swallowed mat er-
nal blood, HDN
● Thrombocyt openia,
Trauma, DI C
● Fact or XI I I def.,
DI C, coagulat ion
fact or def
1. Look for signs of sepsis, j aundice, hepat o
splenomegaly.
2. Cephalhemat oma.
3. Hemangioma.
I nvesti gati ons
Basic screening t est s such as 'Plat elet count , PT, PTT
should be done before giving Vit K or blood t ransfusion.
Test s such as bleeding t ime and clot t ing t ime are not
sensit ive and do not help t o reach diagnosis.
Treatment
● Hemorrhagic disease of newborn
* Vit K 0.5-1mg I V. if bleeding cont inues
* Fresh frozen plasma (FFP) 10-15 ml/ kg I V if
act ive bleeding, can be repeat ed 12 hourly if
needed
* I f Hb is less t han 10 g t hen fresh blood t rans-
fusion 10-15 ml/ kg
* Prevent ion: 1 mg Vit K I M t o every newborn at
birt h is t he prevent ive measure for t his condi-
t ion.
● DI C
* Treat t he underlying cause, i.e. appropriat e
ant ibiot ics in sepsis, correct ion of acidosis,
hypoxia
* Replacement t herapy wit h FFP 10-15 ml/ kg
every 12 hourly
* Exchange t ransfusion using fresh blood less
t han 12 hours old every 12 hourly, t ill condi-
t ion st abilizes.
Hypothermia In Newborn
BABI ES AT RI SK FOR HYPOTHERMI A
● All newborns in first 12hrs of life
● All pret erm and low birt h weight babies
● Asphyxiat ed babies
281
● Associat ed sepsis and meningit is
● I nt ravent ricular hemorrhage
● Mat ernal sedat ives
Signs and sympt oms of hypot hermia
Acrocyanosis
Cool ext remit ies
Decreased peripheral
perfusion
Let hargy
Poor feeding
Shock
Weight loss
Poor weight gain
Tachypnea
Respirat ory Dist ress
Bradycardia
Apnea
Abdominal dist ension
I ncreased gast ric
residuals
Pulmonary
hemorrhage
Definition
Normal axillary temperature
Cold Stress
Moderate Hypothermia
Severe Hypothermia
Temperature
36.5°c – 37.5°c
36°c – 36.4°c
32°c – 35.9°c
<32°c
Implication
Concern
Danger
Grave
Very grave
Action
Warm the baby
Urgent skilled care
Referral
Referral
Treatment Of Hypothermia
Hypot hermic newborns should be re-warmed
quickly. The room t emperat ure should be at least 25°C
(77°F). Cold clot hes should be removed and replaced
wit h pre-warmed clot hes and a cap. I t is very import ant
t o cont inue feeding t he baby. I f t he infant is t oo weak
t o breast-feed, breast milk can be given by nasogast ric
t ube, spoon or cup.
At t he hospi t al
The met hods t o use include:
● Skin t o skin cont act
● Warm room or bed
● 200 wat t s bulb
● Radiant warmer
● Air heat ed incubat or
Radi ant war mer ( open car e syst em)
Radiant warmers provide an int ense source of
radiat ion energy. Suggest ed abdominal skin t emperat ure
set t ings for infant s nursed under radiant warmer or
servo mode incubat or.
<1kg 36.9°C
1-1.5kg 36.7°C
1.5-2 kg 36.5°C
2.0-2.5kg 36.3°C
>2.5kg 36°C
Car e of ski n pr obes
Apply t he probe over ant erior abdominal wall and
frequent ly inspect t he probe for det achment from skin
surface t o prevent over heat ing of t he baby.
“ I t is import ant t o be aware t hat hypot hermia can
be a sign of infect ion. every hypot hermic newborn
should t herefore be assessed for infect ion”
282
283
Prevention of Hypothermia
Concept of “ war m chai n”
Baby must be kept warm at t he place of birt h (home
or hospit al) and during t ransport at ion for special care
eit her from home t o hospit al or wit hin t he hospit al.
The “ Warm Chain” is a set of t en int erlinked
procedures carried out at birt h and lat er, which will
minimize t he likelihood of hypot hermia in all newborns.
1. Warm delivery room (> 25°C)
2. Warm resuscit at ion
3. I mmediat e drying
4. Skin t o skin cont act bet ween baby and t he
mot her
5. Breast feeding
6. Bat hing and weighing post poned
7. Appropriat e clot hing and bedding
8. Mot her and baby t oget her
9. Warm t ransport at ion
10. Training/ awareness of healt hcare providers
The kangar oo mot her car e ( KMC)
Kangaroo Mot her Care (KMC) is a special way of
caring for low birt h weight babies. I t
● Assist s in maint aining t he t emperat ure of infant
● Facilit at es breast-feeding
● Helps t o increase t he durat ion of breast-feeding
● I mproves mot her infant bonding
El i gi bi l i t y Cr i t er i a
All st able LBW babies are eligible for KMC. However,
sick babies needing special care should be cared under
radiant warmer init ially, KMC should be st art ed aft er t he
baby is hemo-dynamically st able.
Guidelines for pract icing KMC include:
1. Birt h weight > 1800 g; These babies are generally
st able at birt h. Therefore, in most of t hem KMC
can be init iat ed soon aft er birt h.
2. Birt h weight 1200-1799 g; Many babies of t his
group have significant problems in neonat al pe-
riod. I t might t ake a few days before KMC can be
init iat ed. I f such a baby is born in a place where
neonat al care services are inadequat e, he should
be t ransferred t o a proper facilit y immediat ely af-
t er birt h, along wit h t he mot her / family member.
He should be t ransferred t o a referral hospit al
aft er init ial st abilizat ion and appropriat e manage-
ment , One of t he best ways of t ransport ing small
babies is by keeping t hem in cont inuous skin t o
skin cont act wit h t he mot her / family member
during t ransport .
3. Birt h weight < 1200g; Frequent ly, t hese babies
develop serious premat urit y-relat ed morbidit y
oft en st art ing soon aft er birt h. They benefit t he
most from in-ut ero t ransfer t o t he inst it ut ions
wit h neonat al int ensive care facilit ies. I t may t ake
days t o weeks before baby’s condit ion allows ini-
t iat ion of KMC.
Kangar oo posi t i oni ng
● The baby should be placed bet ween t he mot her’s
breast in an upright posit ion.
● The head should be t urned t o one side and in a
slight ly ext ended posit ion. This slight ly ext ended
head posit ion keeps t he airway open and allows
eye t o eye cont act bet ween t he mot her and t he
baby.
● The hips should be flexed and abduct ed in a
“ frog” posit ion; t he arms should also be flexed.
● Baby’s abdomen should be at t he level of t he
mot her’s epigast rium. Mot her’ s breat hing st imu-
lat es t he baby, t hus reducing t he occurrence of
apnea. Support t he baby’s bot t om wit h a sling /
binder.
Kangaroo mot her care
Moni t or i ng
Make sure t hat baby’s neck posit ion is neit her t oo
flexed nor t oo ext ended, airway is clear, breat hing
is regular, color is pink and baby is maint aining
t emperat ure. Mot her should be involved in observing
t he baby during KMC, so t hat she herself can cont inue
monit oring at home.
When shoul d KMC be di scont i nued?
284
When t he mot her and baby are comfort able, KMC is
cont inued for as long as possible, at t he inst it ut ion and
t hen at home. Oft en t his is desirable unt il t he baby’s
gest at ion reaches t erm or t he weight is around 2500g.
She st art s wriggling t o show t hat she is uncomfort able,
pulls her limbs out , cries and fusses every t ime t he
mot her t ries t o put her back skin t o skin. This is t he
t ime t o wean t he baby from KMC.
Bat hi ng t he baby
Bat hing should be avoided immediat ely aft er birt h.
Preferably give bat h t o normal baby on second day in
summer. I n wint er bat hing may be avoided for several
days. I n small and / or LBW baby post pone bat h t ill cord
falls or preferably t ill weight is 2.5kg.
Neonatal Transport
Temper at ur e mai nt enance dur i ng t r anspor t
( Weakest l i nk i n war m chai n)
● I deally t ransport of a newborn should be in an
orderly manner i.e. a neonat e who is found t o be
sick by a healt h worker at home visit should be
referred t o a PHC
● I f t he facilit ies or expert ise at t he PHC not ad-
equat e enough t o manage t his sick neonat e, he
should be referred t o t he FRU and t hereaft er t o
t he Medical College. Sickest of t he neonat es re-
quire referral t o an apex inst it ut ion or a t ert iary
care cent re.
● Prepare well before t ransport : I t is of ut most im-
port ance t hat a neonat e is st abilized before t he
t ransport is begun, as an unst able neonat e is go-
ing t o det eriorat e on t he way and may reach t he
referral facilit y in a moribund st at e defeat ing t he
very purpose.
● The neonat e should be assessed for t emperat ure
maint enance, airway pat ency, breat hing effort s,
st at e of circulat ion, fluid and hydrat ion st at us,
medicat ions t o be administ ered and feeding t hat
is t o be provided.
● I f, on assessment any of t he above paramet ers is
found t o be compromised, remedial act ion should
be immediat ely t aken.
* Communicat e and writ e a not e
* Assess and st abilize
* Correct hypot hermia
* Encourage mot her t o accompany
* Arrange a provider t o accompany
● Ensure warm t ransport
* Skin t o skin care (Kangaroo Mot her care)
* Cover t he baby fully wit h clot hes (or cot t on)
including t he head and t he limbs. Avoid un-
dressing t he infant s for cleaning, weighing or
examinat ions. Carry t he baby close t o chest of
t he mot her I mprovised cont ainers: Thermocol
box wit h pre-warmed lines or plast ic bubble
sheet or silver swaddler may be used during
t ransport .
* Transport incubat or
Pr ovi de ot her car e dur i ng t he t r anspor t
● Ensure warm feet
● Ensure an open airway
● Check breat hing
● Provide feeds
● Record t he vit als including t he t emperat ure be-
fore, during and aft er t he t ransport .
● Take t he baby t o t he nearest referral facilit y, by
t he short est rout e, and by a safe mode.
● During Procedures
* Perform t he procedure under a funct ioning ra-
diant warmer
* Monit or t he t emperat ure frequent ly during t he
procedure
Fluid And Electrolyte Management In
Newborn
Tr eat ment gui del i nes f or f l ui d and el ect r ol yt es
Day 1: > 1500 g
Term babies > 1500 g 60 ml/ kg is given. To meet t he
glucose requirement s of 4-6 mg/ kg/ min, t his is given as
10% Dext rose.
Day 1: < 1500 g
● Because of t he higher insensible wat er loss, ba-
285
bies wit h birt h weight 1000 – 1500 g require 80
ml/ kg of 10%D.
● Ext remely premat ure babies < 1000 g require
100 ml/ kg and t his is given as 5%D t o maint ain
glucose homeost asis.
Aft er Day 1:
Sodium and pot assium should be added only aft er
48 hrs of age each in a dose of 2 – 3 mEq/ kg/ day.
Glucose infusion ideally should be maint ained at 4 – 6
mg/ kg/ min in a volume independent manner if possible.
I n pret erms, sodium is supplement ed at 3 – 5 mEq/
kg/ day t ill 32 – 34 wks post-menst rual age. Calcium may
be used in a dose of 4 – 6 ml/ kg/ day of calcium gluconat e
for t he first 3 days in cert ain high risk sit uat ions such as
premat urit y, infant of diabet ic mot hers, birt h asphyxia
et c.,
Treatment guidelines for fuid and electrolytes
Weight > 1500 g 1000 – 1500 g < 1000 g
D1 60 80 100
D2 75 95 120
D3 90 110 130
D4 105 120 140
D5 120 130 150
D6 135 140 160
D7 and > 150 150 170
I ncr ement s 15-20 10-15 10-20
Max 150 150-170 160-180
Moni t or i ng of f l ui d and el ect r ol yt e st at us
Body wei ght
● At least once a day
● Term neonat es lose 1 – 2% of t heir body weight
daily in t he 1st week wit h a cumulat ive loss of
5 – 10%
● Pre-t erms lose 2 – 3% daily in 1st week wit h a
cumulat ive loss of 15 – 20%
● Weight gain should have commenced by 7 – 10
days in a t erm neonat e and by 10 – 15 days in
pre-t erms
I / O char t i ng
I nput out put chart ing has t o be done met iculously
including boluses, NG aspirat es, CSF by lumbar
punct ure, diarrheal loss, fluids used for inj ect ion and
flushing. These will be of import ance especially in VLBW
neonat es.
Cl i ni cal assessment
The usual physical signs of dehydrat ion are unreliable
in neonat es.
● A 10% dehydrat ion (100 ml/ kg) present s as
● Sunken eyes
● Depressed font anelle
● Cold and clammy skin
● Poor skin t urgor and
● Oliguria
● Wit h 15% dehydrat ion (150 ml/ kg
● Shock ensues. As t he normal range of blood pres-
sure is wide, and blood pressure correlat es poor-
ly wit h volume st at us, t hey are not t o be relied
upon for assessing hypo-volemia
● Rat her, import ance is given t o capillary refill t ime
and core – peripheral t emperat ure
● For hyper-volemia, look for weight gain, oedema,
feat ures of CCF and pulmonary oedema.
Pr i nci pl es of Def i ci t cor r ect i on
● Wat er deficit
* Half of it is replaced over t he first 8 hours and
t he ot her half over t he next 16 hours.
● Sodium deficit
* Replaced over 24 hours
● Pot assium deficit
* I f large, replaced over 48 – 72 hours
● Maint ain urine out put 1-3 ml/ kg/ hour
Surgical Problems In Neonates
Tr acheo-esophageal f i st ul a ( TEF)
Point s t o remember
1. TEF should be suspect ed in a neonat e who soon
aft er birt h present s wit h excess salivat ion, respi-
rat ory dist ress, and in whom t here is difficult y in
passing a naso-gast ric t ube.
2. I n suspect ed cases of TEF, even if t he naso-gas-
t ric t ube passes smoot hly, it may be due t o t he
fact t hat t he t ube get s coiled in t he upper blind
pouch. Therefore always confirm t hat t he lower
end of t he t ube is in t he st omach by x-ray in sus-
pect ed cases.
3. Prognosis depends on early diagnosis and pre-
vent ion of aspirat ion of gast ric cont ent s, or milk
int o lungs.
286
4. Look for associat ed cardiac, renal, vert ebral, low-
er GI -anomalies prior t o surgical correct ion.
Cl i ni cal f eat ur es
1. Ant enat al : H/ o polyhydramnios
2. Babies are commonly pre-t erm or small for ges-
t at ional age (SGA).
3. Excessive oral and pharyngeal secret ions wit h
frot hing at mout h.
4. Choking, coughing and cyanosis on feeding.
5. Failure t o pass naso-gast ric t ube, resist ance is
encount ered 8 - 10 cm from t he upper gum line.
6. Sympt oms and signs of pneumonia and sepsis
due t o aspirat ion of gast ric cont ent s wit h super-
added infect ion may be present in cases t hat are
diagnosed lat e.
I nvesti gati ons
● Plain X-ray of neck and chest wit h naso-gast ric
t ube in posit ion
* Upper blind eso-phageal pouch is dilat ed wit h
air and coiled up t ube is seen.
Treatment
1. Nurse t he baby in an upright posit ion of 45o and
carry out frequent suct ion t o prevent aspirat ion.
2. Nil by mout h. st art I V fluids.
3. Ant ibiot ics if pneumonit is or sepsis.
4. Support ive t reat ment
5. Referral t o higher cent re
Congenital Diaphragmatic Hernia
Abnormal presence of abdominal viscera in t he
t horacic cavit y above t he diaphragm.
Si gns and sympt oms
1. Moderat e t o severe respirat ory dist ress wit h or
wit hout cyanosis may be present right from birt h
or lat er
2. Scaphoid abdomen
3. Heart sounds bet t er heard on side opposit e t o
t he hernia
4. Tympanic not e on percussion of chest , and bowel
sounds heard in chest
I nvesti gati ons
1. Ant enat al diagnosis by ult rasound.
2. Post nat al diagnosis by X-ray.
* Mediast inal shift .
* No diaphragm visualized
* Bowel loops in chest .
Treatment
1. Ant icipat e t he problem if diagnosed ant e-nat ally.
Do not vent ilat e wit h bag and mask. Use en-
dot racheal t ube for vent ilat ion.
2. Head high posit ion.
3. Pass naso-gast ric t ube and cont inuous aspirat ion.
4. Correct ion of fluid and elect rolyt e imbalance and
met abolic acidosis.
5. Referral t o higher cent re.
Intestinal Obstruction
1. I nt est inal obst ruct ion should be suspect ed if
t here is mat ernal H/ o polyhydramnios.
2. Abdominal dist ension and failure t o pass meco-
nium are considered cardinal signs of t his condi-
t ion.
I nvesti gati ons
● Abdomen X-ray erect
* Level of obst ruct ion may be det ermined by
configurat ion of fluid levels on X-ray.
Cl i ni cal f eat ur es
● Vomit ing: Non-bilious or bilious
● Abdominal dist ension
● Upper abdominal
* Duodenal at resia
* Annular pancreas
● Generalized dist ension
* Obst ruct ion at t he level of j ej unum and lower
ileum.
● Failure t o pass meconium
* I mperforat e anus
Treatment
1. Nil orally
287
2. Deflat ion and aspirat ion of st omach wit h naso-
gast ric t ube.
3. Fluid and elect rolyt e correct ion and monit oring.
4. Referral t o higher cent re.
5. Thermoregulat ion is ext remely import ant during
t ransport and in t he operat ion t heat re.
Recognition of a critically ill child
Appear ence of t he chi l d
AVPU scale
● Alert
● Voice: Responsive t o voice
● Painful: Responsive t o painful st imuli
● Unresponsive
Ot her feat ures in appearance (Refer t o algorit hm)
Ai r way
Asses airway as clear, maint ainable by posit ioning,
or not maint ainable if it needs advanced int ervent ion
Br eat hi ng
Look for breat hing movement s; cat egorize as
normal, increased or decreased or absent .
Assessment of breathing
Respirat ory rat e: Rapid respirat ory rat e (t achypnea)
by age
● Age < 2 mont hs 60/ mt or more
● 2 mont hs < 12 mont hs 50/ mt or more
● 12 mont hs < 5 years 40/ mt or more
● Work of breat hing
* Look for nasal flaring, grunt ing
* I nt ercost al, subcost al and suprast ernal ret rac-
t ions
* Presence of t hese indicat es increased work of
breat hing
* I ncreased work of breat hing (I WB), head bob-
bing and see saw respirat ions are lat e signs.
● Air ent ry and breat h sounds
* Look for unequal air ent ry, st ridor, wheeze and
silent chest
* Based on t he above, classify t he child as nor-
mal, in respirat ory dist ress or respirat ory fail-
ure
● Check oxygen sat urat ion if available.
● Tidal volume
* Clinically assessed by chest expansion and
auscult at ion for dist al air movement s simul-
t aneously
Ci r cul at i on
Heart rate in children
* Newborn 80 - 200 / mt
* 1-8yrs 80 - 180 / mt
* > 8 yrs 60 - 160 / mt
● Pulses
* Comparison of cent ral and peripheral pulses
t o be done
* Bot h should be of equal volume
* I n early shock peripheral pulse volume is de-
creased.
● Skin Perfusion
* Skin Temperat ure
* Color and Capillary refill t ime (CRT) are al-
t ered in shock.
● Blood pressure
* Use t he following syst olic blood pressure as
cut off for defining hypot ension
Blood pressure (Hypo-tension)
● New born < 60 mm Hg
● Up t o 1 year < 70 mm Hg
● 2 years and above < 70 + (2 x age in
years) mm Hg
● Aft er 10 years < 90 mm Hg
* Based on above circulat ory assessment clas-
sify as normal, compensat ed shock or hypo-
t ensive shock.
● Based on t he appearance, breat hing and circu-
lat ory st at us, physiologic st at us of a crit ically ill
child is charact erized as:
1. St able
2. Respirat ory dist ress charact erized by I WB and
increased respirat ory rat e
3. Respirat ory failure charact erized by cyanosis,
alt ered sensorium, poor muscle t one and poor
respirat ory effort s.
4. Compensat ed shock –Shock wit h normal BP
288
5. Hypot ensive shock
6. Cardiorespirat ory failure – Shock + Respira-
t ory failure
Not e: ( 3 - 6 need ur gent r ef er r al af t er
st abi l i zi ng.)
I ni t i al r esusci t at i on and st abi l i zat i on
When a child is assessed t o be crit ically ill, init ial
management comprises of t aking care of airway,
breat hing and circulat ion.
a. Airway: is kept pat ent – if necessary by posit ion-
ing, suct ioning and or int ubat ion.
b. Breat hing: I n respirat ory dist ress only supple-
ment at ion wit h O2 in a non-t hreat ening manner
is sufficient in respirat ory failure; vent ilat ory sup-
port is oft en needed
c. Circulat ion: Vascular access and volume expan-
sion wit h isot onic fluids such as RL or NS.(20ml /
kg) I f unable t o get a venous access or in hypo-
t ensive shock immediat e int ra-osseous access
should be obt ained
d. I f child present s wit h seizures, t ake care of air-
way and breat hing and cont rol seizures wit h in-
t ravenous Diazepam or Lorazepam. I f no int rave-
nous access, int ramuscular Midazolam 0.15 mg/
kg is relat ively safe, effect ive and fast .
289
Treatment Of Acute Respiratory Distress And Respiratory Failure Beyond Newborn Period
Di agnosi s Tr eat ment
Respirat ory dist ress
1. Tachypnea
2. I ncreased work of breat hing.
3. Presence of st ridor, wheeze, grunt ,
ret ract ions
4. Colour
● Keep t he child in posit ion of comfort (infant
in mot her’s lap)
● Oxygen in a non-t hreat ening manner ( by
simple mask 5 l/ min or by hood 10-12 l/ min
or non-rebreat hing mask.10-12 l/ min
● Monit or Spo2
● Cardiopulmonary assesment
● Ant icipat e worsening and be prepared for
vent ilat ory support
● Specific management for underlying illness
Respirat ory failure (RF)
I n addit ion t o feat ures of respirat ory dist ress
child will have
● Rest lessness, anxiet y
● Alt ered level of consciousness: drowsiness,
let hargy, unresponsiveness
● Signs of exhaust ion, sweat ing, head bobbing
● Loss of t one and post ure
● Cyanosis is a lat e finding
● Bradypnea, shallow breat hing
● Heart rat e and perfusion will be abnormal
● SpO2 < 92% (pulse oximet ry)
(RF can occur wit hout respirat ory dist ress in
CNS depression, muscular weakness and very ill
children)
Diagnosis of RF and decision t o int ubat e and
vent ilat e should be made on clinical signs
● Airway posit ioning, suct ioning
● Bag – mask vent ilat ion wit h 100% O2 using
a reservoir
● Prepare t o int ubat e and vent ilat e
● I f t here is no improvement or det eriora-
t ion occurs aft er int ubat ion and vent ilat ion
consider ‘DOPE’
* Displaced t ube
* Obst ruct ed t ube
* Pneumot horax
* Equipment failure
● Assess circulat ion – RL / NS boluses if shock
present
● Ongoing Cardiopulmonary assesment and
monit oring is import ant
● Never leave t he child unat t ended during
t ransport , t ill t he child recovers.
This is only t he general guidelines for respirat ory dist ress and respirat ory failure. Specific management of illnesses
is described separat ely under specific diseases.
290
Treatment Of Shock In Children
Shock can be
1. Hypovolemic shock
2. Sept ic shock
3. Cardiogenic shock
Feat ures of shock: Tachypnea, t achycardia, normal
or low BP, weak or absent peripheral pulses/ cent ral
pulses, delayed capillary fill, cool peripheries, oliguria,
change in ment al st at us.
Gener al pr i nci pl es
1. Resuscit at ion
2. Treat t he underlying condit ion
3. Treat t he associat ed met abolic dist urbances
4. Support ive t herapy t o prevent or t reat mult i-or-
gan dysfunct ion syndrome
Resuscit at ion: Maint ain airway and breat hing.
Administ er oxygen by a non-rebreat hing mask 10-15 L/
min in spont aneously breat hing children.
Vascular access
● Large bore I V cat het er
● I nt ra-osseous (I O): When I V access not obt ained
or child is in hypot ensive shock, immediat e I O ac-
cess; proximal t ibia preferred sit e in infant s and
small children
Fluid t herapy
● I nit ial fluid bolus for shock
* RL or NS 20ml/ kg rapidly in hypo-volemic
shock. Repeat boluses 2-3 t imes aft er reas-
sessment of cardiopulmonary st at us at t he
end of each bolus
● Cardiogenic shock due t o sepsis
* 100- 240ml / kg in aliqout s of 20 ml / kg at 20
minut es per hour may be needed in t he init ial
6 hours of rescuscit at ion
● 2 or 3 fluid boluses will be required in hypovo-
lemic or sept ic shock
● I n case of blood loss, at t empt replacement wit h
blood aft er 2 boluses of fluids
● Reassess cardio-pulmonary st at us following each
bolus: by pulse volume, heart rat e, skin per-
fusion, urine out put , sensorium, blood pressure,
liver size and lung signs.
● Wit hhold furt her boluses if cardiogenic shock oc-
curs (airway inst abilit y, pink frot h, apnea, devel-
opment of grunt , ret ract ions, abdominal respira-
t ions, fresh rales, gallop rhyt hm, enlargement of
liver).
● Child wit h shock refract ory t o fluid boluses needs
t o be shift ed t o a t ert iary care facilit y urgent ly as
t he delayed referral will increase t he mort alit y in
shock.
I not r opes may be needed i n car di ogeni c and
sept i c shock
Dopami ne
● St art at 10 mcg/ kg/ min; t it rat e dose by incre-
ment of 2-3 mcg/ kg/ min every 15 minut es upt o
20 mcg/ kg/ min
● Weight × 6 = mg of dopamine t o be added t o
100 ml of NS; 1ml/ hr will deliver 1mcg/ kg/ mt ; I n-
dicat ed in hypot ensive shock aft er fluid boluses.
Dobut ami ne
● I ndicat ed in cardiogenic shock wit h normal or in-
creased blood pressure
● I not rope of choice, dose: 10-20 mcg/ kg/ min
preparat ion similar t o dopamine.
Epi nephr i ne
● I n case of low blood pressure
Treat underlying condit ion and correct any met abolic
imbalance, document ed hypo-glycemia, hypo-kalemia
and met abolic acidosis.
Caut ion in replacing Sodium bicarbonat e and
pot assium replacement in hypoxia on shocked child
Anaphyl act i c shock
● Epinephrine 0.1 ml/ kg 1: 10000 deep I M, 0.1ml/
kg 1: 1000 I V,
● Oxygen. Early int ubat ion t o secure airway, rapid
volume expansion wit h NS or RL ; repeat ed bo-
luses t o rest ore perfusion.
● St eroids, ant ihist amines
Airway: To be maint ained; Oropharyngeal suct ion;
Nasogast ric decompression
Breat hing: Spont aneous breat hing: oxygen t hrough
NRM 10-15 lit res/ min
Apneic: BMV wit h 100% O2 10 lit res/ min
If not improved, consider intubation
Circulat ion: I V access and correct shock; 25%
Dext rose 2ml/ kg if
hypoglycemic
291
When to refer:
Seizures refractory after phenobarbitone
Persistent altered level of consciousness
Treatment of status epilepticus
0 Min: Inj. Lorazepam 0.05-0.1 mg/kg; IV; max.4mg/dose: at 2mg/min
(or)
Inj.Diazepam 0.2mg/kg; IV; max.10mg/dose
(or)
Inj. Midazolam 0.2mg/kg; IM (If IV access immediately not available)
10 Min: Inj. Lorazepam/ Diazepam - Same dosage (Second dose)
Plan Shift to ICU; Start Midazolam infusion at 1µg /kg/min
Increase every 15 min upto 20µg/kg/min
60 Min: Plan intubation with Midazolam 0.2 mg/kg bolus
IV Phenobarbitone 20mg/kg at 2mg/kg/min
IV Sodium valproate 15 –20mg/kg loading dose over 1-5 min
If seizures stop at any stage, continue to evaluate the cause for
seizures and complications.
20 Min: Inj.Phenytoin 20mg/kg IV Loading dose; max.50mg/min at 1mg/kg/min
Mix with NS as phenytoin is incompatible with glucose containing solutions
Monitor HR, perfusion and blood pressure.
If t continues additional 5mg/kg up to a max of 30mg/kg
STATUS - EPILEPTICUS
Seizures > 5 min or sudden unconsciousness
Not regained consciousness in between two episodes
292
● Smear for MP
● Blood glucose for hypoglycemia and hyperglyc-
emia,
● Serum elect rolyt es for hyponat remia, hyper-
nat remia and ot her imbalances,
● Blood Urea and serum creat inine, calcium
● SGOT, SGPT, CSF analysis if no cont raindicat ions.
Ot her invest igat ions as necessary
PT, PTT, X-ray bones, Cult ures, MSAT, Widal, Viral
st udies, CT scan, EEG, Gast ric aspirat e analysis in
poisoning.
Treatment

● ABC as ment ioned earlier
● Posit ion t he child in semi-recumbent post ure
● Specific management depending on underlying
condit ion
● Ot her support ive measures
* Ant i-convulsant s as per management of St a-
t us epilept icus
* Ant i-edema measures in cases wit h raised
I CP Keep t he head elevat ed 15- 30 degrees;
Cont rol fever and seizures; 20% mannit ol 1.5
ml/ kg eight hourly if not in shock
* Vent ilat ory support
* Blood component s t herapy if indicat ed
* Elect rolyt e/ Glucose correct ion
* Neurosurgical int ervent ion.
● Support ive care
* Eye care, skin care, bladder care.
● Monit or urine out put , elect rolyt es, renal param-
et ers, blood glucose.
● Nut rit ional support
* I VF as Dext rose wit h ½ NS at t he following
rat e
* Up t o 10 Kg 4 ml/ kg/ hour
* 10 –20 Kg 40 ml + 2ml/ kg.hour for every
kg above 10
* > 20 Kg 60ml + 1ml/ kg/ hour for every
kg above 20
● St art oral feeds as early as possible.
I ndicat ions for referral
1. Worsening sensorium
Treatment Of A Child With Altered Level Of
Consciousness (ALOC)
How t o r ecogni ze ALOC?
An older child not responding t o simple commands
and simple quest ions appropriat ely. I n an infant > 8
weeks, absence of eye cont act and unresponsiveness t o
mot her’s call. I rrit ablit y, rest lessness, refusal of feeds,
excessive sleepiness, inconsolable cry, failing t o cry even
wit h painful st imuli such as inj ect ions are indicat ive of
ALOC. Rapid assessment can be done by AVPU scale
Hi st or y
Try t o find out if t he problem is acut e, chronic or
acut e on chronic illness. Acut e sympt oms: Fever,
headache, vomit ing, ALOC, drug ingest ion, inj ury,
predisposing illness. Underlying Chronic illness such
as CHD, CRF, seizure disorder, development al delay,
bleeding disorder. Hist ory should point t owards t he
gross cat egories as follows: -
● I nfect ion, Raised I CP, t rauma, bleeds, syst emic
illness.
● Hist ory not correlat ing t o t he present at ion/ vac-
uum in t he hist ory should alert about poisoning,
animal bit es and met abolic encephalopat hies.
Cl i ni cal f eat ur es
Tachypnea, shock
Hy p e r t e n s i o n ,
oedema
Mast oid swelling,
ear discharge.
Pallor, j aundice,
bleed
Bit e marks, fang-
marks, cellulit is
Arryt hmia, murmur
Hemat oma of scalp
N e u r o c u t a n e -
ous markers
Bulging AF
Hepat osplenomegaly
● Raised int ra-cranial pressure is suspect ed wit h
neurogenic hypervent ilat ion, neurogenic st ridor,
unequal pupils, dilat ed non-react ive pupil, ab-
normal post ure, presence of Cushing’s t riad wit h
bradycardia, hypert ension and abnormal breat h-
ing pat t ern may be seen in advanced cases.
● Fundus examinat ion and Glasgow Coma Scale
(GCS)
I nvesti gati ons
● Complet e blood count
293
2. Suspect ed increased int ra-cranial pressure
3. Suspect ed int racranial focal pat hology
RR, Stridor, work of breathing
Air entry
Colour normal or abnormal
HR, core peripheral temperature gap
Temperature
Compare central and peripheral pulses
AVPU=Alert voice, pain unresponsive
294
Algorithm For Acute Loss of Consciousness
Note
ALOC: Acute loss of consciousness
ICP: Intracranial pressure
HSV: Herpes simplex virus
295
Febrile Seizures
● Common bet ween 6 mont hs and 5 years of age
● Family hist ory of febrile convulsion may be
present
● Occurs frequent ly when t he core t emperat ure is
more t han 39oC (102oF)
● Convulsions t ypically of generalized t onic, clonic
t ype
● Durat ion of seizures from few seconds t o 10 min-
ut es
● Causes of febrile seizures are commonly
* Respirat ory infect ion
* Ear infect ion
* Acut e dysent ery
● Nearly 50% of children have recurrent febrile sei-
zures
● No evidence of underlying meningeal disease
● Febrile seizures occurring less t han one year of
age for t he first t ime have more recurrences.
Treatment
Prevent ion of furt her febrile seizures is mainly
by early and effect ive t reat ment of fever. Only few
children require long-t erm ant i-convulsant s t o prevent
recurrence.
● Tepid sponging
● Reassurance t o t he parent s
● Ant ipyret ics – Paracet amol 10-15 mg/ kg/ dose
● Sympt omat ic t reat ment
● Ant iconvulsant not required rout inely
● I nt ermit t ent diazepam 0.3 mg/ kg/ dose t wice
daily st art ing on t he day of fever for 2 t o 3 days
(low dose clobazam is t he ot her opt ion).
I ndi cat i ons f or ant i convul sant pr ophyl axi s
● At ypical febrile seizures
* Age below 6 mont hs or above 5 years
* Focal seizures and
* Prolonged seizures – more t han 15 minut es
● Post-ict al palsy
● I nt er-ict al EEG abnormalit y
● Family hist ory of febrile / afebrile seizures
● Recurrent febrile seizures
* Long-t erm Sodium valproat e or phenobarbi-
t one may be used
* I nt ermit t ent diazepam or Clobazam at t he on-
set of fever is t he ot her opt ion
Treatment of Acute Respiratory Infection
Acut e phar yngot onsi l l i t i s
● Fever, sore t hroat , foul breat h, difficult y in swal-
lowing, voice change, referred ot algia and cough
are t he clinical feat ures
● Nasal sympt oms may be seen (nasopharyngit is)
● Aet iology can be bact erial
* Group A β-hemolytic streptococcus – GABHS
or
* Viral: Rhinovirus
● Clinical different iat ion bet ween bact erial (st rep-
t ococcal) and viral aet iology is not foolproof, but
t he following feat ures help
Nasal discharge, conj unct ival involvement or
cough besides t hroat involvement are more common
wit h viral infect ion; severe pharyngeal congest ion
wit h yellow, t hick exudat es, t ender ant erior cervical
lymphadenopat hy, t oxicit y and absent coryza or cough
point t owards st rept ococcal t onsillit is.
Treatment
● Support ive care: I ncreased fluid int ake, paracet a-
mol
● Ant ibiot ics in suspect ed st rept ococcal t onsil-
lit is t o reduce morbidit y and prevent long-t erm
complicat ions such as rheumat ic fever:
* Oral Penicilin V
» 250 mg bid X 10 days for children < 30 kg
» 500 mg bid X 10 days for children > 30 kg
* Oral Amoxycillin
» 40 mg/ kg/ day in 3 doses X 10 days for chil-
dren < 30 kg
» 250 mg t id X 10 days for children > 30 kg
* I nj . Benzat hine Penicillin 12 lac unit s deep I M
once (6 lac unit s for children < 30 kg)
● I f allergic t o Penicillin
* Oral eryt hromycin 40 mg/ kg/ day in 3 doses
for 10 days
296
Pneumonia
● ARI (Pneumonia) is responsible for 20% of Under
5 mort alit y.
● Aet iology varies wit h age
* Upt o 3 mont hs of age
» Gram negat ive bact eria and Group B st rep-
t ococcus
* 3 mont hs – 5 years
» St rept ococcus pneumoniae
» H.influenzae, viruses
» St aph. aureus
* > 5 years of age
» S pneumoniae
» Mycoplasma pneumoniae
» viruses
Cl i ni cal f eat ur es
● Fever
● Fast breat hing (RR: Up t o 2 mont hs of age: 60/
minut es or more; 2 mont hs - up t o 12 mont hs: 50
or more; 12 mont hs – up t o 5 years: 40 or more)
count RR for full 1 minut e when child is not crying
● I ncreased work of breat hing – I WB (Nasal flaring,
chest indrawing and grunt )
● Crackles/ bronchial breat hing on auscult at ion is
heared if pneumonia is confined t o a lobe
Treatment
● Chest X-ray need not be done rout inely if no
complicat ion (pleural effusion, non improvement )
suspect ed
● Children up t o t hree mont hs of age and children
wit h severe pneumonia (I WB, not feeding, cya-
nosis, int ermit t ent apnea, signs of dehydrat ion)
are t reat ed as in-pat ient s wit h parent eral ant ibi-
ot ics.
● They may also require close monit oring (clinical
and pulse oximet ry), I V fluids, oxygen and some-
t imes vent ilat ory support
● All pneumonias are t reat ed as ‘bact erial’ wit h an-
t ibiot ics
For non-sever e pneumoni a ( domi ci l i ar y or al
t r eat ment and f ol l ow up)
● 3 mont hs – 5 years
* Amoxycillin 40 mg/ kg/ day in 3 doses X 7-10
days or
* Chloramphenicol 50-100 mg/ kg/ day in 4
doses X 7-10 days
● 5 years plus
* Amoxycillin (First line)
* Eryt homycin or chloramphenicol or coamoxi
– clav (second line)
For sever e pneumoni a and chi l dr en upt o
3 mont hs of age ( Hospi t al i zat i on and I V
ant i bi ot i cs)
● Upt o 3 mont hs (for 7 - 10 days)
* I nj cefot axime 100 mg/ kg/ day in 3 or 4 di-
vided doses
+
* I nj Garamycin 5-7.5 mg/ kg/ day 2 divided
doses or
* I nj Amikacin 15 mg/ kg/ day 2 divided doses
● 3 mont hs – 5 years:
● First line for 7 t o 10 days
* I nj Ampicillin I V 100 mg/ kg/ day in 4 divided
doses or
* I nj Chloramphenicol 50-100 mg/ kg in 4 di-
vided doses
● Second line
* I nj Cefot axime 150-200 mg/ kg/ day
I n al l age gr oups
● I f st aph. pneumonia is suspect ed t reat for 14
days:
* I nj cefot axime / ceft riaxone
+
* I nj cloxacillin 100-200 mg/ kg/ day in 4 di-
vded-doses (wit h support ive measures, I V
fluids and oxygen administ rat ion)
When t o r ef er
● Respirat ory dist ress not improving
● Respirat ory failure as indicat ed by increasing fa-
t igue, cyanosis or alt ered sensorium
297
Bronchiolitis
● Viral in aet iology (Respirat ory syncit ial virus)
● Most frequent ly in children < 12 mont hs of age
● I nit ial URI sympt oms followed by
* I ncreasing cough
* Respirat ory dist ress
* Wheeze and
* Feeding difficult y
I nvesti gati ons
● CXR: Hyperinflat ed lungs wit h pat chy infilt rat es
Treatment
● Support ive measures such as oxygen by hood
(10 lit res / mt ) or by mask (5 lit s / mt ); I V fluids
if child is not able t o feed orally.
● Monit oring (RR, Respirat ory dist ress, pulse oxi-
met ry)
● A t rial dose of Nebulised salbut amol / epinephrine
if wheezing is marked
● As child improves wean off oxygen and increase
oral feeds.
● I f child develops severe respirat ory dist ress, in-
creasing hypo-xemia, cyanosis or fat igue – vent i-
lat ory support may be required.
Guidelines For Diagnosis And Treatment Of
Empyema
● Charact erised by presence of pus or microorgan-
isms in t he pleural fluid
● Occurs as a complicat ion of pneumonia
● St aph aureus, St rept ococcus pneumoniae, He-
mophilus influenzae and St rept ococcus pyogenes
are t he common organisms
● Common sympt oms are
* Fever
* Chills
* Toxemia
* Respirat ory dist ress
* Grunt and
* Chest pain (pleurit ic pain)
On exami nat i on
● Decreased chest expansion
● Diminished breat h sounds and
● Dullness on percussion on affect ed side and
● Mediast inal shift t o opposit e side
I nvesti gati ons
● CXR: oblit erat ion of cost ophrenic angle; diffuse
homogenous opacit y
● USG chest : size, sit e of effusion, adhesions or
loculat ions can be made out
● Diagnost ic t horacocent esis usually in fift h int er-
cost al space over mid-axillary line using a large
bore needle
● Pleural fluid for Gram st ain, cult ure and sensit ivit y
● Pleural fluid pH and sugar are reduced and pro-
t ein is elevat ed.
Treatment
● Treat ment comprises of chest drain and ant ibiot-
ics
Chest dr ai nage
● Using an int ercost al drainage t ube insert ed in t he
region of maximal dullness (usually V or VI int er-
cost al space in axillary region) and connect ing t o
a st erile under wat er drainage bot t le
● Chest drainage is kept t ill t he drainage decreases
t o < 25 ml/ day and t here is good lung expansion.
● I f t here is no chest expansion by clinical or radio-
logical met hods, surgical opinion is sought
Ant i bi ot i cs
● Cloxacillin wit h cefot axime or ceft rioxone is t he
first line ant ibiot ic; swit ch over t o oral ant ibiot ics
aft er child becomes afebrile and chest t ube is re-
moved. Tot al durat ion of 4-6 weeks of ant ibiot ic
t herapy.
● Cloxacillin: 100-200 mg/ kg/ day in 4 div. doses
● Cefot axime: 150-200 mg/ kg/ day in 3 or 4 div.
doses
● Support ive care: oxygen, good nut rit ion
298
299
Approach to Fever
Hi st or y
● Type of fever
● Associat ed sympt oms – chills / rigor, cough, sore
t hroat , ear pain, urinary sympt oms, bleeds et c
● Previous illness and t reat ment if any
● Feeding difficult y, respirat ory dist ress
Clinical examinat ion
Check Temperat ure. Blood pressure, Pulse, Per-
fusion
Skin: Rashes, Bleed, Cyanosis
Eyes: Pallor, I ct erus
Mout h: Ulcer, Thrush
Ear: Discharge, Redness, Tenderness
Throat : Congest ion, Tonsillit is
CNS: Meningeal irrit at ion, Alt ered sensorium
Abd: Hepat omegaly, Splenomegaly
RS: Tachypnea, Ret ract ion, Creps, Wheeze
Basi c i nvest i gat i ons i n hi gh r i sk gr oup and f ever
beyond 5 days i n l ow r i sk:
● Tot al count , different ial count , peripheral smear,
● Plat elet count
● Urine analysis, urine c/ s
● Blood cult ure and sensit ivit y
● Chest x-ray
● C-react ive prot ein
● Mant oux t est
● CSF analysis if required
Ot her i nvest i gat i ons
● Liver funct ion t est
● Renal funct ion t est
● USG abdomen
● Blood for lept ospirosis
● Serology for dengue
● Widal
● Bone marrow
Not i f i cat i on
Remember t o I nform t he healt h aut horit ies in No-
t ifiable diseases.
Ref er r al
● Fever wit h unconsciousness
● Fever wit h shock
● severe respirat ory diseases
● Bleeding diat hesis
● Refract ory seizures
Treatment Of Malaria In Children
Approximat ely 2.48 million malaria cases are
report ed annually from Sout h Asia of which 75% cases
are cont ribut ed by I ndia alone. Plasmodium falciparum
resist ance t o st andard ant imalarial drugs part icularly
chloroquine is on t he rise.
Cl i ni cal f eat ur es
● Fever: Though t he classical int ermit t ent fever is
described in Malaria, any t ype of fever can occur.
● Chills, rigors and sweat ing are t he ot her charac-
t erist ic feat ures.
● Pallor and splenomegaly are oft en seen in Malaria
● High grade fever, j aundice, alt ered sensori-
um and shock can occur in falciparum malaria
(complicat ed malaria)

I nvesti gati ons
● Microscopy
* Light microscopy of well-st ained t hick and
t hin films. Blood sample collect ion for smear
should be done before st art ing ant imalarials
and smears should be prepared soon aft er
blood collect ion.
● Rapid diagnost ic t est s
* These are immunochromat ographic t est s t o
det ect plasmodium ant igens in blood
● Hist idine rich prot ein (HRP-I I ) t est
* To det ect P.falciparum (bot h asexual st ages
and young gamet ocyt es)
● Parasit e lact at e dehydrogenase (LDH) t est
* To det ect falciparum and vivax malaria.
Treatment
● Chloroquine 10 mg base/ kg st at followed by 5
mg/ kg at 6, 24 and 48 hours.
or
300
● Chloroquine 10 mg base / kg st at followed by 10
mg / kg at 24 hours and 5 mg / kg at 48 hours
( Tot al dose 25 mg / kg).
● I n case of vivax malaria t o prevent relapse, Pri-
maquine 0.25 mg / kg / dose for 5 days
* Age group 12 mont hs – 5 years
* 1 t ablet Primaquine t ablet cont aining 2.5 mg
base once daily for 5 days
● Primaquine should not be given t o children up t o
1 year of age and during pregnancy.
Ant i mal ar i al t her apy of sever e and compl i cat ed
mal ar i a ( due t o P. f al ci par um)
I V Quinine or parent eral Art emisinin
Qui ni ne:
● 20 mg salt / kg (loading dose) dilut ed in 10 ml /
kg of isot onic fluid by infusion over 4 hours.
● Aft er 12 hours of st art ing t he loading dose, give
maint enance dose of 10 mg / kg over 2 hours.
● This maint enance dose is t o be repeat ed every 8
hours unt il t he pat ient can swallow, t hen quinine
t ablet s 10 mg / kg 8 hourly t o complet e a 7 day
course.
or
Ar t esunat e
● 2.4 mg / kg / I V loading dose followed by 1.2 mg
/ kg at 12 and 24 hours, t hen 1.2 mg / kg daily
for 6 days.
● I f pat ient is able t o swallow, t hen t he daily dose
can be given orally.
or
Ar t emet her
● Art emet her 3.2 mg / kg I M loading dose followed
by 1.6 mg / kg daily for 6 days.
● I f t he pat ient is able t o swallow, t hen t he daily
dose can be given orally.
● At t he end of t herapy a single dose of Sulfadox-
ime – Pyrimet hamine (calculat ed as 25 mg / kg
of sulfadoxime) or Mefloquine 25 mg / kg (in 2
doses of 15 mg / kg and 10 mg / kg 4-6 hours
apart ) is t o be given.
● A single dose of Primaquine (0.75 mg / kg) is t o
be given for gamet ocyt ocidal act ion.
Suppor t i ve management i n compl i cat ed mal ar i a
● Cont inuous clinical monit oring
● Care of Airway, Breat hing and Circulat ion ( A B
C )
● Blood Sugar values.
● Promt t reat ment of seizures
Dengue Infection
Dengue infect ion is caused by one of t he four
serot ypes of Dengue virus (Dengue 1 t o Dengue 4)
t ransmit t ed by t he mosquit o vect or, Aedes aegypt i.
WHO est imat es t hat 20 million dengue cases occur
every year worldwide of which, about 5 lakh cases are
t hose of Dengue Hemorrhagic fever wit h case fat alit y
rat e of 1-5%. Dengue infect ion causes t wo import ant
clinical syndromes:
● Dengue fever
● Dengue hemorrhagic fever (DHF) including Den-
gue Shock Syndrome (DSS).
Dengue f ever
I t is a benign, non-fat al febrile illness indist inguishable
from ot her common febrile illnesses.
● Acut e fever – biphasic (init ial fever of 1-7 days,
t hen afebrile for 1-2 days followed by fever
again).
● Headache, myalgia, art hralgia
● Rash (Macular, generalized rash seen in t he first
48 hours of fever)
● Lymphadenopat hy
● Leukopenia
● A second rash may appear wit hin 1-2 days of de-
fervescence.
DHF / DSS
● Fever of 2-7 days durat ion.
● This is followed by rapid det eriorat ion in t he
form of rest lessness, irrit abilit y, abdominal pain,
vomit ing, liver enlargement .
301
WHO criteria for DHF
● Fever of 2-7 days
● Thrombocyt openia (plat elet count of
< 1,00,000/ cmm)
● Bleeding manifest at ion (skin and mucosal
bleeding)
● Evidence of plasma leak (Great er t han 20% rise
in average hemat ocrit level for age and sex,
great er t han 20% drop in hemat ocrit level fol-
lowing volume replacement or pleural effusion,
ascit es or hypoprot einemia)
DSS
Above crit eria plus circulat ory failure charact erized
by:
● Rapid, weak pulse
● Narrow pulse pressure (< 20 mm/ kg)
● Hypot ension
● Cold, clammy skin
The crit ical period of fluid leak and shock is t he peri-
defervescence period, i.e. about 1-2 days before and 1
– 2 days aft er t he fever subsides. Hence close wat ch is
required from 2nd day of fever for early signs of shock.
I f t his phase is not recognized and t reat ed prompt ly,
fat al shock and hemorrhage can occur rapidly. Plasma
leakage, somet imes sufficient t o cause shock, is t he
most import ant complicat ion of dengue infect ion in
children
I nvesti gati ons
● I n dengue fever non-specific feat ures such as
leucopenia and mild t hrombocyt openia may oc-
cur.
● I n DHF, increase in haemat ocrit of more t han
20% of base line value and t hrombocyt openia
(< 1,00,000/ cmm).
● Moderat e elevat ion of SGPT and hypoalbumine-
mia
● X-ray: Pleural effusion, usually right sided.
● USG abdomen: Ascit es
● Dengue serology: I t has some pit falls and limit a-
t ions. I n early dengue infect ion (first 5 days of
fever) serology may be negat ive. A single sample
may be sent for I gG and I gM dengue ant ibodies
aft er 5 days of illness
● The ELI SA t est s (I gM capt ure ELI SA and I gG cap-
t ure ELI SA) and rapid immunochromat ographic
card t est s are most commonly used.
I n primary dengue infect ion I gM is posit ive (80%
by day 5, 99% by day 10-20). I n secondary dengue
infect ion t here is a brisk and rapid I gG response wit h a
slower and lower I gM response.
Treatment
● I n uncomplicat ed dengue fever, rest , oral para-
cet amol and oral fluids will be sufficient . Avoid
NSAI Ds
● All dengue pat ient s must be observed for com-
plicat ions for at least 2 days aft er recovery from
fever.
● Parent s must be informed of t he following danger
signs which require hospit alizat ion: -
* Abdominal pain
* Any bleeding
* I rrit abilit y, drowsiness
* Alt ered sensorium
* Poor feeding
* Sweat ing and cold skin
Danger signs are feat ures of shock (rapid, weak
pulse, narrowing of pulse pressure, hypot ension),
hemat ocrit of > 40 or rising hemat ocrit , plat elet count of
< 1,00,000/ cmm or evidence of plasma leakage.
Gradation of severity of
Dengue Hemorrhagic fever
Gr ade Sympt oms Lab f i ndi ngs
DHF I Dengue fever feat ures
plus
posit ive t ourniquet t est
Plat elet s <
1,00,000/
cmm
Hct rise >
20%
DHF I I Above signs plus
spont aneous bleeding
Plat elet s <
1,00,000/
cmm
Hct rise >
20%
DHF I I I Above signs + circulat ory
failure (weak pulse,
hypot ension,rest lessness)
Plat elet s <
1,00,000/
cmm
Hct rise >
20%
302
DHF I V Profound shock wit h
undet ect able BP and pulse
Plat elet s <
1,00,000/
cmm
Hct rise >
20%
DHF III and IV= Dengue shock syndrome
(DSS)
DHF gr ade I and I I
● DHF I can be managed wit h oral rehydrat ion t her-
apy and close monit oring. I f oral fluids are not
t olerat ed and for DHF I I , I V fluids are required
● Early volume replacement of lost plasma wit h iso-
t onic cryst alloid solut ion can reduce t he severit y
of disease and prevent shock
● Usually I V fluid t herapy for 12-24 hours wit h fre-
quent clinical and lab (Hct ) monit oring is required.
I V fluid t herapy is not recommended in dengue
infect ion when plasma leak is not suspect ed.z
DHF gr ades I I I and I V
● All children wit h DSS should be managed in t he
hospit al, where facilit ies for frequent clinical and
ht aemat ocrit monit oring are available.
● Guidelines for volume replacement in DHF I I I &
I V (DSS) are depict ed in fig. 2.
● To ensure adequat e volume replacement and t o
prevent excessive fluid administ rat ion t he rat e of
fluid administ rat ion should be carefully adj ust ed
during t he 24-48 hour period of plasma leakage.
● Fluid overload may occur due t o
* Excess and / or t oo rapid I V fluids
* I nappropriat e use of hypot onic rat her t han
isot onic cryst alloid solut ion
* Cont inuat ion of I V fluids for t oo long even af-
t er t he plasma leak has resolved
* Unnecessary use of large volume of I V fluid in
children wit h severe leak.
● Fluid overload may cause respirat ory dist ress
from massive pleural effusion, ascit es and pul-
monary oedema. This can be dangerous.
Cl i ni cal Feat ur es of r ecover y
● Child becomes more alert ,act ive
● Want s feed
● Urine out put improves
● Clinical signs of shock disappear
Typhoid Fever
● Caused by Salmonella t yphi
● Also by Salmonella parat yphi
Clinical pat t ern:
● Ranges from mild gast roent erit is t o severe bact e-
rial sepsis
● Fever, coat ed t ongue
● Vomit ing, abdominal dist ension, loose st ools
● Alt ered sensorium can be present in severe cases
● Hepat omegaly and soft splenomegaly may be
present
Complicat ions:
● I nt est inal perforat ion
● Hemorrhage
● Toxic encephalopat hy
Diagnosis:
● Blood cult ure – 1st week
● Widal – 2nd week
* Significant if ‘O’t it er > 1: 160
Di f f er ent i al Di agnosi s
● Sept icemia, malaria, lept ospirosis, UTI
Treatment
● Uncomplicat ed t yphoid: Oral cefixime 15-20mg/
kg/ day (I Pine for 14 days or Oral chloramphen-
icol 50-75mg/ kg/ day or TMP-SMX 40mg/ kg/ day
of SMX for 14 days
● I V fluids if child doesn’t t ake oral feeds
● I nj ect ion ceft riaxone 75-100 mg/ kg in t wo divid-
ed doses – 14 days
● Oral cefixime can be used for follow up t hereby
aft er improvement t o complet e 14 days course.
● I nj ect ion Ciprofloxocin 10-15 mg/ kg in t wo divid-
ed doses – 2 weeks in life-t hreat ening infect ion
resist ant t o ot her drugs
● Ant ipyret ics
● Tepid sponging
Pr event i on
● Typhoid vaccine (0.5 ml) available in single dose
or mult i dose vial
303
● Take care of hygiene, sanit at ion, cooked food
● Eat well cooked food including boiled milk
Not i f i cat i on:
● Not ify aut horit ies
Urinary Tract Infection (UTI)
● Approximat ely 8% of girls and 1-2% of boys are
likely t o get an UTI during childhood.
● A significant proport ion of children less t han 2
years developing UTI have underlying urinary
t ract anomalies, most oft en vesico uret eric re-
flux (VUR). UTI in a set t ing of VUR may lead
t o renal scarring, an import ant cause of chronic
renal disease. Early recognit ion and t reat ment of
UTI and urinary anomalies is essent ial t o prevent
such complicat ions.
Cl i ni cal f eat ur es of UTI
● Neonat es
* Sepsis like feat ures wit h fever or hypot her-
mia, let hargy, poor feeding, Poor weight gain,
j aundice and shock; urinary sympt oms may
be absent .
● I nfant s and children below 2 years
* Unexplained fever; urinary sympt oms minimal
or absent .
● Adolescent s
* Most ly relat ed t o lower urinary t ract such as
dysuria, frequency, urgency and suprapubic
pain. Renal parenchymal involvement is in-
dicat ed by high fever, chills, rigors and flank
pain.
I nvesti gati ons
● Urine analysis
* May suggest UTI in t he form of increased leu-
kocyt es in urine. Gram st ain of cent rifuged
urine specimen may show bact eria.
● Dipst ick for nit rit e reduct ion and leukocyt e est e-
rase may help in rapid diagnosis.
● Urine cult ure
* This is t he only confirmat ory t est for UTI .
Every effort must be made t o properly collect and send
a urine sample before ant ibiot ic is st art ed. I n infant s
and young children UTI should be suspect ed if t here is
unexplained fever.
● A midst ream clean cat ch specimen is ideal. Soap
or ant isept ic solut ion should not be used before
collect ion. I n infant s urine can be obt ained by
suprapubic aspirat ion.
● Common organisms responsible for UTI are
* E. coli
* Occasionally Klebsiella
* St aph epidermidis or St rep fecalis may be re-
sponsible.
● A colony count of > 105 colony forming unit s
(CFU) / ml of single species in a clean cat ch spec-
imen indicat es significant bact eriuria. Presence
of any bact eriuria in suprapubic specimen is sig-
nificant .
Treatment
For t he purpose of management UTI is divided int o
complicat ed and uncomplicat ed UTI .
Compl i cat ed UTI
● Temperat ure > 390C, persist ent vomit ing, renal
angle t enderness and syst emic t oxicit y are fea-
t ures of complicat ed UTI
● I nfant s below 3 mont hs of age and t hose wit h
complicat ed UTI should receive parent eral ant i-
biot ics init ially.
Opt i ons
1. Cefot axime 100-150 mg/ kg/ day in 3 div doses
2. Ceft riaxone 75 mg/ kg/ day in 1-2 doses
3. Gent amycin 5-7.5 mg/ kg/ day single dose
4. Amikacin 15-20 mg/ kg/ day single dose
● I n young infant s (< 3 mont hs) ent ire t reat ment
is parent eral
● For older children, aft er first 2-3 days, oral an-
t ibiot ics may be st art ed based on ant imicrobial
sensit ivit y
● Tot al durat ion of t reat ment is 10-14 days.
Or al ant i bi ot i cs
Amoxicillin 20 - 40 mg/ kg/ day in 2-3 doses
Cefadroxil 30 mg/ kg/ day in 2 doses
Cephalexin 50 mg/ kg/ day in 3 doses
Cefixime 8 mg/ kg/ day in 2 doses
Ciprofloxacin 10 - 20 mg/ kg/ day in 2 doses
304
Uncompl i cat ed UTI
Children > 3 mont hs of age and t hose who do not
have feat ures of complicat ed UTI can be t reat ed wit h
oral amoxicillin or cefadroxil for 7 t o 10 days (based on
sensit ivit y). Though fluoroquinolones are effect ive and
safe for UTI , t hey are not t he first-line ant ibiot ics
Ot her i nvest i gat i ons
To ident ify urologic abnormalit ies t hat predispose t o
renal scarring t he following st udies are recommended.
1. Ult rasonography
2. Voiding cyt ouret hrography: For diagnosing VUR
and defining bladder and uret hral anat omy
3. Radionuclide scint igraphy: For ident ifying
pyelonephrit is and renal scarring.
4. Special invest igat ions t o rule out predisposing
causes
Ant i bi ot i c pr ophyl axi s
Recommended in
● I nfant s wit h UTI pending evaluat ion
● Children wit h VUR
● Recurrent febrile UTI
Cot rimoxazole (1-2 mg/ kg/ day of Trimet hoprim),
Cephalexin (10 mg/ kg/ day) or low dose Cefixime are
commonly used in prophylaxis.
Leptospirosis
● Lept ospirosis is a zoonot ic disease which has re-
cent ly emerged as a maj or public healt h issue.
Rat s and dogs are t he maj or reservoirs in urban
areas.
● Human infect ion occurs t hrough cont act wit h
urine of an infect ed animal or t he organisms en-
t ering t hrough abrasions in skin or t hrough con-
j unct iva; cont aminat ion of wat er supplies also
can result in out breaks.
Cl i ni cal f eat ur es
Biphasic clinical present at ion; variable, non-specific
clinical feat ures at different phases
I phase ( Acut e or sept i cemi c phase)
● Usually last s for a week
● Fever, headache, phot ophobia, myalgia, abdomi-
nal pain, conj unct ival suffusion and skin rash.
● Different ial diagnosis in t his phase includes viral
fever, dengue, t yphoid fever, malaria, viral hepa-
t it is and pneumonia.
I I phase ( I mmune phase)
● This follows a brief febrile period of variable dura-
t ion aft er t he I phase of illness, may last for 4-30
days.
● Liver and kidneys are t he most commonly in-
volved organs
● Some develop j aundice (Weil’s disease) followed
by renal failure
● Many pat ient s do not have j aundice. They may
develop fever, rash and headache.
● Pulmonary manifest at ions such as cough, dysp-
noea and hemoptysis may occur in a few.
● Unusually CNS manifest at ions (encephalit is,
asept ic meningit is), CVS feat ures (arrhyt hmias)
or hepat obiliary manifest at ions (cholecyst it is,
pancreat it is) may occur.
I nvesti gati ons
● Urinalysis: prot einuria, pyuria, microscopic he-
mat uria
● Leukocyt osis wit h t hrombocyt openia in severe
forms
● Feat ures of hepat ic and / or renal involvement
● Organisms (Lept ospires) can be visualized in
blood or urine by dark-field microscopy or im-
munofluroresence (High degree of false posit iv-
it y)
● Cult ures from blood, CSF or urine t hough are
confirmat ory, are t edious t o carryout .
● Ant ibody det ect ion (serology): commonly used
t est s in spit e of cert ain limit at ions
e. Microscopic agglut inat ion t est (MAT) is t he
st andard serologic t est 1 : 100 / MSAT - 2+
f. Enzyme Linked I mmunosorbent Assay
(ELI SA) for det ect ion of I g M ant ibodies
increasingly used in view of it s simplicit y.
Treatment
1. Support ive care including adequat e hydrat ion.
2. I n case of renal failure, perit oneal / hemodialysis.
3. Ant ibiot ics:
305
* Effect ive ant imicrobials should be inst it ut ed
early.
* Parent eral penicillin G 2-3 lacs / kg / day in 4
t o 6 divided doses for 7 days is t he t reat ment
of choice.
* Doxy / Tet racyclines in children more t han
eight years of age
* Oral amoxicillin, eryt hromycin and 3rd gen-
erat ion cephalosporins (Cefot axime / Ceft riax-
one) are also effect ive.
Ref er ear l y t hose chi l dr en wi t h
● Alt ered level of consciousness
● Renal / hepat ic failure or mult i-organ dysfunct ion
● Respirat ory dist ress, shock
Viral Hepatitis
Aet i ol ogy
● Wat er born viruses: Hepat it is A and E
● Spread by blood and body fluids
* Hepat it is B and C
● Hepat it is A virus (HAV) account s for 20-25% of
clinical hepat it is
● HAV and HEV t ransmission occurs primarily by
faeco-oral rout e t hrough cont aminat ed wat er.
● HAV t ransmission can also occur person-t o-per-
son and also t hrough food handlers.
Hepatitis A Infection
Cl i ni cal f eat ur es
Hepat it is in children due t o HAV may be anict eric or
ict eric and t hese children may have mild sympt oms t o
severe and prolonged forms.
Prodromal phase (few days t o 1 week): Anorexia,
fat igue, abdominal pain nausea, vomit ing, fever.
I ct eric phase: Jaundice appears. High-coloured
urine, pale st ools; I t ching may occur; fever, nausea and
vomit ing subside.
Convalescent phase: All sympt oms gradually subside.
Normalcy ret urns aft er variable period.
I n children all t hese phases usually have a short
durat ion.
I nvesti gati ons
1. I ncrease in liver enzymes (SGPT, SGOT).
2. I ncrease in serum bilirubin; usually does not ex-
ceed 10mg/ dl
3. Det ect ion of I gM ant i HAV indicat es recent infec-
t ion
Ful mi nant Hepat i t i s A
Very rarely hepat it is A may lead on t o fulminant
hepat it is charact erized by deepening j aundice, GI
bleeding, ascit es and alt ered sensorium. Underlying
chronic liver disease is a risk fact or.
Treatment
● Only support ive t reat ment
● Diet ary rest rict ion does not have any role
● Pot ent ially hepat ot oxic drugs are t o be avoided
● Ant iviral agent s do not have any role
Hepatitis E Virus (Hev) Infection
● HEV infect ion generally occurs in out breaks, pri-
marily aft er first decade of life.
Cl i ni cal f eat ur es
● Mild gast roent erit is followed by j aundice, anorex-
ia, abdominal pain, nausea, vomit ing, fever and
prurit us.
● Self-limit ed course; Can be severe in pregnant
women
● Serological diagnosis: I gG, I gM and I gA ant ibod-
ies t o HEV ant igens by enzyme immunoassay.
Hepatitis B Infection
Spread occurs t hrough cont act wit h infect ed blood
and body fluids. Vert ical t ransmission (from mot her
t o newborn) and lat er horizont al t ransmission t hrough
body fluids can occur.
Cl i ni cal f eat ur es
● I f infect ion is acquired in perinat al period 90%
cases will develop chronic hepat it is; if it is ac-
quired 1-5 years of age, t hen 20-50% risk of
developing chronic hepat it is; older children and
adult s have < 5% chance of progressing t o chron-
ic hepat it is.
● Children may be asympt omat ic or may present
wit h acut e viral hepat it is.
● Ext ra- hepat ic feat ures such as art hralgia and
skin manifest at ions (urt icaria, maculopopular
lesions) may occur.
306
● Ot her immune mediat ed feat ures such as polyar-
t erit is, glomerulonephrit is and papular acroder-
mat it is may occur.
● The course is insidious and last s longer t han HAV
infect ion
● Chronic HBV infect ion includes chronic hepat it is,
cirrhosis and hepat ocellular carcinoma.
I nvesti gati ons
Ser ol ogy
● Following acut e infect ion, HBs Ag (Hepat it is B
surface ant igen) appears first . I t may event ually
disappear aft er clinical recovery.
● HBe Ag is normally present during t he acut e
phase and is indicat ive of a highly infect ive st at e.
● HBV DNA is also det ect able in t his phase.
Treatment
Ant iviral drugs (I nt erferon and lamivudine) are used
in t he t reat ment of chronic HBV infect ion wit h t he aim of
suppressing HBV replicat ion and ult imat ely eliminat ion
and also t o decrease necro inflammat ion in liver and
prevent hepat ic decompensat ion. However t hey are
not used rout inely.
Pr event i on of Hepat i t i s B i nf ect i on
I mmunizat ion wit h 3 doses of hepat it is B vaccine is
effect ive (eit her st art ing at birt h or lat er at 6 weeks
along wit h DPT) (Ref. Chapt er. I mmunizat ion).
I f mot her is HBsAg posit ive, newborn baby is given
hepat it is B immunoglobulin in addit ion.
Screening blood for HBsAg before t ransfusion and
safe inj ect ion pract ices also will prevent hepat it is B
t ransmission.
Hepatitis C Infection
Hepat it is C virus (HCV) is fast emerging as an
import ant cause of chronic hepat it is and primary
hepat ocellular carcinoma. Blood t ransfusion is t he
principal mode of infect ion followed by vert ical
t ransmission.
Cl i ni cal f eat ur es
● Acut e hepat it is can occur in a small minorit y of
pat ient s.
● Chronic infect ion is charact erized by chronic
hepat it is, cirrhosis and hepat ocellular carcinoma
slowly developing over decades.
I nvesti gati ons
● The following lab t est s are useful: -
* Ant i HCV ant ibodies
* HCV RNA levels
* Liver biopsy t o st age t he necro inflammat ory
changes.
Treatment
● To get a sust ained virological response by clear-
ing of HCV RNA.
● Interferon α and Ribavirin are used under specific
indicat ions.

Pyogenic Meningitis
● Causat ive organisms depend on t he age group
● I n t he neonat al period and upt o 2 mont hs t he
common organisms are
* Gram negat ive bacilli
* Group B st rept ococci
* List eria monocyt ogens et c
● I n t he age group more t han 2 mont hs t he com-
mon organisms are
* Hemophilus influenzae
* St rept ococcus pneumoniae
* Neisseria meningit idis et c
Sympt oms and si gns
Upt o 2 mont hs of age
● Let hargy unconsciousness
● Not t aking feeds
● Bulging ant erior font analle
● Movement s less t han normal
● Hypert hermia or hypot hermia
● Feeble cry
● I rrit abilit y or incessant cry
● Seizures
> 2 mont hs
● Fever
● Headache
● Vomit ing
● I rrit abilit y
307
● Bulging ant erior font analle (Upt o 18 mont hs)
● Alt ered level of consciousness
● Neck st iffness
● Seizures
● Pet echiae / rashes
● Hypot ension
I nvesti gati ons
Di agnosi s of Pyogeni c Meni ngi t i s
1. Early diagnosis depends on high index of suspi-
cion
2. Definit e confirmat ion is by CSF analysis only.
There are very few cont ra indicat ions for lumbar
punct ure such as
* Signs of raised int racranial t ension
* Bleeding diat hesis
* I nfect ion at t he sit e of Lumbar Punct ure (LP)
3. CSF has t o be sent for:
* Cell count
* Smear for Gram st ain
* Biochemist ry (CSF prot ein raised; sugar de-
creased < 40% of simult aneous blood sugar)
* Cult ure and sensit ivit y
* P. C. R. t est s / Lat ex agglut inat ion t est s may
help in rapid diagnosis and also in part ially
t reat ed cases of pyogenic meningit is
4. I ndicat ions for neuro–imaging
* When t he diagnosis is doubt ful
* Signs of increased int racranial t ension
* Focal neurological signs
* When t he clinical response is not sat isfact ory
Treatment
Select ion of ant ibiot ics as per age, et iology and
immune st at e.
1. For immuno compet ent children I nj . Ceft riaxone
100 mg/ kg/ day I V in 2 div. doses for 10 – 14 days
Or I nj . Cefot axime 200mg/ kg/ day I V in 3 or 4 div.
doses for 10 – 14 days
* Modify ant ibiot ic based on clinical improve-
ment and C/ S report if necessary
* Durat ion of ant ibiot ic for Gram negat ive men-
ingit is (Usually in newborn): 14-21 days
2. St eroids: I nj . Dexamet hasone - 0.1 t o 0.2 mg/ kg/
dose, once in 6 – 8 hours
* Not indicat ed in newborn
* To be given 1 – 2 hours before first dose of
ant ibiot ics.
3. When t o repeat C. S. F. analysis?
* Young children
* No sat isfact ory clinical response
* Gram negat ive bact erial meningit is
4. Ot her support ive measures:
* St abilizat ion of airway, breat hing and circula-
t ion
* Fluid balance: No need t o rest rict int ake.
Maint ain normal circulat ing volume
* Ant i-oedema measures:
» Mannit ol (20%) - 1 – 2 ml/ kg/ dose, once
in 8 hours
» I nj . Dexamet hasone – 0.25 – 0.5 mg/ kg/
dose, may be repeat ed once in 6 hours
» Frusemide 1 mg/ kg per dose
* Cont rol of fever
* Ant iconvulsant s - Phenobarbit one or Pheny-
t oin
5. During follow-up look for
* Head circumference
Hearing
* Neuro cognit ive defect s
* Epilepsy
* Cranial nerve palsies
Ref er r al
● Complicat ed or difficult cases
● When t herapeut ic response is not sat isfact ory
● Modify if meningococcal meningit is is suspect ed
308
( RL or NS)
D
D
309
Management Of Pediatric Tuberculosis
Under RNTCP
● Diagnosis
Suspect when:
* Fever and / or cough for more t han 3 weeks
* Weight loss ± / no weight gain
● Based on:
* Clinical present at ion
* Sput um examinat ion wherever possible
* Chest X-ray
* Mant oux t est
Neuro-imaging if diagnosis doubtful or focal pathology or
no improvement or complications such as hydrocephalus
ALGORITHM: MANAGEMENT OF BACTERIAL MENINGITIS
Bacterial (pyogenic) meningitis
(Diagnosis based on clinical and CSF ndings)
Stabilize A,B,C
Anitconvulsants as per SE protocol; continue maintenance phenobarb ± phenytoin
LP after child stabilized and if no contraindication
IV dexamethasone 0.15 mg/kg 1 – 2 hrs before rst dose antibiotic
and continue 6th hourly for 2 days
IV ceftriaxone 100mg/kg in 2 divided doses or IV cefotaxime
200mg /kg in 3-4 doses x 10-14 days
If increased ICP present IV mannitol and frusemide ;
Maintain uid and electrolyte balance
* Cont act hist ory
● Tuberculous meningit is suspect ed in presence of:
* Neurological sympt oms such as irrit abilit y, re-
fusal t o feed, headache, alt ered sensorium
* Vomit ing
Tr eat ment of Pedi at r i c Tuber cul osi s
● DOTS is t he recommended st rat egy for t reat ment
in adult s as well as in children
● All paediat ric TB pat ient s should be regist ered
under RNTCP
● Cat egory of t reat ment
310
● Cat egory I : This cat egory is generally pre-
scribed t o new sput um smear-posit ive pat ient s.
They have a high bacillary populat ion wit h
higher chances of having nat urally occurring
drug-resist ant mut ant s. Therefore, four drugs
are prescribed during t he I nt ensive Phase (I P).
Cat egory I I : These are cases t hat have had
previous ant i-t uberculosis t reat ment . There-
fore, t he chances of harboring resist ant ba-
cilli are higher. Hence, a 5 drug regimen is
prescribed in t he int ensive phase, and t he
t ot al durat ion of t reat ment is 8 mont hs.
Cat egory I I I : These are sput um smear-negat ive
cases wit h a low bacillary populat ion. There is a
lower chance for drug-resist ant mut ant s. There-
fore, a 3 drug regimen is prescribed.
Pr i nci pl es i n t r eat ment
Pat ient s are classified int o t hree cat egories for
t he purpose of t reat ment . The number of drugs
and t he durat ion of t reat ment are different in t he
t hree t reat ment cat egories of RNTCP ( Table 2).
I n pat ient s wit h TBM on cat egory I t reat ment ,
t he four drugs used during t he int ensive phase
should be HRZS(inst ead of HRZE).
● Cont inuat ion phase of t reat ment in TBM and spi-
nal TB wit h neurological complicat ions should be
given for 6-7 mont hs, t hus ext ending t he t ot al
durat ion of t reat ment t o 8-9 mont hs.
● St eroids should be used init ially in hospit alized
cases of TBM and TB pericardit is and reduced
gradually over 6-8 weeks.
● I n all inst ances, before st art ing a child on cat-
egory I I t reat ment , s/ he should be examined by
a pediat rician or TB expert .
● Any pat ient , pulmonary or ext ra-pulmonary,
who is known t o be HI V posit ive based on
volunt ary sharing of result s and / or hist ory of
ant i-ret roviral t herapy, is considered seriously ill
For t he purpose of cat egorizat ion, HI V t est ing
should not be done. Also, HI V st at us should not
be revealed / recorded in any RNTCP document .
● All effort s should be made t o ensure t hat every
dose of medicine in t he int ensive phase and at
least t he first dose every week in t he cont inua-
t ion phase are direct ly observed.
● Treat ment observat ion should be done by some-
one who is accessible and accept able t o t he
pat ient and account able t o t he healt h syst em.
One of t he most import ant responsibilit ies is t o
ensure t hat during t he int ensive phase of t reat-
ment (which is 2 t o 4 mont hs of direct ly observed
administ rat ion of drugs) pat ient s are swallowing
every dose of t heir drugs under t he direct obser-
vat ion of a DOT provider.
● To ensure proper drug administ rat ion, observe
t he DOT provider administ ering drugs t o t he pa-
t ient s and speak direct ly t o pat ient s t o det ermine
whet her t hey have been receiving t he correct
number and type of drugs.
● Aft er t he pat ient s swallow t heir drugs in t he pres-
ence of a DOT Provider, t hose receiving st rept o-
mycin should be given t he inj ect ions wit h st erile
syringes and needles.
Chemopr ophyl axi s
● Recent infect ion wit h t ubercle bacilli is one of t he
risk fact ors for disease development . The young-
er t he child, t he higher is t he risk of breakdown of
infect ion int o disease. Therefore, child cont act s
of smear – posit ive t uberculosis cases, especially
t hose below 6 years of age, must be screened for
sympt oms of t uberculosis.
● I n cases of sympt oms being present , t he diag-
nost ic algorit hm for pediat ric t uberculosis should
be followed and t he child should be given a full
course of ant i-t uberculosis t reat ment if she/ he is
diagnosed as a t uberculosis case.
● For asympt omat ic children and t hose who are not
found t o be suffering from t uberculosis , chemo-
prophylaxis wit h isoniazid (5mg per kg body wt )
should be administ ered daily for a period of six
mont hs. This is regardless of t he BCG vaccinat ion
st at us.
Moni t or i ng
● Child is reviewed at t he end of 2 mont hs of t reat-
ment . Sat isfact ory response is ident ified by im-
provement in sympt oms and weight gain.
● Clinical follow-up and t reat ment is cont inued.
On review, unsat isfact ory response is assessed
by non-adherence t o t reat ment , weight loss and
worsening sympt oms. This child is referred t o
pediat rician or a t uberculosis specialist t o decide
whet her he has t o receive Cat egory I I t reat ment
(Non-responder).
311
Immunization
Nat ional I mmunizat ion Schedule
Age Vacci nes
Birt h
6 weeks
10 weeks
14 weeks
9 mont hs
16-18 mont h
5 years
10 years
16 years
Pregnant
women
BCG, OPV-O
DPT 1, OPV 1
DPT 2, OPV 2
DPT 3, OPV 3
Measles
DPT boost er, OPV 4
DT
TT
TT
TT (2 doses at 4
weeks int erval)
BCG Vacci ne
Supplied as a lyophilized (freeze-dried powder)
preparat ion; reconst it ut ed wit h t he recommended
diluent supplied. Once reconst it ut ed, t he vaccine should
be used wit hin 4-6 hours.
Dose: 0.1ml
Rout e: I nt radermal over delt oid insert ion sit e of left
arm
Following t he vaccinat ion t here is no immediat e
react ion. A papule develops in 2-4 weeks, ulcerat es and
heals slowly over 6-12 weeks leaving a small scar.
Or al pol i o vacci ne ( OPV)
● Rout ine immunizat ion wit h 6 doses
● Nat ional schedule 5 doses
RNTCP Treatment Categories And Regimens For Children
Tr eat ment
cat egor y
Type of pat i ent s
Tr eat ment Regi men* * *
I P CP
Cat egory I New sput um smear – posit ive PTB,
New sput um smear – negat ive PTB seriously ill
*
New ext ra – PTB, seriously ill*
2H
3
R
3
Z
3
E
3
* * * 4H
3
R
3
Cat egory I I Sput um smear – posit ive relapse, sput um smear
– posit ive t reat ment failure
Sput um smear – posit ive t reat ment aft er default
2H
3
R
3
Z
3
E
3
S
3
+
1 H
3
R
3
Z
3
E
3
5H
3
R
3
E
3
Cat egory I I I New sput um smear – negat ive, not seriously ill
* *
New ext ra – PTB, not seriously ill * *
2H
3
R
3
Z
3
4H
3
R
3
* I n children t hat are seriously ill, sput um
smear negat ive pulmonary t uberculosis (PTB)
includes all forms of sput um smear negat ive
PTB ot her t han t he primary complex including
milit ary TB, cavit ary disease. Seriously ill ext ra
pulmonary TB (EPTB) includes TB meningit is
( TBM), disseminat ed TB, TB pericardit is, TB
perit onit is and int est inal TB, bilat eral ext en-
sive pleurisy, spinal TB wit h or wit hout neuro-
logical complicat ions, genit o–urinary TB, and
bone and j oint TB.
Not e:
* * Not seriously ill sput um smear-negat ive PTB
includes primary complex. Not seriously ill EPTB
includes lymph node TB and unilat eral pleural effusion
* * * Prefix indicat es mont h and subscript indicat es
t hrice weekly
I P = I nt ensive Phase CP = Cont inuat ion
Phase
Suggested Pediatric Dosages For Intermit-
tent Therapy
Dr ugs Dosage ( Thr i ce a week)
I soniazid 10- 15 mg/ kg
Rifampicin 10 mg / kg
Pyrazinamide 30-35 mg/ kg
Et hambut ol 30 mg / kg
St rept omycin 15 mg / kg
312
mont hs).
Dose: 0.5ml (10 microgram in children)
Rout e: I M over ant erolat eral t high or delt oid region.
Local pain and eryt hema may occur following t he
vaccinat ion.
I mpor t ant poi nt s t o r emember i n i mmuni zat i on
1. Proper handling of vaccines and maint enance of
cold chain is import ant
2. Minor illnesses such as cold, cough or mild di-
arrhea are not cont raindicat ions for immuniza-
t ions.
3. I f due t o some reason a vaccine is delayed, t he
schedule need not be repeat ed; it should only be
complet ed.
4. I f any adverse react ion follows immunizat ion, re-
port t o healt h aut horit ies immediat ely.
Acute Flaccid Paralysis (Afp) Surveillance
Def i ni t i on of AFP
● Sudden onset of weakness and floppiness in any
part of t he body in a child less t han 15 years of
age or paralysis in a person of any age in whom
polio is suspect ed.
● AFP surveillance helps t o det ect reliably areas
where polio virus t ransmission is occurring. To
ensure t hat no case of polio is missed, all cases
of AFP wit hin 6 mont hs of onset are report ed and
invest igat ed wit h collect ion of t wo st ool speci-
mens wit hin 14 days of onset .
● The non-polio causes of AFP include
* Guillain – Barre syndrome (GBS)
* Transverse myelit is and
* Traumat ic neurit is.
St ool sampl e col l ect i on
● 2 st ool samples from t he child at a minimum in-
t erval of 24 hours.
● At t empt t o collect t he st ool samples wit hin 14
days of onset of paralysis t o maximize t he prob-
abilit y of posit ive result . I f not possible, t he spec-
imens should st ill be collect ed up t o 60 days of
paralysis onset .
● Each st ool sample should be 8 grams (approxi-
mat ely t he size of adult t humb).
● I t should be t ransport ed t o regional laborat ory
● I n Tamil Nadu, one more dose given wit h mea-
sles vaccine at 9 mont hs.
● To achieve polio eradicat ion and t o int errupt cir-
culat ion of wild polio virus in communit y annual
polio immunizat ion in t he form of pulse polio (2
doses in Tamil Nadu) is given t o all children upt o
5 years irrespect ive of t heir prior immunizat ion
st at us.
● Polio vaccine is t emperat ure sensit ive, hence
proper maint enance of cold chain t ill t he vaccine
is delivered t o t he child is ext remely import ant .
Dose: 2 drops orally
DPT Vacci ne
I t is a combinat ion of dipht heria t oxoid, whole-cell
killed pert ussis and t et anus t oxoid. Dose: 0.5ml. Rout e:
I M – over ant erolat eral aspect of t high (Avoid inj ect ion
over glut eal region). The prot ect ion following 3 doses
is more t han 95% for dipht heria and t et anus and 70-
80% for pert ussis. Following an inj ect ion, fever, local
pain and indurat ion may last for 1-2 days. Paracet amol
may be given for t hese sympt oms
Tet anus t oxoi d ( TT)
Tet anus t oxoid is given at 10 years and 16 years.
Following t his, boost er doses are required only aft er
every 10 years. There is no need t o give I nj TT for every
wound if t he child has received t he immunizat ions at
t he recommended age.
Measl es vacci ne
Measles vaccine is supplied in freeze – dried st at e
(lyophilized powder) wit h t he required diluent . The
vaccine does not cont ain any ant ibact erial preservat ive.
Hence st rict asept ic t echnique should be used during
reconst it ut ion and administ rat ion. Reconst it ut ed vaccine
should be used wit hin 4 hours.
Dose: 0.5ml
Rout e: Subcut aneously over arm or ant erolat eral
t high. Fever, coryza and mild measles like illness may
occur in up t o 10% of children bet ween 5-10 days aft er
immunizat ion.
Ot her vacci nes under consi der at i on f or i ncl usi on
i n Nat i onal I mmuni zat i on schedul e
Hepat i t i s B vacci ne
I t is a recombinant DNA vaccine. I mmunogenicit y is
more t han 95% wit h various schedules (Birt h, 6 and 14
weeks; 6, 10 and 14 weeks at t he same t ime of DPT
vaccine but at a different sit e; Birt h, 1 mont h and 6
313
under proper cold chain (20 – 80C) condit ions so
t hat it arrives at t he lab in a good condit ion (no
desiccat ion, no leak, wit h adequat e document a-
t ion and evidence t hat t he cold chain was main-
t ained).
● Document t he proper address of child so t hat fol-
low up examinat ion for residual paralysis can be
carried out bet ween 60-90 days following paraly-
sis onset .
Out br eak r esponse i mmuni zat i on ( ORI )
● Aft er AFP invest igat ion and st ool collect ion, ORI
is organized in t he communit y t o administ er one
dose of OPV t o approximat ely 500 children below
5 years of age form t hat localit y / village.
Vi r ol ogi cal cl assi f i cat i on of AFP cases
● An AFP case is ‘confirmed’ as polio only by isola-
t ion of polio virus from any st ool specimen.
● An AFP case is classified as “ non-polio AFP” if
wild polio virus is not isolat ed from adequat e
st ool specimens.
● I f st ool specimens are inadequat e, t hen t he clas-
sificat ion will depend on 60 days follow up ex-
aminat ion. I f t he 60 days follow up examinat ion
shows no residual weakness, t he case is classi-
fied as “ non-polio AFP”.
Repor t i ng
● All cases of AFP should be report ed t o t he not i-
fied surveillance medical officer immediat ely for
furt her evaluat ion and act ion.
Treatment
● Support ive measures
● Avoid I M inj ect ion
● Vent ilat ory support may be required in progres-
sive paralysis
Rheumatic Fever In Children
● Caused by Group A β hemolytic streptococcus
● Children from 5 t o 15 years are t he most suscep-
t ible.
● I ncreased number of cases occur in socially and
economically disadvant aged groups
Diagnosis Of Rheumatic Fever - Modifed Jones
Crit eria
● Maj or
* Cardit is
* Migrat ory polyart hrit is,
* Chorea
* Subcut aneous nodules
* Eryt hema marginat um
● Minor
* Fever
* Art hralgia
* Previous rheumat ic fever
* I ncrease in ESR, CRP
* Prolonged P-R int erval in ECG
For diagnosis of Rheumat ic fever 2 maj or or 1
maj or and 2 minor crit eria Plus Evidence of previous
Group A st rept ococcus infect ion.
Di f f er ent i al Di agnosi s
● Juvenile rheumat oid art hrit is
● I nfect ive endocardit is
● Sept ic art hrit is
● Serum sickness
I nvesti gati ons
● Throat cult ure for Group A st rept ococcus
● ASO for recent st rept ococcal infect ion
● Chest X-ray
● ECHO
Management
● Treat st rept ococcal infect ion:
● I nj . Benzat hine Penicillin G 12 lakhs unit s single
dose deep I M (6 lacs unit s for < 27 kg)
or
● Oral penicillin V 250 mg bid (500 mg bid for > 30
kg) for 10 days
or
● Oral eryt hromycin 40 mg/ kg/ day in 3 divided
doses for 10 days.
● Aspirin 90-120 mg/ kg/ day for 4 weeks
I n car di t i s
314
● Prednisolone 2 mg/ kg/ day – 2 t o 3 weeks and
t aper over anot her 2-3 weeks
● To t reat cardiac failure as applicable
Tr eat ment of r heumat i c chor ea
● Haloperidol 0.5 mg/ day in 2 divided doses
Pr event i on
● Primary (Refer t reat ment of st rept ococcal infec-
t ion given above)
● Secondary
* I nj . Benzat hine Penicillin 12 lakhs unit s
(6 lakhs < 27 kg) once in every 3-4 weeks
or
* Oral Penicillin V 250 mg BI D daily
Congenital Heart Diseases (CHD)
● I ncidence 58 per 1000 live birt hs
● Commonest CHD – VSD, ASD, PDA, TOF

↑PBF (Pulmonary Blood Flow)
↓PBF
DORV (Double out let right vent ricle)
TOF
TGA wit h VSD
VSD wit h PS
Truncus art eriosus
Common at rium
Sympt oms
● Recurrent respirat ory t ract infect ions
● Failure t o t hrive
● Diagnosed usually in first 3 mont hs of life
● Feeding problem
● Respirat ory dist ress
● Presence of CCF
Sever e cyanosi s at bi r t h
● Cyanot ic spells
● Squat t ing episodes
● Ej ect ion syst olic murmur
X-r ay
● Cardiomegaly
Small heart
● Pulmonary plet hora
Pulmonary oligemia
● ECHO diagnost ic
● Treat CCF as applicable (Ref. Chapt er on CCF)
● Surgery is t he definit ive t reat ment
Appr oach –Acyanot i c hear t di sease
● To look for shock or arrhyt hmia
● Look for facial dysmorphism
● Look for congenit al malformat ion
● Growt h paramet er
Cl i ni cal f eat ur es
Pul se
● Absence of art erial pulse in lower limb / radio
femoral delay – coarct at ion of aort a
● Low volume pulse – aort ic st enosis
● Collapsing pulse - aort ic regurgit at ion, PDA
● Pulsus paradoxus – pericardial effusion
● Pulsus alt ernans – LVF
Bl ood Pr essur e
● Wide pulse pressure – aort ic regurgit at ion, AV
fist ula
● Narrow pulse pressure – valvular aort ic st enosis
Par ast er nal heave
● Present in right vent ricular hypert rophy
Thr i l l s
● Aort ic area – aort ic st enosis
● Pulmonary area – pulmonary st enosis
● Left st ernal lower border – VSD
315
Var i ous f eat ur es of acyanot i c CHD:
● VSD – asympt omat ic or sympt omat ic
* some t imes present s wit h CCF
* Presence of pansyst olic murmur in t he left
lower st ernal border
● PDA – cont inuous murmur in t he left first int er-
cost al space
● ASD – most ly asympt omat ic
* Wide split of second heart sound
● Coarct at ion of aort a – signs of acut e circulat ory
shock in first 6 weeks of life
* Weak lower limb pulses
I nvesti gati ons
Echocardiogram is diagnost ic for acyanot ic CHD
To t reat CCF appropriat ely (Refer chapt er 34)
Appropriat e surgical management for each dis-
ease
Congestive Heart Failure (CHF)
Pr i nci pl es
● Cont rol of excessive salt and wat er ret ent ion wit h
diuret ics
● I mprove cardiac cont ract ilit y wit h digoxin
● Prevent and reverse neurohormonal changes t hat
lead t o progressive worsening of cardiac st at us
wit h bet a blockers, ACE inhibit ors
Di goxi n
● Drug of choice in chronic CHF wit h at rial fibrilla-
t ion
● I n CHF wit h sinus rhyt hm it gives sympt omat ic
benefit
Dose
● Tot al digit alizing dose
* I n children 30-40 mcg/ kg ½ t he t ot al dose
st at : ¼ aft er 8 hrs; ¼ aft er 16 hrs
● Daily maint enance dose
* ¼ of t ot al digit alizing dose. Once daily or 2
divided doses
Not e:
Hypokalemia may aggravat e digit alis t oxicit y
especially wit h concomit ant diuret ic administ rat ion. Use
oral Kcl supplement or use pot assium sparing diuret ic
such as spironolact one.
Or al Di ur et i cs
● Furosemide: 1-2 mg/ kg/ day
● Hydrochlorot hiazide: 1-1.5 mg/ kg/ dose
every 12-24 hours
● Spironolact one: 1-2 mg/ kg/ day
ACE i nhi bi t or s
● I ndicat ed for all pat ient s wit h congest ive heart
failure.
● Capt opril: 0.1 t o 0.5 mg/ kg/ dose oral every 8 t o
12 hourly up t o 4 mg/ kg/ day
● Enalapril: 0.1 mg/ kg/ dose oral every 12-24 hour-
ly up t o 0.5 mg/ kg/ day
β-blockers
● I nt egral part of congest ive heart failure t herapy
nowadays.
● Met aprolol or carvedilol is used
Di et
● Calories - Recommended daily diet ary allowance
plus 20-30% in shunt lesions
● Avoid salt y foods and addit ional salt in cooking
● I ron supplement at ion
When t o r ef er
● Severe respirat ory dist ress
● Acut e pulmonary oedema
● Refract ory CCF
● Cardiogenic shock
Nephrotic syndrome in children
Nephrot ic syndrome is a clinical ent it y charact erized
by
● Massive prot einuria (> 50mg/ kg/ day)
● Hypoalbuminemia (< 2.5gm/ dl)
● Edema
● Hyperlipidemia.
Def i ni t i ons
● Frequent relapses
* Eit her 2 or more relapses wit hin 6 mont hs of
316
init ial response or 3 or more relapses wit hin a
12 mont h period.
● St eroid dependent
* 2 or more consecut ive relapses while st eroids
are st ill being t apered or wit hin 4 weeks of
st opping st eroids.
● St eroid resist ant
* Failure t o respond t o oral Prednisolone of
2mg/ kg/ day for 4 weeks or t o t hree doses of
pulse Met hyl prednisolone
Cl assi f i cat i on
● Congenit al or Primary (idiopat hic)
● Secondary. I n children maj orit y of NS are pri-
mary or idiopat hic; 90% of t he idiopat hic NS are
minimal change NS.
Cl i ni cal exami nat i on
● Periorbit al puffiness/ gain in weight , generalized
edema wit h pleural effusion, ascit es, diminished
urine out put .
I nvesti gati ons

Ur i ne I nvest i gat i ons
Prot einuria
● Preferable early morning specimen
● 24 hour urine prot ein
● The rat io of spot urine prot ein t o creat inine (PCR)
more t han 3 is diagnost ic of NS.
● Urine microscopy: broad waxy cast s, hyaline
and granular cast s.
● Urine cult ure: Rule out infect ion before inst it u-
t ion of st eroid t herapy.
Bl ood Chemi st r y
● Blood urea, serum creat inine
● Serum t ot al prot ein will be reduced
● Serum albumin level is less t han 2.5gms/ dl.
● Serum cholest erol and t riglycerides are raised in
a nephrot ic child
● Serum elect rophoret ic pat t ern will reveal a de-
crease in albumin level and a raised alpha 2 and
bet a globulins.
● Mant oux and chest X-ray should be done t o rule
out t uberculous infect ion.
● Ult rasound of t he kidneys is rout inely done t o
confirm t he number, sit e and size of t he kidneys.
Pr obl ems i n nephr ot i c syndr ome
I nfect ion, acut e renal failure, increased t hrombo
embolic manifest at ions, hypocalcemia
Management
● Diet
* A balanced diet adequat e in bot h calories and
prot eins (1-2gms/ kg) is recommended.
* Salt is rest rict ed t o 1-2gms/ day if edema is
present .
* Fluid rest rict ion is advised only if gross edema
is present .
● Diuret ics
* Fluid is rest rict ed t o insensible loss-
es in massive edema. Fluid rest rict ion is
not necessary in moderat e edema Diu-
ret ics such as frusemide (1-2mg/ kg) /
spironolact one (2mg/ kg) are used. I n
refract ory cases 20% salt poor albumin 2ml/
kg or 20ml/ kg plasma followed by int ravenous
frusemide is advised.
● I nfect ions: Associat ed infect ions such as UTI ,
skin infect ion, ARI , t uberculosis or perit onit is
must be cont rolled, prior t o st eroid t herapy.
Speci f i c
Oral prednisolone 60mg/ m2/ day daily for 6weeks
I f urine is prot ein free it is followed by 40mg/
m2/ alt ernat e days for next 6 weeks and st opped.
(APN regimen). More t han 50% of children who
respond wit hin t wo mont hs do so wit hin first t wo
weeks and 95% wit hin first mont h.
Relapses: There is no single clinical or hist ological
t est t o predict frequent relapses but occurrence
of first relapse soon aft er init ial at t ack predict s
furt her relapses. Regular follow up in OPD t o
det ect relapses at early st ages before edema de-
velops is sufficient t o st art t herapy.
Frequent Relapses (> 2 relapses in 6 mont hs):
The st andard prednisolone schedule is st art ed
and t apered t o a low dosage of 0.5mg/ kg/ 48hrs
in order t o minimize side effect s. Most children
can t olerat e a dosage of 0.5mg/ kg/ 48 hrs and
t reat ment should be given for a period of 12-18
mont hs.
317
I nfrequent Relapse (Less t han t wo relapses in
6 mont hs): St andard st eroid t herapy is st art ed
and if urine is prot ein free it is cont inued for 2
weeks and swit ched over t o alt ernat e days for
four weeks and st opped.
St eroid Resist ant : About 10-15% of t he pat ient s
do not show remission of prot einuria and t his
is t ermed as a st eroid-resist ant nephrot ic syn-
drome. For t hese pat ient s alt ernat e t herapy can
be considered.
Al t er nat e Tr eat ment
Alt ernat e drugs should be considered in t he fol-
lowing circumst ances:
● Relapse on Prednisolone dosage of more t han
0.5mg/ kg/ 48hrs, st eroid t oxicit y, pubert al age
and st eroid resist ant NS.
I mmunosuppr essi ves
● Levamisole
● Cyclosporin A
● Tacrolimus
● Angiot ensin convert ing enzyme inhibit ors(ACE)
and
● Angiot ensin recept or blockers
● Pulse met hyl prednisolone
● Lipid lowering agent s.
Par ent al Counsel l i ng
The parent s should be educat ed about t he course
and out come of t he illness.
Ref er r al
Resist ant nephrot ic syndrome, frequent relapses,
and complicat ions need referral.
(missing algorit hm for management of nephrot ic
syndrome book pg 70)

Acute Nephritic Syndrome
Et i ol ogy
Post-infect ive glomerulonephrit is
Commonest cause is st rept ococcal infect ions of t he
t hroat and skin.
Cl i ni cal f eat ur es
Abrupt onset of hemat uria, edema, prot einuria,
hypert ension, oliguria, azot emia
I nvesti gati ons
● Colour of urine (cola coloured)
● Urine deposit s / RBC cast / prot einuria
● Urine prot einuria
● 24 hours urine prot ein
● Spot prot ein creat inine rat io (0.3 –3)
● Urea/ creat inine/ elect rolyt es
● Chest skiagram
● USG abdomen
● ASO/ CRP
● Serum C3 levels if indicat ed
Moni t or i ng
Blood pressure
Daily weight
Urea, creat inine
I nt ake/ out put
Compl i cat i ons
Pulmonary edema, hyert ensive encephalopat hy ,
hyperkalemia, uremic encephalopat hy
Treatment
Cont r ol of edema
● Salt free diet / I nj Frusemide 1- 2 mg/ kg/ dose/
● Fluid rest rict ion in severe edema-rest rict t o in-
sensible wat er loss(400ml/ m2 / day)
Cont r ol of hyper t ensi on
● T. Alpha met hyl dopa 20- 40 mg/ kg/ day
● T.Enalapril 0.3 – 0.5 mg/ day
● Sublingual Nifedepine 0.25 – 0.5 mg/ kg/ dose 6
hourly
I nf ect i on cont r ol
Appropriat e ant ibiot ics t o cont rol infect ion
Hyper kal emi a
● Sodabicarbonat e 1 ml/ kg.dose int ravenously very
slowly
● 10% calcium gluconat e 1 ml/ kg/ dose I V slowly
● I nj Frusemide 1- 2 mg/ kg/ dose
318
● Salbut amol nebulisat ion
● Sodim polyst erone sulfonat e 1 gm/ kg/ dose eve-
ry 6 hours
● Perit oneal dialysis
Pul monar y edema
Support ive oxygen t herapy, vent ilat ion, I nj .
Frusemide 5 mg/ kg/ I V
Hyper t ensi ve encephal opat hy
● Sublingual Nifedepine 0.5 mg/ kg/ dose
● Seizure cont rol wit h Diazepam, Phenyt oin
I ndi cat i ons f or r ef er r al
Pulmonary edema, persist ent anuria, uremic
encephalopat hy and rapid det eriorat ion of renal funct ion

Protein Energy Malnutrition (PEM)
Def i ni t i on of PEM
WHO (1973) has defined PEM as a range of
pat hological condit ions arising from coincident lack, in
varying proport ions of prot ein and calories, occurring
most frequent ly in infant s and young children and
commonly associat ed wit h infect ions.
Welcome classifcation of PEM
Wei ght f or
age
Oedema Type
Less t han 60% + Marasmic kwashiorkor
Less t han 60% Nil Marasmus
60 – 80% + Kwashiorkor
60 – 80% Nil Under nut rit ion
Wei ght f or age
● 1-7 years (age x 2) + 8 = Expect ed Weight
● > 7 years (age x 7) - 5 ÷ by 2 = Expect ed
weight
Look f or t he f ol l owi ng
● Visible severe wast ing
● Edema bot h feet
● Very low weight for age
● Look for associat ed infect ion
● Look for underlying vit amin/ t race element defi-
ciencies.
I nvesti gati ons
● To det ermine cause and degree of malnut rit ion
● To ident ify infect ions, infest at ions, vit amin and
mineral deficiency
* Examinat ion of st ools
* Urine rout ine, cult ure and sent ivit y
* Hemoglobin, smear st udy
* Blood sugar, elect rolyt es
* Mant oux, X-ray chest
* Blood grouping
* Serum prot ein, albumin, globulin
* HI V st at us
Treatment
Phase I ( 24 – 48 hour s - Resusci t at i ve phase) :
Chi l dr en pr esent i ng wi t h l i f e-t hr eat eni ng
compl i cat i ons:
1. St abilize airway, breat hing and circulat ion
2. Look for life-t hreat ening complicat ions:
* Hypoglycemia
» Treat wit h 10% Glucose I V 2ml/ kg followed
by infusion wit h dext rose cont aining I VF
* Hypot hermia
» Maint ain warmt h
* Hypokalemia
» Provide adequat e pot assium in t he flu-
ids at 40 meq/ lit re ( 2ml KCL / 100ml of
maint enance fluid)
* Shock
» Treat wit h normal saline boluses
* Dehydrat ion
» Correct ion as per guidelines
3. Treat ment of associat ed problems:
* Anemia
» Treat wit h oral iron aft er smears, st ool
st udy; 6 mg/ kg element al iron/ day
* CCF
* Severe Vit . A deficiency
319
* Sepsis management wit h parent eral ant ibiot-
ics
Phase I I ( Rest or at i ve phase)
I dent ify and t reat underlying cause and cont inue t o
t reat already ident ified complicat ions. Oral feeds can
be gradually st art ed.
Phase I I I ( Rehabi l i t at i ve phase)
Diet ary Treat ment
1. Principle
* Diet according t o Recommended Diet ary Al-
lowance (RDA) and calculat ed for ideal weight
for age
2. I n Pract ice
* Correct diet ary imbalances
* I ncrease what ever t he child rout inely t akes at
home
* Add sugar and oil (wit hin RDA) t o make up
calories (upt o 30% of required calories can be
in t he form of sugar and oil)
* Low cost : cereal - pulse preparat ion (NI N mix)
as a nut rit ional supplement at ion.
3. Vit A supplement at ion (as in t able)
4. Nut rit ional monit oring and follow up
5. Deworming wit h Albendazole 400mg as a single
dose in children 2 years and above.
Cereal pulse multi-mix preparation
NIN mix
Ragi - 40 gm
Wheat - 35 gm
Roast ed Bengal Gram - 15 gm
Ground Nut s - 10 gm
This provides 13 gm of prot ein and 360 calories
per 100 gm.
Treatment of vitamin A defciency
Or al Oi l mi sci bl e
Vi t ami n A
< 1 year > 1 year
I mmediat ely 1 lakh I U 2 lakhs I U
Next day 1 lakh I U 2 lakhs I U
Aft er 2 – 4 weeks 1 lakh I U 2 lakhs I U
I nj ect ion Vit amin A (wat er soluble)
● Oral vit amin A for infant < 6 mont hs is 50,000
unit s/ dose
* I n t he presence of diarrhea and vomit ing,
Kerat omalacia
» Below 1year - 50,000 unit s I M/ dose
» Above 1 year - 1 lakh unit s I M/ dose
● Given on day 1 and day 2 and day 14.
● Encourage green leafy veget ables, yellow veg-
et ables, milk fort ified wit h vit amin A.
● Prophylact ic vit amin A single dose of vit amin
100,000 unit s at 9 mont hs followed by 200,000
unit s at 18, 24, 30, 36 mont hs.
When t o r ef er i n PEM
● Children wit h fulminant sepsis needing parent ral
nut rit ion
● Children suspect ed t o have any life-t hreat ening
complicat ion
● Children wit h no weight gain despit e adequat e
t herapy.
Management of Anemia
The most common form of anemia is iron-deficiency
anemia caused by reduced diet ary int ake. I t is easil