Amniotic Fluid Optical Density (AFOD) and its Correlation with Fetal Functional maturity and labour

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President : Dr. Lalithambika
Secretary General: Dr. Fessy Louis T
Immediate Past President: Dr.Kunjamma Roy
President Elect: Dr.Chellamma
Vice President: Dr.Chellamma,
Vice President Elect: Dr. Vijayan C.P.
Joint Secretary: Dr. Bindu K.M.
Treasurer :Dr.lola Ramachandran
Journal Editor: Dr. Sangeetha Menon
Mat. Fetal Med. Chair
: Dr.K. Ambujam
CRMD
: Dr.Paily V.P.
Chair, Reproductive Health : Dr .Philips Abraham
Chair,Oncology : Dr.Chitrathara
Chair, Research Committee: Dr. Nirmala C
EMOCALS: Dr. Bindu M.
KFOG Managing Committee
Dear friends,
Hope you enjoyed
re a ding pr e vious
is s ue of KFOG
JOURNAL. We will
be able to improve
the quality and quantity of the
contents of our journal only if each one of us try
to make it better. Sub editor of our journal dr.
Prameela was very keen to release this issue
du r ing 37th A K COG and tha t ha s bee n
materialised. In addition to scientific material ,it
would be nice if we can publish social activities
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Vol: 9 No: 1
February 2015
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Wish you all a
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Editorial
Sepsis in Obstetrics
Dr Joe John Chirayath
Amniotic Fluid Optical
Density (AFOD)
DR.H. SAMARTHA RAM
HOW TO APPROACH YOUR
FERTILITY PROBLEMS
Dr. FESSY LOUIS. T
ONCO CORNER
02 07
12
Dr. Prameela Menon.
Sub Editor KFOG Journal
prameelapramod@gmail.com
KFOG Head Quarters: TOGS Academia,
East Sooryagramam, Thrissur- 5 Ph: 0487 2320233
smritidesign.in
Dr. Lalithambika
President KFOG
Dr.Fessy Louis T
Secretary KFOG
..................................................................
From KFOG
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22
The death of a mothe r, a young
woman who had hopes and dreams of a
happy future, but who dies before her
time is one of the cruell est events
imaginable. The short and long term
impact of such a tragedy on her surviving
ch i ldren , partn e r, wi der fa m ily,
community and the health workers who cared
for her, cannot be estimated at all 1.
Worldwide, sepsis accounts for 15% of all
maternal deaths2. In the most recent Confidential
Enquiry into Maternal and Child Health in UK
(CEMACE 2012, formerly CEMACH), sepsis
was the leading cause of direct maternal deaths
and the maternal mortality rate from sepsis has
almost tripled in the last 25 years2.
Sepsis is the 3rd leading cause of maternal
deaths in Kerala3. The mortality rate is high in
septic patients with both hypotension and lactate
>/= 4 mmol/L (46.1%) and is also increased in
severely septic patients with hypotension alone
(36.7%) and lactate >/= 4 mmol/L alone (30%)4.
History2:
It has long been recognised that puerperal
fe ver occu rre d in ep ide mics in ‘l yin g-in ’
(m a ternit y ) hos p itals . I n 186 7 Flor e nce
Nightingale was forced to close the lying-in ward
she had established at King’s College Hospital,
within 5 years of opening it because of excessive
rates of puerperal fever. The earliest recognition
that puerperal fever was contagious came from
Alexander Gordon’s ‘Treatise on theEpidemic
of Puerperal Fever’ in Aberdeen published in
1795.In America this observation was later
supported by Oliver Wendell Holmes’ 1843
pa p er ‘T he Contag i ousne s s of Pue r peral
Fever’.A significant contribution was made by
Igna z Semmelw eis worki ng at the Vien na
Maternity Hospital. He recognised that medical
students, who were attending post-mortems and
then labourin g women, wer e tra nsm itting
infection. In 1847 he introduced hand washing
using disinfectants, after which there was a
dramatic fall in the incidence of puerperal fever
from 18% to 1.27%.
A government-commissioned investigation
into maternal deaths in England published in
1937, found that sepsis accounted for 39% of all
deaths.In 1935 Leonard Colebrook, a physician
worki ng at Que en Charl otte’s Hospital in
London, gave the first sulphonamide, Prontosil,
to a woman who was severely ill with puerperal
sepsis and she made a full recovery.This event
heralded the introduction of antibiotics in the
treatment of puerperal sepsis2.
RISK FACTORS IN OBSTETRICS2:
Obstetric factors:
xAmniocentesis, and other invasive
intrauterine procedures
xCervical suture
xProlonged rupture of membranes
xProlonged labour with multiple (>5)
vaginal examinations
xVaginal trauma
xCaesarean section
xRetained products of conception after
miscarriage or delivery
Patient factors:
xObesity
xImpaired glucose tolerance/diabetes
xImpaired immunity
xAnaemia
xVaginal discharge
xHistory of pelvic infection
xHistory of Group B streptococcal infection
SOME DEFINITIONS:
Systemic inflammatory response syndrome
(SIRS) is a widespread inflammatory response
to a variet y of severe clinical insults. For
diagnosis it needs at least two of the following
signs and symptoms.
xTemperature >380C or <360C
xHeart rate >90 beats/min
xRespiratory rate >20 breaths/min or PaCO2
< 32 mmHg
Dr Aliena Sharon P, MD Student
Dr Joe John Chirayath MD, MRCA (London),FCARCSI (Ireland)*
Associate Professor,Department of Anaesthesiology
Amala Institute of Medical Sciences,Thrissur
* All correspondences to joechirayath@yahoo.co.in

33
xWhite blood cells >12 x 109/dL or <4 x 109/
dL or >10% immature (band) forms2
Sepsis is defined as the presence (probable or
documented) of infection together with systemic
manifestations of infection4. Thus sepsis is SIRS
and suspicion of new infection.
Severe sepsisis defined as sepsis with sepsis-
in d uced o rgan dysfu n ction or ti ssue
hypoperfusion.
Sepsis-induced hypotension is defined as a
systolic blood pressure (SBP) < 90 mm Hg or
mean arterial pressure (MAP) < 70 mm Hg or a
SBP decrease of > 40 mm Hg or less than two
standard deviations below normal for age, in the
absence of other causes of hypotension.
Sepsis- induced tissue hypoperfusion is defined
as hypotension persisting after initial fluid
challenge or blood lactate concentration e” 4
mmol/L.
Se ptic shoc k is de fine d as sepsis -ind uced
hypotension persisting despite adequate fluid
resuscitation4.
MANAGEMENT:
Th e Royal C olleg e o f Obs t e trici a ns and
Gynaecologists UK (RCOG) recommends that
se p sis s hould be ma n aged in a c corda n ce
withthe Surviving Sepsis Campaign (SSC)
guidelines2.
Surviving Sepsis Campaign: History and
perspective.
The Surviving Sepsis Campaign was launched
in 2002 as a coll ab orative initiative of the
European Society of Intensive Care Medicine
(ESICM), the International Sepsis Forum (ISF)
and the Society of Cri tical Care Med icine
(SCCM)with hopes that mortality rates will be
reduced by standardizing care. Its objective was,
through the development and promulgation of
evidence-based guidelines, to effect a 25%
reduction in the relative risk of death from severe
sepsis and septic shock5.
To be completed within 3 hours: 1) Measure
lactate level 2) Obtain blood cultures prior to
administration of antibiotics 3) Administer broad
spectrum antibiotics4) Administer 30 mL/kg
crystalloid for hypotension or lactate >/=4mmol/L
To be completed within 6 hours:5) Apply
vasopressors (for hypotension that does not
respond to initial fluid resuscitation) to maintain
a mean arterial pressure (MAP) >/=65 mm Hg 6)
In the event of persistent arterial hypotension
despite volume resuscitation (septic shock) or
initial lactate >/= 4 mmol/L (36 mg/dL): -
Measure central ven ous pressu re (CVP) -
Measure central venou s oxygen saturation
(ScvO2)7) Remeasure lactate if initial lactate was
elevated
(R e pro duc e d from Surv i ving Sep s is
Campaign:International guidelines for management
of severe sepsis and septi c shock:2012Crit Care
Med.2013 Feb;41(2):580-637)
Initial resuscitation:Goal-directed therapy4
a) CVP 8–12 mm Hg
b) MAP >/=65 mm Hg
c) Urine output >/= 0.5 ml/kg/hr
d) Superior vena cava oxygenation saturation
(Scvo2) 70% or mixed venous oxygen
saturation (SvO2) 65%.
Resuscitation targeting the physiologic goals
expressed in the recommendation above for the
initial 6-hr period was associated with a 15.9%
absolute reduction in the 28-day mortality rate4.
Diagnosis:
x Cultures, as clinically appropriate before
antimicrobial therapy, if there’s no significant
de l ay ( > 4 5 mi n s) i n t h e st art o f t h e
antimicrobial(s).
xAt least two sets of blood
cu l tures (b o t h a e r obic and
anaerobi c bottles) should be
obtained before antimicrobial
therapy with at least one drawn
percutaneously and one drawn
through each vascular access
device, unless the device was
recently (<48 hrs) inserted4.
The most common organisms
identified in pregnant women
dying from sepsis are Lancefield
gr o up A beta - haemol y tic
Streptococcus and E.Coli.Mixed
in fecti ons wit h both Gr a m-
po siti ve an d Gra m-ne gati ve

4
or ganis m s a re commo n , e speci a lly in
ch o rioam n ionit i s . C o lifor m in f ectio n is
particularly associated with urinary sepsis,
preterm premature rupture of membranes, and
cervical encerclage6
Antimicrobial therapy1:
xAdministration of effective intravenous
antimicrobials within the first hour of severe
sepsis.
xWhen a specific organism is identified,
antibiotic therapy can then be modiûed to
the most appropriate regimen.
xAntimicrobial regimen should be reassessed
daily for potential de-escalation.
Some suggested choices of initial empirical
intravenous antibiotic therapy in genital tract
sepsis are outlined below1.
Where the organism is unknown and the
woman is not critically ill:
xco - amoxi c l av 1 .2 g 8 - h ourly pl u s
metronidazole 500 mg 8-hourly or
xce f uroxi m e 1.5 g 8 - h ourl y p lus
metronidazole 500 mg 8-hourly or
xcefotaxime 1–2 g 6- to 12-hourly plus
metronidazole 500 mg 8-hourly
In cas es of all ergy to penicilli n and
cephalosporins, clarithromycin (500 mg twice
daily or clindamycin (600 mg to 1.2 g by
intravenous infusion three or four times daily)
plus gentamicin to give Gram-negative cover
are possible alternatives while waiting for
microbiological advice
In severe sepsis or septic shock (seek
urgent microbiological advice): Piperacillin–
tazobactam 4.5 g 8-hourly or ciprofloxacin
600 mg 12-hourly plus gentamicin (3–5 mg/
kg daily in divided doses every 8 hours by
slow intravenous injection).
A carbapenem such as meropenem (500 mg
to 1 g 8-hourly by intravenous injection over
5 minutes or by intravenous infusion) plus
gentamicin may also be added
Metronidazole 500 mg 8-hourly may be
considered to provide anaerobic cover
If Gr oup A strep t ococc a l i n f ectio n i s
suspected, clindamycin (600 mg to 1.2 g by
intravenous infusion three or four times daily)
is more effective than penicillin as it inhibits
exotoxin production
If there are risk factors for MRSA, add
teicoplanin 10 mg/kg 12-hourly for three doses
then 10 mg/kg 24-hourly or linezolid 600 mg
twice daily
Fluid therapy4:
Crystalloids are recommended as the initial fluid
of choice in the resuscitation of severe sepsis and
septic shock.
Albumin is suggested in the fluid resuscitation
of severe sepsis and septic shock when patients
require substantial amounts of crystalloids.
Initial fluid challenge in patients with sepsis-
induced tissue hypoperfusion with suspicion of
hypovolemia to achieve a minimum of 30 ml/kg
of crystalloids (a portion of this may be albumin
equivalent). More rapid administration and
greater amounts of fluid may be needed in some
patients.
Hydroxyethyl starches are not recommended for
fluid resuscitation.
Vasopressors & inotropes4:
No r epine p h rine (N E) is the firs t c h o ice
vasopressor.
Epinephrine (added to and potentially substituted
for norepinephrine) when an additional agent is
needed to maintain adequate blood pressure.
Vasopressin 0.03 units/minute can be added to
NE with the intent of either raising MAP or
decreasing NE dosage.
All patients requiring vasopressors should have
an arterial catheter placed as soon as practical if
resources are available.
A tria l of dobu t amine inf u sion up to 20
micrograms/kg/min may be administered or
added to the vasopressor in the presence of
myocardial dysfunction, as suggested by elevated
cardiac filling pressures and low cardiac output
or on-going signs of hypoperfusion, despite
achieving adequate intravascular volume and
adequate MAP.
Supportive therapy:
Corticosteroids4,7,8 :
If adequate fluid resuscitation and vasopressor
therapy are not able to restore hemodynamic
stability,intravenous hydrocortisone at a dose of
200 mg per day as a continuous infusion is
recommended.
In treated patients hydrocortisone is tapered when
vasopressors are no longer required.
Blood products4:
Once tissue hypoperfusion has resolved and in
the severe hypoxemia, acute haemorrhage or
is c hemic heart disea s e , a r ed bl o od ce l l

5
transfusion should be given only when the
haemoglobin concentration decreases to <7.0 g/
dl, to target a haemoglobin concentration of 7.0
–9.0 g/dl in adults.
Fresh frozen plasma should not be used to correct
laboratory clotting abnormalities in the absence
of bleeding or planned invasive procedures.
In patients with severe sepsis, administer platelets
prophylactically when counts are<10,000/mm3
(10 x 109/L) in the absence of apparent bleeding.
Prophylactic platelet transfusion should be
considered when counts are < 20,000/mm3 (20
x 109/L), if the patient has a significant risk of
bleeding. Higher platelet counts of >/= 50,000/
mm3is advised for active bleeding, surgery, or
invasive procedures.
Glycaemic state4:
A protocolized approach targeting an upper blood
glucose of </= 180 mg/dl rather than </=110 mg/
dl, with an insulin infusion, if needed.
Blood glucose values should be monitored every
1–2 hrs. until they are stable and then every 4
hrs thereafter.
Renal replacement therapy4:
Continuous renal replacement therapies and
in t ermit t e nt ha emodi a l ysis are eq ually
efficacious in patients with severe sepsis and
acute renal failure, provided that the patient is
haemodynamically stable enough to tolerate the
dialysis.
Nutrition4:
Oral or enteral feeds as early as possible.
Use intravenous glucose and enteral nutrition
rather than total parenteral nutrition (TPN) alone
or parenteral nutrition in conjunction with enteral
feeding in the first 7 days after a diagnosis of
severe sepsis/septic shock.
Deep Vein Thrombosis(DVT) prophylaxis4:
Daily subcu tan eou s low-m olecular weight
he par in (LMWH) is nee ded .If creati nine
clearance is <30 mL/min, use dalteparin or
another form of LMWH that has a low degree of
renal metabolism.
Patients with severe sepsis be treated with a
combination of pharmacologic therapy and
intermittent pneumatic compression devices
whenever possible.
Ventilator Associated Pneumonia (VAP)
care bundle:
1 Seda tion revi ewed and, if appro pri a te,
stopped each day
2 Patient assessed for weaning and extubation
each day
3 Avoid supine position. Aim to have the head
of bed elevated to at least 30°
4 Use chlorhexidine as part of daily oral care
(0.12-2.0% applied 6-hourly).
5 Use subglottic secretion drainage in patients
likely to be ventilated for more than 48 hours9.
6 Pharm a copro p h ylaxi s agains t venous
thromboembolism (VTE)4,10,12
7 Stress ulcer prophylaxis4,10,11,12
INFECTION PROPHYLAXIS IN
OBSTETRICS1:
Routine antenatal antibiotic prophylaxis with
erythromycin 250 mg orally 6-hourly for 10 days
is recommended in women who have PPROM
before 37 weeks of gestation.
For prelabour rupture of the membranes at term
(i.e. after 37 weeks of gestation), if there is
evidence of infection, a full course of broad-
spectrum intravenous antibiotics should be
prescribed.
Women having a caesarean section should be
offered prophylactic antibiotics, such as a single
parenteral dose of first-generation cephalosporin
or ampicillin, to reduce the risk of postoperative
infections.
Broad-spectrum antibiotics are recommended
following obstetric anal sphincter repair (third-
and fourth-degree tears) to reduce the incidence
of posto p erati v e infe c tions and wo und
dehiscence.
RECENT ADVANCES
Given that a high proportion of critically ill
patients have systemic inflammatory response
syndrome (SIRS) , the ability to accu rately
distinguish between SIRS and sepsis has become
one of the holy grails of medicine. It is therefore
unsurprising that there has been considerable
interest, debate and, sometimes, argument over
the last two decades rega rdi ng the use of
biomarkers to achieve this goal.
Procalcitonin (PCT)13,14:
PCT is a precursor of the hormone calcitonin and
is synthesized physiologically by thyroid C cells.
In normal physiological conditions, PCT levels
in the serum are low (0.1 ng/mL). However, in
bacterial infection PCT is synthesized in various
extra thyroidal neuroendocrine tissues and so
cause the highest rises in PCT. In bacterial
infections, serum PCT levels start to rise at 4 h

66
after the onset of systemic infection, and peak at
between 8 and 24 h.If all microbiological cultures
are negative and a clear source of infection has
not declared itself by 24 h, a repeat low PCT
combined with clinical judgement, provides a
strong argument for discontinuing antimicrobial
th e rapy and search i n g fo r an alter n ative
diagnosis13.
Procalcitonin to Reduce Antibiotic Treatments
in Acutely ill patients (PRORATA) trial was a
large multicentre randomized control trial aimed
at establishing the effectiveness of an algorithm
based on procalcitonin to reduce unnecessary
antibiotic exposure in critically ill patients with
su s pecte d se p sis. A pr o c alcit o nin-g u i ded
antibiotic strategy will help the physicians to
start, continue, or stop antibiotics once the PCT
level declines below a certain cut-off point or
reduces to a certain percentage of its initial value.
(1’!3)-â-D-glucan assay15,16:
The culture independent serum (1’!3)-â -D-
glucan (BG) detection test may allow early
diagnosis of invasive fungal disease15. A single
point BG assay based on a blood sample drawn
at the sepsis onset, alone or in combination with
candida score(CS), may guide the decision to
start antifungal therapy early in patients at risk
for candida infection16.
Mannan antigen (Mn) and anti-mannan
antibodies (A-Mn)17:
Timely diagnosis of invasive candidiasis (IC)
remains difficult as the clinical presentation is
not specific and blood cultures lack sensitivity
and need a long incubation time. Thus, non-
culture-based methods for diagnosing IC have
been developed. On the basis of the literature
review, Mn antigen and A-Mn antibody offer
diagnostic help in patients with suspected IC17.
Intravenous immunoglobulins (IVIG)4,6:
IV I G is sugg e s ted f or se v ere i n vasiv e
streptococcal or staphylococcal infection if other
therapies have failed. IVIG has an immune
modulatory effect, and in staphylococcal and
streptococcal sepsis it als o neut ralis es the
superantigen effect of exotoxins, and inhibits
production of tumour necrosis factor (TNF) and
interleukins. High dose IVIG has been used in
pregnant women and is effective in exotoxic
shock (i.e. toxic shock due to streptococci and
staphylococci) but with little evidence of benefit
in gram-negative (endotoxin related) sepsis6. But
as per the SSC guidelines, IVIG is not still
recommended for the treatment of severe sepsis
and septic shock4.
Modified Early Obstetric Warning System
(MEOWS)18:
The development of early warning systems from
simple bedside observation charts arose from the
knowledge that physiological abnormalities
precede critical illness.The triennial Confldential
En q uiry i nto Ma terna l and Ch ild Health
(CEMACH) report recommends the routine use
of the modified Early ObstetricWarning System
(MEOWS), which is an early warning system
adapted for the obstetric population.In its current
state, the chart has high sensitivity and reasonable
speciûcity.
CONCLUSION:
Sepsis in the obstetric population in early stages
is often clinically masked due to the many
physiological changes that happen at the time.
We should thus have constant vigilance; prompt
recogn ition and mana gement strategies, to
prevent this serious disease with such deadly
outcomes to the person, family and community.
REFERENCES:
1) Ce ntr e for Mate rna l and Chil d Enqu iri es
(CMACE). Saving Mothers’ Lives: Reviewing
maternal deaths to make motherhood Safer:
2006–2008. The Eighth Report on Confidential
Enquiries into Maternal Deaths in the United
Kingdom. BJOG 2011;118(Suppl. 1):1–203.
2) Lucas D N,Robinson P N,Nel M R. Sepsis in
ob s tetr i cs an d t he ro l e of th e
anaesthetist.InternationalJournal of Obstetric
Anesthesia 2012; 21: 56–67
3) Paily VP, Ambujam K, Rajasekharan Nair V,
Thomas B. Conûdential Review of Maternal
Deaths in Kerala: a country case study. BJOG
2014; 121: (Suppl. 4): 61–66.
4) Dellinger RP1, Levy MM, Rhodes A, Annane
D, Gerlach H, Opal SM, Sevransky JE, Sprung
CL , Do u glas IS , Jae s chk e R, Osbo r n
TM, Nunnal ly ME, Townsend SR, Reinha rt
K, K le inp el l RM, A ngus DC , Deu tsc hm an
CS , Ma c hado FR , Rub e nfel d GD , Web b
SA, Beale RJ, Vincent JL, Moreno R; Surviving
Se p sis C a mpa i gn Gu i deli n es Co m mitt e e
including the Pediatric Subgroup.Surviving
sepsis campaign: international guidelines for
management ofsevere sepsis and septic shock:
2012 Crit Care Med. 2013 Feb;41(2):580-637

77
Introduction:We, Obstetricians regularly do
artificial ruptur e of membranes(ARM) and
observe the color and turbidity of amniotic
fluid(AF). Sometimes the liquor looks watery,
milky, buttermilk like or curdy. This color &
turbidity of AF is having correlation with fetal
functional maturity and onset of spontaneous
labor.
Observation: Prematurity was associated with
less turbid watery liquor. Optimally mature
babies were associated with milky or buttermilk
like liquor. Post maturity, sometimes dysmaturity
was associated with curdy liquor1.
Stud y : Obser v ation a l stud y i nvolv i ng360
uncomplicated singleton pregnant women whose
dates were confirmed by first trimester scan for
CRL and who were in spontaneous labor. Medical
di s order s com p l icati n g pr e gnanc y wer e
excluded1.
Sa m ple col l e ction : AF sa m p les we r e
collectedwhile doing LSCS, and while doing
amniotomy.
Measuring the Color and turbidity of AF:
Color and turbidity of fresh uncentrifuged AF
sampleswere measured in terms of Optica l
Densit y at 650n mwith a simple laborator y
colorimeter (CostsRs.7000/- only). This is what
we call as Amniotic Fluid Optica l Density
(AFOD). This procedure hardly takes 5minutes.
Babies were evaluated for functional maturity in
terms of respiratory distress (RDS), color of the
skin, and adherence of vernix caceosa on skin
surface at birth. Birth
weights andgestational
age at delivery were
also recorded. Informed
consent was obtained
from all women who
pa r t icipa t ed in t h is
study1.
The colour & turbidity of fresh uncentrifuged AF
was measu red in term s of Optica l Density
(AFOD) at 650nm with colorimeter.
Results:
Gestational age at Delivery.
360 spontaneous labors were spread widely from
35wks to 41wks, within 95% CI (249 to 288
days).
The mean GA at spontaneous labor was found to
be 38wk 3ds ±7days.Maximum number of
deliveries (82%) occurred between 37 to 40wks.
11% womendelivered after 40wks. 7% women
delivered before 37wks. Only 2.28% women
delivered on EDD (280) by Naegle’s rule.
360 Spontaneous labours were spread widely
from 35wks to 41wks. 95% CI(249 to 288 days).
The mean GA at spontaneous labor: 38wk 3ds
±7days
AFOD and functional maturity of the new
born.
The Mean AFOD at the onset of spontaneous
labor was found tobe 0.98±0.27.
At this AFOD value all the babies were fully
functionally mature and none of them developed
RDS.
DR.H. SAMARTHA RAM
Consultant Obstetrician and Gynaecologist.
Sandhyaram Hospital, Katampazhi puram, Palakkad, Kerala Pin: 678633
drsamartharam@gmail.com 09447737327
Histogram
Mean =272.01
Std. Dev=7.595
N=352
Innovative Thinking
contd.to pg 10

8
QUALITY STANDARDS training the trainers
KFOG management committee meetings
Dr Betsy Thomas – Kamini Rao oration
Dr Samarth Ram.H – C S Dawn prize
Dr Reshma Sajan – Dr.Amarendhranath Dan prize
Congrats
winners AICOG 2015
8

99

1010
But, this AFOD 0.98± 0.27, completion of fetal
functional maturity, and onset of spontaneous
labor, which all went together, occurred at any
time from 36wks to 43wks. In other words, babies
attained completion of functional maturity and
goes for spontaneous labourat any time from
36wks to 43wks, indicating2‘Individual Term
for Each fetus’.
All the babies born with AFOD around 0.98 were
functionally mature, and none of themdeveloped
RDS irrespective of GA (gestational age)& B.W
AFOD and functional prematurity of the
new born.
Babies born with AFOD < 0.40 were functionally
premature and developed varying degrees of RDS
irrespective of GA andbirth weight.
Babiesborn remote from term with AFOD value
< 0.40 developed severe RDS of longer duration.
Babies born towards term with AFOD value
< 0.40 developed milder RDS of shorter duration.
To sum up these observations a baby can be fully
functionally mature even at 35+wks GA if AFOD
is around 0.98. On the other hand a baby can be
functionally premature even at 40+wks if AFOD
is < 0.40.
Babies born with AFOD <0.40 were functionally
premature and developed varying degrees of RDS
irrespective of GA & B.W
At a cross section of any G.A it is possibleto
observe all scenarios of functional maturity.
Red dots: functionally mature babies delivered
at different GA, with AFOD around 0.98.
Bl ue dots : funct i onal ly prem ature babies
delivered at different GA, with AFOD <0.40.
Blue circle: Functional prematurity. Red circle:
optimal maturity.Green circle: post-maturity
Discussion:
The physiology of onset and progression of
labour is undoubtedly multi factorial involving
various rate limiting complex sequential inter
related and mutually supportive cascades1.
Narendran V, et al reportedthe concept of lung
skin interaction3.Amniotic fluid surfactant
lecithin is produced by fetal lungs. Letner C et.al,
reported that rapid surge like raise in AF lecithin
occur few days before the onset of spontaneous
labor4. Narendran V, et al reported that, this
raising level of A.F lecithin,causes the induction
of verni x deta c hmen t from the fet al ski n
surfacewhich is the primary factor leading to
progressive increase in AF turbidity3.
S. Ram et.alreported,AFOD surge coincide
wi t h th e o n s et o f sp o ntane o us l a bor2.
Rapid and progressive surge like raise in amniotic
fluid lecithin induces rapid and progressive
detachment of vernix from foetal skin surface,
which get mixed with AF resulting in rapid surge
li k e raise in AFO D (color an d turbi d ity)
coinciding the onset of spontaneous labour. The
contd.from pg 6

1111
duration of surge was found to be 8-10days2.
Si mila r rai se in ma ny biolog ical ly act ive
substances which participatein the process of
spontaneous labourlike, serum hyaluronic acid,
amniotic fluid L/S ratio, AF macro score were
reported by different authors5.
There was a slow and prolonged raise in AFOD
till a val ue around 0.4 0was reached . After
attaining this value, there was a surge like raise
in AFOD which coincided with the onset of
spontaneous labor (N=12).
Mazzucchelli et.al reportedHuman amniotic
fl u id cell s can pro duce pr o
labourcytokineslike IL-6, IL-8, IL-1 beta,
EGF6.
The exact mechanism of onset of spontaneous
labourwhich results due to pro labour cytokine
rich vernix detachment into AF has to be further
explored.
The concept of individualized term for each
foetus is having a significant impact in obstetrics.
A preterm baby at 35+wks gestation can be fully
functionally matureand do not develop RDS, if
the AFOD value is around 0.982. On the other
ha nd, a te rm baby even at 40wks ca n be
functionally premature and develop RDS(term
RDS)2 if the AFOD value is <0.40.
A foetus which completes maturation as early as
36wks(early maturer) becomes post mature or
dysmature (idiopathic IUGR and IUFD) by
37+wks, if labour does not start for some reason.
On the other hand a foetus destined to complete
maturation by 42wks (de lay ed matu rer ), if
delivered at 40wks, it becomes premature by
2wks and develop RDS (term RDS)7.This could
be the reason for ACOG8 and RCOG9 guidelines
recommending confirmation of lung maturity
before 38wks+6days gestation for induction of
labour or elective caesarean sections.
Induction failures even at 40wks gestation could
be due to functionally unprepared uterus (labour
cascades are not established) with functionally
premature babies.
The definitions of preterm, term, post-term, and
post-dated pregnancies are made by obstetricians
for clinical convenience. Nature does not have
these definitions. Nature’s philosophy is only to
push the baby out whenever the baby is fully
functionally mature and fit to survive outside6
Conclusions: There is individual term for each
fetus. Babies can be fully functionally mature
even at 36wks gestation if AFOD around 0.98.
Babi es can be funct ion ally premature and
de v elop RD S ev en at 40wk s gestat i on if
AFOD<0.40. There is definite surge like raise in
AFOD with the onset of spontaneous labor. The
duration of surge is found to be 8 to 10days,
during which time preparations for spontaneous
labor take place. Further research in this area will
help us to solve many problems like induction
of labor,preterm labor, and atonic PPH. Under
the light of this scientific information there is
every need to review and redefine the concept of
term pregnancy.
xThis scientific information was first published
in Calicut Medical Journal.
x Republished as an invitation article in Dr.
Pankaj Desai website.
x Awarded Dr. C.S. Dawn prize (first prize) at
AICOG Varanasi.
x First dissertation on this subject was done at
Andhra Medical College Visakhapatnam-AP.
xCurrently one more dissertation is going on
at Guntur Medical College- AP.
References:
1. Ram S et al, A mniotic fluid optical density at spontaneous
onset of labor and its correlation with gestational age,
birth weight, functional maturity and vernix caseosa of
new born. Calicut Medical Journal 2009;7(4)Vol 7 Issue
4 2009www.calicutmedicaljournal.org/2009/4/e2.pdf
2. Samartha Ram. H, D. Sandhya, Individualized Term for
Each Fetus: From Surge in Amniotic Fluid Optical
Density (AFOD). Internet Journal of Gynecology&
Obstetrics; 2014, Vol. 18 Issue 1, p1.
3. Narendran V et.al, Interaction between Pulmonary
Surfactant and Vernix: A Potential Mechanism for
induction of Amniotic Flu id Turbidity. J Pediatric
Research 2000; 48:120-124.
4. Lentner C .Scientific Tables. New Jersy: Medical
Education Division ,Ciba Geigy Corporation; 1981
5. Samartha Ram. H, Shankar Ram SR,. Sandhya S,
Individual Term for Each Fetus: with Surge in Amniotic
Fluid Optical Density. BJOG, An international Journal
of Obstetrics and Gynecology: Volume 121, EP7.99,
Issue supplement S2
6. Mazzucchelli I, Avanzini MA , Ciardelli L,Pagani S,Greco
R,Belloni C,Castellazzi AM,Marconi M,Rondini G,Polatti
F. Human Amniotic Fluid cells are able to produce IL -
6 and IL- 8. AmJReprodImmunol . 2004 ; 51 :198-203
7. Samartha Ram H, Shankar Ram HS, et.al, Role of
Amniotic Fluid Optical Density (AFOD) and Low dose
Isox sup rin e Hcl rap id in fusion toc oly sis for the
management of PTL. IOSR Journal of Dental and
Medical Sciences (IOSR-JDMS) Volume 13, Issue 11
Ver. III (Nov. 2014), PP 09-14
8. A COG Practi ce b ulleti n. C linica l ma nage men t
guidelines for obstetrician-Gynecologists. Number 97,
September2008.
9. Royal College of Obstetricians and Gynecologists,
Antenatal Corticosteroids to Reduce Neonatal Morbidity
and Mortality .Green-top Guideline No. 7. October 2010.

1212
Infertility is a personal problem with lot of
family and social implications. The diagnosis and
treatment of infertility has gained much importance
because of increase in the number of infertility
couples and their awareness. The advances in
treatment facilities have increased the number of
patients attending the clinics. Increased age of
marriage, voluntary infertility practiced by the
upper class of patients and absentee husbands are
the main contributory factors responsible for the
decrease in fertility.
Normal Fecundity (pregnancy expected per
cycle in a healthy couple) in a cycle is only 15-20
%; h ence the infertilit y investigation may be
delayed up to one year. But in special situations
like late marriages, or when there is a known
problem in a couple, investigation and treatment
can be started early.
In a normal female, eggs are produced from the
ovary in the middle of the menstrual cycle. During
sexual act the sperms are deposited in the vagina,
which travel through the cervix, uterine cavity and
meets the egg to fertilize in the tube. Embryo
formed after fertilization travels through the tube
into the uterus and gets implanted in the uterine
cavity and grows to a full term baby. Anything
that interferes with these normal physiological
events can cause infertility, like
1. Defective ovulation
2. Problems with spermatozoa
3.Problem with transport of gametes
4. Defective implantation
5. Sexual problems
6. Unexplained infertility
Though it was ignored for a long time, male
fact or is now cons idere d as the sin gle most
important cause for infertility. Either the sperms
cannot be produced in sufficient amount, or if at all
produced they are not normal. Even if normal they
get blocked in male genital
tract or male has some sexual
problems, which interferes
wi t h eja c u lati o n and
deposition of sperms in to the
vagina. In extreme cases
where the sperm production
is not possible for the male
there is no treatment. Many
ot h er cau s e s of mal e
in fer til ity can be trea ted
medically or by various surgeries. When there is
no r e spon s e t o t hese t r eatm e nts ad vanc e d
te c hniq u es know n a s I UI (Int r aute r ine
Insemination), ICSI (Intracy toplasmic Sperm
Injection) has helped many couples to parent a child.
Ovulation problem is the second most important
cause of infertility and most common cause of
female infertility. In 90% of the cases ovulation
problem is due to polycystic ovarian syndrome.
Rarely it may be due to increase in hormones like
prolactin or decrease in hormones like Thyroid,
FSH and LH or abnormal levels of different
hormones. Typical pattern in the PCOS may present
with an irregular or prolonged period, obesity and
increased hair growth, multiple small cysts in the
ovary in ultrasonography or may not have all the
above features. Because PCOS is multi factorial
in origin the response to treatment also varies from
patients to patients. Treatment options for PCO in
infertility vary from ovulation induction, ovarian
drilling or ART. From simple tablets to costly
hormon e inje ction or surgi cal treatment like
laparos co pic surgery to assisted reproductive
techniques like IVF / ICSI may be necessary in
these group of patients. A small group of patients
may not respond to any treatment at all. A woman
with normal menstrual cycles should not be labelled
as a case of anovulation problem.
Endometriosis: Is one of the common causes
of infertility in females especially in our part of the
world. In this disease uterine lining cells are found
in sites other than uterus and there will be cyclical
bleeding from these sites during menstruation. This
blood cannot go out of the body, which may lead to
adhesion of these structures. This commonly occurs
in ovaries, tubes and around the uterus, leading to
painful menstruation. It also destroys the normal
anatomy and affect normal ovulation. Also it affects
transport of ovum through tubes there by preventing
fertilization. Many a time diagnosis is possible by
ultrasound, but sometimes can be diagnosed only
by laparoscopy. The best treatment now available
is laparoscopic surgery, but again few cases may
end up in IVF, ICSI treatment.
Different causes like pelvic infection may
produce tubal block and adhesions. Isolated tubal
HOW TO APPROACH YOUR
FERTILITY PROBLEMS
Dr. FESSY LOUIS. T
Consultant, IVF- Coordinator
CIMAR Fertility Center Cochin

1313
block in the proximal part of tube and adhesions
can be treated with laparosc opy or may need
laparotomy, otherwise they will conceive only with
IVF/ICSI
Hydrosalpinx is a condition in which there is
collection of fluid inside the tube resulting in tubal
block. If there is bilateral hydrosalpinx only 10-
20% of patient will get normal conception after
su rge r y. Rema i nin g patie nts ma y need IV F
treatment. Tubal block secondary to tuberculosis
has only IVF as treatment option. Sexual problem
is an important cause of infertility. But fortunately
most of the cases can be treated with psychological
counselling.
Di a gnos t ic Pr oced u res: Dram a tic
developments in the field of science have helped
to diagnose and treat infertility in a more scientific
manner. Semen analysis is the integral part of
infertility investigation. Interpretation will be
sensible only when it is done by a reliable lab. In
addition to count and motility, morphological
staining may be done as a routine part of semen
analysis. Endocrine studies has helped to diagnose
most of anov ulatory infert il ity. Transvaginal
ultrasound can be used as a diagnostic tool for most
of problems related with female infertility. And it
also helps in the treatment monitoring. Perhaps that
is the only non-invasive weapon by which we can
judge the quality of endometrium. Also it can
diagnose the tubo ovarian pathology.
In t rodu c tion o f Hys t ero laprosc o py ha s
revolutionized the treatment of infertility. It is
considered as a gold standard for diagnosis of
certain infertility conditions. It is the last option to
treat most of the surgical problems related to
infertility.
Tre atme n t Op t ions : In t ra U t erin e
Insemination (IUI) is a very simple treatment, which
can increase the fertility rates in a sub fertile couple.
The concentrated good quality sperms, separated
from the toxic contents are deposited into the upper
part of uter us, at the tim e of ovu latio n in a
stimulated cycle. Unexplained infertility, cervical
hostil ity, poor spe rm cou nt are the accep ted
indications for IUI. But unless it is done with all
precautions, by itself it can cause pelvic infection.
Test Tube Baby Treatment (IVF& ICSI) -
Bi r th of Lo u ie Brow n in 1978 by Ass i sted
reproductive Technique (Infertility treatment in
which both the egg and sperm are handled outside
the bod y) was an impor tant lan dmark in the
treatment of infertility. It was done on a patient
with tubal block, which could not be corrected by
surgery. Till then there was no treatment for such a
condition. Later this was done for indications like
un e xpla i n ed in fert i l ity, pe lvic a dhes i ons,
endometriosis, PCOS and moderate OAT.
But unfortunately there was no treatment for
severe OAT, obstructive azoospermia and in many
cases of fertilization problem. Another landmark
in infertility treatment was the birth of a baby born
in 1992 with ICSI (Intra Cytoplasmic Sperm
Injection). Here a single sperm was injected into
egg resulting in fertilization and embryo formation.
In ICSI only one sperm was sufficient to produce
an embryo. Most of the male problem could be
co rre cted by thi s meth od. Co mpa red to the
conventional IVF, fertilization failure is minimal
and it could give better pregnancy rates. Now most
of the couples for IVF treatment are treated by ICSI.
Advances in infertility techniques: Even with
all modern treatments ultimate pregnancy rates with
ART is about 30%. Many advanced techniques have
come up in the field of ART to improve the success
rate. Many of these are available in India.
Laser : This technique has improved the ICSI
procedure by immobilization of sperm, zona drilling
of embr yo. Zona drilling facilitate s As si sted
Hatching, which improves the pregnancy in elderly
females and in repeatedly failed cases.
Blastocyst Culture : In this technique if there
are facilities like triple gas incubators and special
medias, embryos can be grown upto blastocyst stage
outside the body before inserting back into uterus.
This may help to select best embryos which help to
reduce multiple pregnancy, improve pregnancy
rates, reduce maternal and foetal morbidity and
mortality during treatment.
PGD (Pre Implantation Genetic Diagnosis):
This is the most rec en t development in ART
treatment. The idea is to identify the euploid
embryos before it is transferred to mother. It has
the potential to identify and exclude the embryos
wi t h an e uplo i dy an d va riou s chr o moso m al
anomalies like Down syndrome. Once this is fully
established, it can improve the success of treatment
in many patients.
IMSI: In this technique we identify the sperms
without vacuoles and morphologically normal
sp e rms b y m a gnif y ing t h em usin g s p ecia l
equipments and using them for ICSI in patients with
repeated ART failures.
Cryopreservation: Is the process of storing
sperms, oocytes and embryos in liquid nitrogen for
many years. If there are excess embryos or oocytes,
they can be cryopreserved and can be used in the
subsequent cycles, which in turn increases the
cumulative pregnancy rate and decreases the overall
cost of IVF treatment.
Conclusion : Any couple looking for infertility
treatment, it is better they have a basic knowledge
about infertility and available investigative and
treatment options. This will help the couples to
approach the treatment more confidently.

14
FIGO Ovarian Cancer Staging
Effective Jan. 1, 2014
STAGE II: Tumor involves 1 or both ovaries with pelvic extension
II A
II B
II C
Extension and/or implant onuterus and /or
Fallopian tubes
Extension to other pelvic intraperitoneal
tissues
IIA or IIB with positive washings/ascites.
II A
II B
OLD NEW
Extension and/or implant on uterus and/or Fallopian
tubes
Extension to other pelvic intraperitoneal tissues
**Old stage IIC has been eliminated**
IA
Tumor involves both ovariesotherwise like IA.
STAGE I: Tumor confined to ovaries
OLD NEW
Tumor limited to 1 ovary, capsule intact, no tumor
onsurface, negative washings/ascites.
IB
IC Tumor involves 1 or bothovaries with any of
thefollowing: capsule rupture, tumor on surface,
positivewashings/ascites.
IA
IB
IC Tumor limited to 1 or both ovaries
IC1
IC2
IC3
Tumor limited to 1 ovary,capsule intact, no tumor
onsurface, negative washings.
Tumor involves both ovariesotherwise like IA.
Surgical spill
Capsule rupture before surgery or tumor on ovariansurface.
Malignant cells in theascites or peritoneal washings.
STAGE III: Tumor involves 1 or both ovaries with cytologically or histologically confirmed spread to the
peritoneum outside the pelvis and/or metastasis to the retroperitoneal lymph nodes
OLD NEW
Microscopic metastasis
beyond the pelvis.
IIIA
Macroscopic, extrapelvic,
peritoneal metastasis d”
2 cmin greatest dimension.
IIIB
Macroscopic, extrapelvic, peritoneal
metastasis > 2 cm in greatest dimension
and/ or regional lymph node metastasis.
IIIC
IIIA ( Positive retroperitoneal lymph nodes and
/or microscopic metastasis beyond the pelvis)
Positive retroperitoneal lymph nodes only
IIIA1
Metastasis d” <10 mm
IIIA1(I)
IIIA1(II) Metastasis d” >10 mm
Microscopic, extrapelvic (above the brim) peritoneal
involvement ± positive retroperitoneal lymph nodes
IIIA2
Macroscopic, extrapelvic, peritoneal metastasis d” 2
cm ± positive retroperitoneal lymph nodes. Includes
extension to capsule of liver/spleen.
IIIB
Macroscopic, extrapelvic, peritoneal metastasis > 2
cm ± positive retroperitoneal lymph nodes. Includes
extension to capsule of liver/spleen.
IIIC
STAGE IV: Distant metastasis excluding peritoneal metastasis
OLD NEW
IV Distant metastasis excluding
peritoneal metastasis. Includes
hepatic parenchymal metastasis.
Pleural effusion with positive cytology
IVA
Hepatic and/or splenic parenchymal metastasis, metastasis
to extraabdominal organs (including inguinallymph nodes and
lymph nodes outside of the abdominal cavity)
IVB
(Changes are in italics)
Other major recommendations are as follows:
Histologic type including grading should be designated at staging Primary site (ovary, Fallopian tube or peritoneum) should be
designated where possible
Tumors that may otherwise qualify for stage I but involved with dense adhesions justify upgrading to stage II if tumor cells are
histologically proven to be present in the adhesions
Onco Corner

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