Philippine 0bstetrical and Gynecological

Society (Foundation), lnc.

CtINICAI PRACTICE GUIDETINES

on
DIABETES MELTITUS IN PREGNANCY

Second Edition

November 2011
[D \\.{fVER OF RESPONSIBILITY
Historical Background ...................... 1
Dr Virgilio B. Castro
ru-:, :.:s (CPG) on Diabetes Mellitus in
!r ,'- i1. II Epidemio1ogy................. ...................4
Dr. Valerie T. Guinto
nr - l:sietrical and Gynecological Society III. Normal Glucose Metabolism in Pregnancy ........... 6
Dr. Sol M. Pangan

$ ,.:e:s. and its entire membership. IV Maternal and Fetal Complications .............. ....... 1l
Dr Ma. Victoria V Torres
::1.-titioner, the patient, the student, V. Diagnosis and Classification.......... .....................23
. :raiter. any capacity of the person Dr. Ernesto S, Uichanco and Dr. Ma Cristina P. Crisologo
:'=: :o. or acknowledge, any, or part, YI Screening and Detection ............... .....................21
,-:: Jiagnostic condition or idea/s Dr. Walfrido W Sumpaico and Dr. Angelita R. Teotico
:: ::.1 responsibilities of the POGS,
: -:i :he Committee on the Clinical u-II Management Issues: Pregestational and Gestational Diabetes Mellitus
A. Preconception Evaluation and Prevention .............
'." .:r an)' or all clinical or other ..........39
Dr Marjorie L Santos and Dr Mo Victoria V Torres
-': -rltroversies, case discussions/
B. AntepartumManagement
1. Blood Glucose Management
', - -:-r, case as a distinct and unique a. Nutritional Management ................. .................... 46
::, .\act location if reference is Dr. Cecilia C, Santos-Acuin

b. Blood Glucose Management........ 50

Dr. Nemesio A. Nicodemus
' )-:\'e as a guide, to clarify, to
-':-r --m or objective of this CPG 2. Antepartum Fetal Surveillance.......... ......54
Dr Pilar T. Lagman-Dy
- - :. and treatment for clinical
--:r:'J :o refer to the individual C. Intrapartum Management
-:
-: j; ::t question, not this CPG. 1. Intrapartum Glucose Management 63
Dr. Nemesio A. Nicodemus

2. Intrapartum Fetal Monitoring, Timing and Mode of Delivery ........ 66

: .': :.r :he discovery of clinical Dr Rosa Ninez B. Velante
. :: --rr"'ef\'.
D. Postpartum Management: Short and Long Term Considerations.......... 75
Dr. Susan T. Nagtalon and Dr. Brenda Bernadette B. Zamora
: -- -:rnittee on The Clinical
-...; e ach one of us a perfect III. The Infant of Diabetic Mother ......... 86
Dr. Jose B. Salazar

IX Summary of Recommendations .92

X Appendix
;s$ .......106
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 HISTORTCAL BACKGROUND
Virgilio B. Castro, MD

Diabetes mellitus is undoubtedly of ancient origin. The first systematic

:escription was written by Aretaeus of Cappadocia in Asia Minor, probably in
:he flrrst century AD. He described the excessive thirst and the constant need to
;rinate, dry mouth, parched skin and lost of weight, and interpreted the disease as
melting down of the flesh into the urine". This derives from the Greek meaning
ro pass through." The ancient Hindu Vedas, however, include information
:ttributed to Susruta) which shows that many cenluries earlier than Aretaeus,
-:rdian physicians were familiar with the fact that ctiabetic urine is sweet. The
:iveet taste was associated with glucose in the i8'h century. The discovery of Von
).{ering and Minkowski, in 1889, that pancreatectomy causes a metabolic disorder
-:ke that of spontaneous diabetes mellitus, followed by the discovery of insulin by
Santing and Best in 1921, leci to the conclusion that diabetes mellitus is a result of
::sulin deficiency. This point of view proved too simple when it was shown that
,-','eractivify of the adrenal cortex, the anterior pituitary and the adrenal medulla
--.:uld all produce a diabetes mellitus-like syndrome. More recently, the discovery
iat many diabetics have appreciable amounts of insulin in their pancreas and
:,asma has led to the hypothesis that resistance to the effect of insulin may be
::sponsible for the disease.

Prior to the 20th century, pregnancy in a woman with diabetes mellitus

:rrtended death of mother, fetus, or both. An early review of diabetic pregnancies
:'.' Duncun in 1882 reported the survival of only l0 of 22 newborns and death
'.rithin 5 years of delivery of 9 of 15 of their mothers. Only l0 children survived,
:rd only 6 of the patients were alive at l-year delivery. Joslin (1916) chronicled
ieven pregnant women with severe insulin-dependent diabetes mellitus, 5 of
-.'.hom died of diabetic complications. Later descriptions of diabetic pregnancies
:r Craigin and Ryder (1916), Delee (1920), and Williams (1925) reported an
-.r'erall 30% incidence of abortion and premature labor, stillbirth in over 50oh, and
:nflant death in about 74oh.

Before the discovery of insulin, the only method of treatment of diabetes

nellitus was a general hygienic approach to life, including diet and exercise.
''\'ith the discovery of insulin in 1921 by Banting and Best, treatment in
Jiabetes mellitus became both more specif,rc and more successful. Early insulin
:reparations were effectivc for only a few hours after injection. The de_velopment
:i insulin preparations with longer periort' ot riberated
"""""*iig$gqgF
,
 need References
the diabetic from some of the restrictions of her activity imposed by the to
oral preparations'
for frequent injections. Early attempts at introducing L Bendy PK, Rosenberg LE (Eds,
controldiabetesmellituswereunsuccessfulbecauseinsulinisnotabsorbed Metabolism and Endocrinolog.
hypoglycemt'c.p-teparations (e'g'
unchanged and because other oraily active
-
Company Philadelphia, LonCcn.
und aiguunides, introduced in
synthalin A) were too roxic. The sulfonylureai 2. Kahn CR, Weir GC (Eds). Josl:r.
themidlg50,s,permittedsomediabeticstoremainhealthywithouttheuseof Baltimore, Hong Kong, Londc: l
daily insulin injections 3. Creasy RK, Resnik R (Eds). \1a:::
Company, A Division of Harc::::
Thediscoveryofinsulininlg2lheraldedanewerainrvhichreproduction White and
possible- nf
by women with diabetes mellitus became ]e]e .Priscilla
colleaguesreportedsuccessful*onugt,ntt'tof245diabeticpregnancies'and
diabetic ketoacidosis (DKA) had fallen
they noted that the i*id.nc. of maternal
dramaticallyandttrattlrelrequencvorantepartumfetaldeathwashalfofthat
recorded in the pre-insulin period'
that pregnancy outcome
The next three decades brought the recognition
andmetaboliccontrolwereclosel-,-linked(Pee"I.19,2).Theadventofportable
reflectancemetersallowedmeaSLllenelrtsolbloorJsugalsathomeandonthejob,
permittingmore..physiologic..bloodsugarcontrolduringpregnancy(Karlsson
of care
the development
and Kjellme r, lg72).irrtut.r,-,ut death became a rariq and
protocolsfortheinfantoftlrediabeticpregnanc}hadenormousimpactoninfant
survival. The perinaiaimortality rate feil
io- l:'; to 10r: during the period'
"team care cf pregnant women with
Since the 1970s, the concept of
diabetes mellitus has become accepted,
involr'ing the obstetrician (perinatologist)'
and nurse educator' New
pediatrician lnroruiotogist), endocrinologist. dieticran
sonographic gron'th assessment,
technologies such as reti bioph_vsical monrtoring.
reduce'J neonatal morbidiry markedly
and amniotic fluid lung maturtty asse ssment
1990)
(Gabbe, 1981; Johnstone, 1990; Lassman-Vague

Nonetheless,majorproblems*,ithbothfetalandmaternalmanagement
erpensi'e biophysical
persist. Although stilibirth rates ha'c fallen dramaticallr '
testinganddisturb,ngtyhighratesofpretermbirthandcesareansectionare
beingquestionedbyhealthCareeconomistan.Jinsurers'Congenitalfetal
debilitating. remain ,11:.'_::
anomalies, many oi them life-threatening and
*ol-. l..qu.nt in diabetic than nondiabetic pregnanC}.. Macrosomra
four times
andbirthinjuryo..u.,i0timesmorefrequentllindiaL.eticfetuses.our
StresS. glucose level,-and
understanding in th. i,]te,r.lation of diet, activit}..
fetalwell-beingcontinuestoberudimentary,arrd\\'earelargel."-unableto
preventmacrosomiaandbirthinjtrrywithoutunaccep.,tat.lvhighratesof
Cesareandelivery,Thekeychangestodayaretovaginallr.delir.eranormally
at tcrm wiihout injury or asphvria This goal
formed, normal-;ize4*'Xf1nt
requ ires m c ticu df.s.'t$'Taltutii a r I d obs te tric ma na ge m e n t
-. r?- tl' :
1
E::: - a her activity imposed by the
need References
lf,i i-: :ntroducing otal pteparations'to
t. Bendy PK, Rosenberg LE (Eds). Duncan's Diseases of Metabolism, Genetics
c,-',- because insulin is not absorbed Metabolism and Endocrinology, 7th Edition Asian Edition. WB. Saunders
a: .= h1'poglycemic preparations (e'g' Company Philadelphia, London, Toronto Igaku Shoin LTD, Tokyo, 1974.
iur -::as and diguanides, introduced in 2. Kahn CR, Weir GC (Eds). Joslins Diabetes Mellitus 13th Edition. Philadelphia,
@:. - :.main healthy without the use of Baltimore, Hong Kong, London, Munich, Sydney, Tokyo, 1994.
3. Creasy RK, Resnik R (Eds). Maternal Fetal Medicine 4th Edition. W.D. Saunders
Company, A Division of Harcourt Brace and Company 1999.
bi :.: a new era in which reProduction
G : ,,;::1e. BY 1939, Priscilla White and
Fr:- :: 2-15 diabetic (DKA)
pregnancies,- ard
had fallen
ir, - ..=,,. ketoacidosis
J L- ,: '::um fetal death was half of that

--.::ttion that Pregnancy outcome

. :=. l9i2). The advent of Portable
- - J sugars at home and on the job,
--

-. -.::,.1 during pregnancy (Karlsson

- : : r 1r'-l' and the development of care
'- - - - -'.. :ad enormous impact on infant
* - -': : : :o i 09/o during the Period.
- -:-ie of pregnant women with
- - -:. obstetrician (perinatologist),
: ::.::an and nurse educator. New
--- : --lographic growth assessment,
: ---: J neonatal morbiditY markedlY
- -: -:9J)
' '.:r- and maternal management
- r - :::- all\'. expensive biophysical
'
'- ::::1 and cesarean section are
' ::: -nsurers. congenital fetal
-, :=:liltating, remain three to
- : :::::, Pregnancy. MaCroSOmia
- ,: -:. . in diabetic fetuses. Our
" .. ..:.. slress. glucose level, and
:.-: ',\'e are largelY unable to
" -: -:.1-.e!.'tably high rates of
.. ..,=:nallr- deliver a normallY
. - -:', .'\r asphyxia. This goal
* ,-::a-:lent.

*qr{tih}'
 EPIDEMIOLOGY o Genetic susceptibilir\. esf (-:
o Infections, like chronic ;:.:.
Asia
Valerie T. Guinto, MD
Exposure to environmerrLl. .:
mellitus
o Moderate iron ot'erload :: ,

Asia
Prevalence

. Worldwide: Approximately 7% of all pregnancies (range: l-l4oh) are Associated Diseases

complicated with gestational diabetes mellitus (GDM). The incidence depends
on the population studied and the diagnostic test used.l . It has been suggested thar Jll
childhood aurism.)
. Western Pacific Region (which included the Philippines in a recent review):
7.60h prevalence of type 2 diabetes mellitus (included GDM and diabetes ' Fetal overnutrition (in gluc-.se .'.
mellitus in both sexes), highest among other regions studied which included and insuli n resistance.
that of Southeast Asia (6%), South and Central America, North America,
Eastern Mediterranean, Middle East and African Countries.a
References
. Philippines: 1.9oh of pregnant women admitted in the last 5 years have GDM.3
1. American Diabetes Assa-:..:. . :-.
. Philippines: 5.loh of women surveyed had type 2 diabetes mellitus or GDM.a position statement. Dia:.:=. J,,:
2. Fuller-Thomson E. Rolr:.::-,.:r:-
. Discrepancy in prevalence of GDM in data from the Philippines may be due pregnancy ot-llcomci .i::: :.- :
2010;32(2):113-119
to underreporting or regional differences (higher prevalence in those living 3. Philippine Obsterrical a::: ,1 .. .
in urban compared to rural areas). The data was also taken from only those 4. Chan JC, Malik \. Ir, -.\ ...,
institutions that are accredited by Philippine Obstetrical and Gynecological epidemiology, risk lacr.-:. .:: :
Sociefy, inc. (POGS), which included only 147 hospitals, and may not really 5. Gardener H, Sprege lrt..:-. I : _-,
reflect the true nationwide prevalence. Psychiatry 2009, l9_r:-- - -
6. Fall C. Maternai ltUrnrrti :r.: i
Res 2009; I 30:-593 -_i9:,
Risk Factors

. Risk factors for the diabetes mellitus epidemic in Asia: l

o Increasing overall and abdominal obesity
o Change in lifestyle (more sedentary) and change in diet (high intake of
food with high glycemic index and glycemic load)
o Cigarette smoking
o Inadequate p cell response to increasing insulin resistance results in loss
of glycemic control and increased risk of diabetes mellitus, even with
relatively tittte,fo*ieltt.gain (as seen in the Japanese population)
o Low birth we.ight and undernutrition in utero, especially for those who
were conceived :.d uunqrlhe war

4
lorocY
I
o
o
Genetic susceptibility, especially those of Southeast Asian descent
Infections, like chronic hepatitis B and tuberculosis, rvhich are high in
Asia
Exposure to environmental irritants has been associated also with diabetes
mellitus
r
o Moderate iron overload, as seen in the hemoglobinopathies common in
I Asia
I

rr :regnancies (range: I-l4oh) are Associated Diseases

F_: .:'rs (GDM). The incidence depends
tb€- ':-c test used.l
. It has been suggested that GDM may play a role in the development of
childhood autism.s
tc, ::e Philippines in a recent review):
.
lt-. ...us (included GDM and diabetes Fetal overnutrition (in glucose excess) is associated with increased adiposity
Er'_ .::r regions studied which included and insulin resistance.6
|! ,- Jentral America, North America,
I:- .-.fircan Countries.a
References
lm- :'.:ued in the last 5 years have GDM.3
1. American Diabetes Association. Diagnosis and classihcation of diabetes mellitus:
position statement. Diabetes Care 2001,;34(suppl l):562-569.
F:- :J ivp€ 2 diabetes mellitus or GDM.a 2. Fuller-Thomson E, Rotermann M, Ray JG. Elevated risk factors for adverse
pregnancy outcomes among Filipina-Canadian women. J Obstet Gynaecol Can
[- '.:a from the Philippines may be due^^-- ___*J
2010,32(2):ll3-119.
h:- , lhigher prevalence in those living 3. Philippine Obstetrical and Gynecological Statistics 2005-2009.
, T', :3ta was also taken from only those 4. Chan JC, Malik Y Jia W, Kadowaki T, Tajnik CS, et al. Diabetes in Asia:
F:rr ::ine Obstetrical and Gynecological epidemiology, risk factors, and pathophysiology. JAMA 2009;301(20):2129-2140.
&: :I'; 117 hospitals, and may not really 5. Gardener H, Spiegelman D, Buka SL. Prenatal risk factors for autism. British J
l;: Psychiatry 2009 ;19 5 :7 -1 4.
6. Fall C. Maternal nutrition: effects on health in the next generation. Indian J Med
Res 2009; 130:593-599.

E ,:.:emic in Asia: a

nr- . -'csirv
!m:.-:.. and change in diet (high intake of
r: =.rcemic load)
uc,: .:sing insulin resistance results in loss
a.,: risk of diabetes mellitus, even with
sr'::-. -n the Japanese population)
or:i-. .:,rn in utero, especially for those who

"'$,N
 Its metabolic function ts to n,.-
NORMAL GLUCOSE METABOLISM IN PREGNANCY hypoglycemia, during the ias:::
and gluconeogenesis. u'hich i:.
So1M. Pangan, MD It also favors hepatic oxidat:,-
bodies, like acetoacetate and .: -
energy sources for the l'rrr::
prolonged fasting. Nletat':----
these ketone bodies are rlp:-:. .

Introduction

. Glucose is the main fuel which supplies the metabolic needs of most body
Changes in Glucose Metabolism Dur
tissues.

. . Changes in carbohydrate att,-l --'-'.

upon entry into the cell, it may undergo glycolysis and form adenosine
accommodate fetal nutrttiorta. :.;:
triphosphaie (ATP), a ne\\' energv unit u'hich fuels biochemical reactions
wiltrin the cell, or it may be stored u'rthin the cell as gly'cogen'r of nutrients to the gros'illg Ii:;: :

. The maintenance of a stable glucose level. and regulation of glucose entry

. Early Pregnancy Changes
into cells, is dependenr on a closed feedback loop relation between:2
o The circulating blood glucose ler el o Early pregnancy can L'e ":. ''
maternal fat stores. and .1e .-:.
o The pancreatic islet hormones insulin and glucagon to meet the increasing llll:.::
o The liver lactation.5
o The peripheral tissues
. Insulin release and actions:r'r
o The pregnancy hormones :*::
previously called humart :--:.
o Insulin secretion by B cells of rhe pancreatic rslets is stimuiated by increased glucose levels and promLr:- :.::
blood levels of glucose and amino acids
reach a nadir by the 1 I th '.'' ::
o On the other hand, insulin release is inhibited bv loti blood glucose levels, normal in early pregnan.',
-

and by epinephrine secretion in response to stress' rrauma and extreme

The postprandial glucose 1e '':.
exerclse.
o In the liver, insulin causes decreased glucose production. by inhibiting o
developing embryo front eie -..'-
gluconeogenesis and glycogenoi,vsls.
o in muscle, insulin increases glucose uptake and gl1-cogen svnthesis. o In summary, hormones ass--
o In fat tissue, insulin increases glucose uptake b1' adipocl'tes, and inhibib storage of energy it-t thefir.: ::.
breakdown of fat stores. to the fetus in late pregnan-'.
'
o In all other insulin-sensitive tissues, it stimulates entrv of amino acids into
cells and protein sYnthesis. . Second Trimester Changes.
o It is therefore, anabolic and anti-catabolic.
. o In the second trimester n:.:::
Glucagon secretion and actions:3 increase. This facilitatL-s r. * -
o Seireted by cr cells of the pancreatic islets, glucagon opposes many of the carrier-mediated active ::.1:-.i --

actions of insulin. maternal valucs.'

o The primary stimulus for glucagon secretion is lori L,lood gJucose level. o Insulin increased secretr,-r-. ::'.
o It is inhibited py elevated blood glucose levels and high insulin blood i. Insulin secretiolt in :..:' :
levels. .,,v;!r-]]A' through out gestatl.':. .'. :
 Its metabolic function is to maintain blood glucose levels, thus preventing
TABOLISM INPREGNANCY hypoglycemia, during the fasting state, by activating hepatic glycogenolysis
and gluconeogenesis, which increase glucose output from the liver.
F.:-:an, MD It also favors hepatic oxidation of fbtty acids, with formation of ketone
bodies, like acetoacetate and B-hydroxybutyrate, which serve as alternative
energy sources for the brain and other vital organs during periods of
prolonged fasting. Metabolic acidosis does not usually result because
these ketone bodies are rapidly cleared by the kidneys.

,::s the metabolic needs of most body Changes in Glucose Metabolism During Normal Pregnancy

Changes in carbohydrate and lipid metabolism occur during pregnancy to

T-. ::Jergo glycolysis and form adenosine
accommodate fetal nutritional requirements and ensure a continuous supply
ry -.tt i.'trictr fuels biochemical reactions ol nutrients to the growing fetus, despite intermittent maternal food intake.a
d ::.:n the cell as glYcogen''

f, -evel, and regulation of glucose entry Early Pregnancy Changes:

!! :rack looP relation between:2
E.:
o Early pregnancy can be viewed as an anabolic phase with increase in
maternal fat stores, and decrease in serum free fatty acid concentration,
G5 --in and glucagon to meet the increasing maternal and letal demands of late gestation and
lactation.s

o The pregnancy hormones human chorionic somatomammotropin (hCS),

previously called human placcntal lactogen (hPL), and cortisol lower
[r, ::creatic islets is stimulatedby increased
glucose levels and promote fat deposition. The lowering of glucose levels
u' :;ids.
reach a nadir by the l2th week, hence fasting levels of 70-80 mg/dL arc
dr -' :s inhibited by low blood glucose levels'
normal in early pregnancy.6
l ::sponse to stress, trauma and exffeme

glucose production, by inhibiting o The postprandial glucose levels are also decreased. This acts to protect the
;@c developing embryo from elevated blood glucose levels.6
-
'sed
]a.
rF-, ., uptut. and glYcogen sYnthesisinhibits o In summary, hormones associated with pregnancy facilitate maternal
15- :,.se uptake by adipocytes, and storage of energy in the first trimester, and assist in the diversion of energy
to the fetus in late pregnancy.6
!@: ; :t stimulates entry of amino acids into
Second Trimester Changes :

tl.r -.-:abolic.
o In the second trimester, maternal fasting and postprandial glucose levels
f, increase. This facilitates glucose transfer through the placenta, via a
-:: islets, glucagon opposes many of
the
FII , carrier-mediated active transport system. Fetal glucose levels are 80% of
maternal values.6
:. secretion is low blood glucose level' o Insulin increased secretion and decreased sensitivity -
- iucose levels and high insulin blood i. Insulin secretion in response to glucose intake progressively increases
through out gestation, with parallel decrease in insulin sensitivity of

' q$.ffiHi
 muscle tissue. This peripheral insulin resistance, which reaches its ' Ketone bodies diffuse freeiv across :

nadir in the third trimester, and rapidly returns to pre-pregnant levels L'lood levels.
after delivery, has been demonstrated in many longitudinal studies'7-rr
ii. The latest srudy, in 2008, confirmed this behavior of insulin secretion ' Neither maternal nor fetal insulrn -:

andsensitivityinalargenumber(903women)olnormalplegnant
women rvith normal bodY weight'r'
iii. Catalano, et al.? found a 56ok reduction, while Buchanan, et al'e ?ossible Causes of Insulin Resistance
showed a 60-80o/oreduction, in insulin sensitivity, in the third trimester
ol normal Pregnant women. Increased blood levels of hCS. h:::
iv. There ls a parittet increase in insulin secretion to maintain a normal cortisol, progesterone, and estrcgr:.
glucose tolerance, so that insulin levels are almost twice that of non-
pregnant women.ro hCS. produced only by sy'ncticr:--
product of the placenta. It has a s:
o Increased hepatic glucose production: basal endogenous glucose rhat:ro
production increases by 16 30ok in late pregnancy, with increase in hepatic c Maternal plasma glucose le','e ;s
gluconeogenesis.s'I: r 3
c Plasma free fatfy acids are rn;.
: Insulin secretion is increaseC ,,i .

Postprandial glucose concentrations are signrficantly elevated and

the
o
glucose peak is Prolonged.r' Reduction of maternal insulin re ;r:
hCS and hPGH, is a suggested n:e ::
through pregnancy.2l
summary of changes in Normal Glucose Metabolism During Pregnancy

Increased insulin secretion R.eferences

Decreased insulin sensitivitY
Elevated postprandial glucose levels and prolonged glucose peak 1. Inzucchi S. Diabetes in plgg-.:1,-
Increased hepatic glucose production Burrow G, Duffi7 T, Eds. \\'B S:-:.
Increased carbohydrate use (by fetus)
:. Kahn S, Porte D. The pathoph.. s--.
mellitus: implications for rreai::--=:.
Accumulation of maternal fat stores in early pregnancy Rifkin H, Porte D Jr, Eds. Eise. :=:
Enhanced fat mobilization in late pregnancy Champe P, Harvey R. Meral..-l:,- ::
-1.
Illustrated Review: Biochen.ris::'. _

{. Butte NF. Carbohydrate and i:':-:

Maternal-Fetal Metabolic Interactions with gestational diabetes ntel1r:,-. ..
5. Catalano P. The diabetose:::: .:
. Glucose molecules traverse the placental circulatron through a process called American Academy of Pedia:::,. _
facilitated diffusion via placental glucose transporters (GLUTs).r5 Fetal glucose 6. Gagarina AK. Metabolisnr in :.-:
Mellitus in Pregnancy. Pror iCe: :'
levels are 20-40 mg/dL lower than matertlal levels
.

. Catalano PM,Tyzbtr EO. Rt-:r,,: ).

in insulin release and ir.rsulin :..,,
. Amino acids pass thc placenta by active transport. Obstet Gynecol l99l; 16-5:1ca- -_
8. Catalano PM, Huston L, Amr:. S_-
. Free fatty acids pass freely, but blood levels are higher in the mother. metabolism during pregnan.', r: r.
gestational diabetes. An.r J O:s:.: .--
. Triglycerides,are blocked, being hycirolyzed in the placenta to free fatty acids 9. Buchanan TA, Metzger BE F:-..
beta-cell responsiveness to gli:- _ .
and glycerol.r"- ..;fr+ =

'
.:?1, g
-.;,!
tt,
.
 -,--::. resistance, which reaches its
-. :.'. returns to pre-pregnant levels
-': : ::. many longitudinal studies.T-1r
* : - .i-rS L'ehavior of insulin secretion
: - -1 ir'omen) of normal pregnant
: -,--lror. while Buchanan, et al.e
' - .:. .ensitivity, in the third trimester
' - : :c.retion to maintain a normal
, -.s are almost twice that of non-
- -. -:. basal endogenous glucose
I i:'ir12r1C!, with inCrease in hepatic
,:: srgnificantly elevated and the
', { etabolism During Pregnancy
:: - -rnged glucose peak
r:, , l.regnancy
--.rculation through a process called
: :: sporters (GLUTs).
i5
Fetal glucose
-... levels.
.:,.-rsport.
,". are higher in the mother.
:J rn the placenta to free fatty acids
Ketone bodies diffuse freely across the placenta, with equal fetal and maternal
blood levels.
Neither maternal nor fetal insulin pass through the placenta.
Possible Causes of Insulin Resistance During Late Pregnancy
' Increased blood levels of hcs, human placental growth hormone (hpGH),
cortisol, progesterone, and estrogen. rare
' hcs, produced only by syncytiotrophoblasts, is the most abundant secretory
product of the placenta.It has a strong lypolytic and anti-insulin action, so
that:20
o Maternal plasma glucose levels are increased.
o Plasma free fatty acids are increased.
o Insulin secretion is increased with the resistance to endogenous insulin.
' Reduction of maternal insulin receptor sites and glucose transport, caused by
hCS and hPGH, is a suggested mechanism for the increasing insulin resistance
through pregnancy.2l
R.eferences
L lnzucchi S. Diabetes in pregnancy. In: Medical Complications in pregnancy.
Burrow G, Duffy T, Eds. WB Saunders Co. PA LISA:1999;25-48.
2. Kahn S, Porte D. The pathophysiology of type II (non-insulin-dependent) diabetes
mellitus: implications for treatment. In: Diabetes Mellitus Theory and Practice.
Rifkin H, Porte D Jr, Eds. Eisevier, NJ USA:1990;436-454.
3. Champe P, Harvey R. Metabolic effects of insulin and glucagon. In: Lippincott's
Illustrated Review: Biochemistry. JB Lippincott Co. pA rJSA:1994;269-2g0.
4. Butte NF. Carbohydrate and lipid metabolism in pregnancy: normal compared
with gestational diabetes mellirus. Amer J Clin Nutr 2000;7i(Suppl 12):56s-61s.
5. Catalano P. The diabetogenic state of maternal metabolism in pregnancy.
American Academy of Pediatrics 2002.
6. Gagarina AK. Metabolism in normal and diabetic pregnancies. In: Diabetes
Mellitus in Pregnancy. Provided by ArmMed Media 2009.
1 . Catalano PM, Tyzbir Eo, Romar NM, Amini SB, Sims FA. Longitudinal changes
in insulin release and insulin resistance in non-obese pregnant women. Am J
Obstet Gynecol 1991; 165:1667 -72.
8. catalano PM, Huston L, Amini sB, Kalhan SC. Longitudinal changes in glucose
metabolism during pregnancy in obese women with normal glucose tolerance and
gestational diabetes. Am J Obstet Gynecol 1999;180903-916.
9. Buchanan TA, Metzger BE, Freinkel N, Bergman RN. Insulin sensitivity and
beta-cell responsiveness to glucose during late pregnancy in lean and moderately
"qffi-
 obese women with normal glucose tolerance or mild gestational diabetes' Am J
MATERNAL AND FET
Obstet Gynecol 1990;1621008- 10 14'
10. DiCianni C, Microli R, Volpe L, Lencioni C, Del Prato S' Intermediate
metabolism in normal pregnancy and in gestational diabetes. Diabetic Metab Res Ma. Victoria'
Rev 2003;19:259-270.
11. Lapolla A, Dalfra MG, Mello G, Parretti E, et al. Early detection of insulin
in
sensitivity and beta-cell function with simple tests indicate future derangements
late pregnancy. J Clin Endocrinol Metab 2008;93(3):876-880'
Ceneralizations about Maternal and
12. Kalhan SC, Angelo LJ, Savin SM, Adam PAJ. Glucose production in pregnant
women at term gestation: sources of glucose for human fetus. J Clin Invest Pregnancv
1979;63:388-94.
13. Assel B, Rossi K, Kalhan S. Glucose metabolism during fasting through human .\[,]ternal Effects
pregnancy: comparison of tracer method with respiratory calorimetry. Am J

Physiol 1993;265:F351-6. . Intensive glucose control reduces rhe

14. Cousin L, Rigg L, Hollingsworth D. The 24-hour excursion and diurnal rhythm complications.
of glucose, inzutln, and C-peptide in normal pregnancy' Am J Obstet Gynecol
1980;1 36:483-8. . With possible exception of diabetic :
l5.ThorensB,CharronM,LodishH.Molecularphysiologyofglucosetransporters. mellitus is not affected by pregnanc'.
Diabetes Care 1990;13:209 .

16. Bonnet B, Brunzel J, Gown A, Knopp R' Metabolism of very low density .
human placental cells. The role of lipoprotein lipase' .\lthough maternal death is uncoin:
lipoprotein triglyceride by
rs increased by lO-fold.
Metabolism 1992;41:596.
17. Freinkel N. Banting Lecture: of
pregnancy and progeny. Diabetes 1980;29:1023.
ig. Kalhoff RK, Richaidson BL, Bect P. Relative eflect of pregnancy human placental ' Deaths most often result from dia:
subclinical
lactogen and prednisolone on carbohydrate tolerance in normal and preeclampsia and pyelonephritis Es:
diabetic subjects. Diabetes 1969;18:153. ',r ith > 50oh mortality rate.
19. Shamoon fi, n"tig P. Effects of estrogen on glucose uptake by rat muscle. Yale J
Biol Med 1.974;47:221. ' tr\'ers, et al, on a prospective studv c:
20. Liu Rebar R. Endocrinology of pregnancy. In: Maternal Fetal Medicine' Creasy
J, rhat even if the glycemic conrrol rs
R, Resnik RR, Eds. WB Saunders Co, PA USA 1999;39'7'389' have HbAlc < 7oh), complicarion ra:(
21. Ciaraldi TP, Kettel LM, El-Roely A, et al. Mechanisms of cellular insulin [PTD] 32ok, cesarean section rate -l-l
resistance in human pregnancy. J Clin Endocrinol Metab 1992;'75:511 .
are still considerably higher than the :

!:;..t1 Effects

There is an important difference .::

o\ ertlpregestational versus gestaria :. j
of complications are proportional tl :

Unlike in those with overt diaberes :.

in GDM.

Likewise, those with overt pres..s:-

, '47,it o
.q. ,
risk of having fetal deaths compar-:
*-.,1*r-
' ..t".' hyperglycemia.'

l0
Iri.. :,.erance or mild gestational diabetes. Am J MATERNAL AND FETAL COMPLICATIONS
l-l =
lx - j encioni C, Del Prato S. Intermediate
;r,c r : :: gestational diabetes. Diabetic Metab Res Ma. Victoria V. Torres, MD

D -- . :-etti E, et al. Early detection of insulin

f n, ' - ,::r]ple tests indicate future derangements in
tr ' t:::: 1008;93(3):876-880.
S : :.:rin PAJ. Glucose production in pregnant Generalizations about Maternal and Fetal Effects of Diabetes Mellitus in
!|:. : glucose for human fetus. J Clin Invest Fregnancy

lu . retabolism during fasting through human \{.zternql Effects

E -=:::od with respiratory calorimetry. Am J
' Intensive glucose control reduces the development and progression of diabetic
rc - rhe 24-hour excursion and diurnal rhythm complications.
p: .- ncrmal pregnancy. Am J Obstet Gynecol

h:. .1 :-ecular physiology of glucose transporters.

' With possible exception of diabetic retinopathy, long term course of diabetes
mellitus is not affected by pregnancy.
!1" --:pp R. Metabolism of very low density
I: .-ental cells. The role of lipoprotein lipase. ' Although maternal death is uncommon, rates in those with diabetes mellitus
is increased by 10-fold.
ff:' :.-lrc-v and progeny. Diabetes 1980;29:1023.
bct 1..-ative effect of pregnancy human placental ' Deaths most often result from diabetic ketoacidosis (DKA), hypertension,
lr;:: .-.',Jrate tolerance in normal and subclinical preeclampsia and pyelonephritis. Especially ominous is ischemic heart disease
i :_:
n'. u'ith > 50% mortality rate.
5: :.:r on glucose uptake by rat muscle. Yale J

Evers, et al, on a prospective study of diabetes mellitus in pregnancies reported

r@r : :i:ienc!. In: Maternal Fetal Medicine. Creasy
k: PA USA 1999;397-389.
that even if the glycemic control is excellent (75% of the study population
have HbAlc < 7o/o), complication rates (preeclampsia 12.7oh, preterm delivery
l:c .i. et al. Mechanisms of cellular insulin
,.:. Endocrinol Metab 1992;7 5:577 . [PTD] 32v0, cesarean section rate 440k, maternal mortaliry rate 601100,000)
are still considerably higher than the nondiabetic pregnancies.6

ktal Effects

There is an important difference concerning adverse fetal consequences of

overt/pregestational versus gestational diabetes mellitus (GDM) because risks
of complications are proportional to the duration and severify of the disease.

Unlike in those with overt diabetes mellitus, fetal anomalies are not increased
in GDM.

Likewise, those with overt/pregestational diabetes mellitus have greater

risk of having fetal deaths compared to those with diet-treated postprandial
hyperglycemia.'

il *'[[!$-TmlJ'o
* t09{19
Uc'
. GDM patients with elevated lasting blood sugar (FBS) have similar risk of . The prevalence during pregna.
having unexplained fetal deaths as those with overt/pregestational diabetes 5- 10%. Pregnancies complicare,i
mellitus.2 maternal and fetal morbidin'an;

. Specifically, the American Diabetic Association (ADA) concluded that FBS

. Microalbuminuria in earlr' pre:
oi ttOS mg/dL is associated with increased risk of unexplained fetal deaths possible onset of preeclampsra
percent of pregnant women u ilh
during the last 4-8 weeks of gestation.3
(White Classification F) rvrth sr;
. Improvement in fetal surveillance, neonatal intensive care and maternal
preeclampsia and low birth rr eigi
metabolic control have lowered perinatal morbidiry and mortality in overt/ . Pregnant women with chronrc :
pregestational diabetes mellitus'r
have 60oh chance to develop pre e
. In type 1 diabetes mellitus, there was dramatic decrease in perinatal mortality . There appears to be no long :
,ut., plrrtR) from 22% in the 1960s to 1% in the 1990s but no change in the diabetic nephropathy. Imp3;1 .-
incidence of fetal overgrowth. Aftenvhich, there was a plateau in the PMR depends on pre-pregnant renal :
because the two majorciuses of fetaldeaths $'hich are congenitalmalformations compromised glomerular fi lrra::,'
and unexplained fetal death in utero (FDU) remained unchanged by
medical
significant risk of permane nr ,1e;.
interventions.5
. Pregnancy neither alters the rir::;
likelihood of transition to enC s:,:
Maternal Complications of Diabetes Mellitus in Pregnancy
):ebetic Retinopathy
1. DiabeticNephroParhY
. Most important cause of visual .
' Pathophysiology of Diabetic Nephropathl': in the United States. Houever. ::,
Hyperglycemia-)excessir'edepositionofglycogentotheglomerular the disease.ra
basementmembrane (BM) ) )
diabeticglomerulosclerosis
BM thickenrng
and papillary necrosis ) albuminuria ) progressive renal destruction/
. Clinical Course/Progression c: -
deterioration ) end stage renal disease and failure Hyperglycemia induce micrcr -.-,
red blood cells (RBCs) exrra', a:
. Diabetic nephropathy will eventuall,v appear in 30-'10% of patients with serous fluid will form hard eru;
type 1 diabeies mellitus and is the leading cause of end stage renal disease progressive occlusion of retina- ',
in the United States. Incidence of renai farlure in t1'pe 1 diabetes mellitus rvith development of cotton \\'c.. r

is 30% compared to 4.2o/o among rype 2 diabetes mellitus'

) compensatory neovascular:z:
space (Proliferative Retin opa th',

Clinical Course of Diabetic Nephropathr':::

) tractional retinal detachme::
. 5 years from onset of diabetes mellitus ) microalbuminuria (30-300 rctinal/yitreous hemorrhages ) ',
mg/24 hours) .
. S-iO years later ) overt proteinuria (> 300 mg/24 hours) with or According the Diabetes Nlell:::.
with impaired glucose resr .i:: -
without hypertension among those destined to have end stage renal have retinopathy.
-:

disease
. 10-15 years later ) renal failure . Almost all of those u'ho te;c::
/
/tL duration of the disease is > l[j '.;,

12
:t i
 ,,:,: sugar (FBS) have similar risk of The prevalence during pregnancy has been estimated to range from
',.: .,'\rth ovefi/pregestational diabetes 5-10%. Pregnancies complicated by nephropathy are at increased risk for
maternal and fetal morbidity and perinatal mortality.

,, :.:tion (ADA) concluded that FBS Microalbuminuria in early pregnancy is a very sensitive predictor of
-
-. r.;d risk of unexplained fetal deaths possible onset of preeclampsia later in the course of pregnancy. Five
percent of pregnant women with diabetes mellitus have renal involvement
(White Classification F) with significantly increased risk for developing
-.-::tal preeclampsia and low birth weights and indicated preterm delivery.
intensive care and maternal
',..- morbidity and mortality in
ovett/
Pregnant women with chronic hypertension with diabetic nephropathy
have 60oh chance to develop preeclampsia.

:: ,1:latic decrease in perinatal mortality
.: : in the 1990s but no change in the
:::h. there was a Plateau in the PMR
'.:is s'hich are congenital malformations
:lU) remained unchanged bY medical
=:
: .
\.{elLirus in PregnancY
ls
Diabetic Retinopathy
There appears to be no long term sequelae of pregnancy per se on
diabetic nephropathy. Impact of pregnancy on diabetic nephropathy
depends on pre-pregnant renal ftrnction, such that in those with markedly
compromised glomerular filtration rate (GFR) prior to pregnancy, there is
significant risk of permanent decline in renal function later.
Pregnancy neither alters the time course of renal disease nor increase the
likelihood of transition to end stage renal disease.r3

. Most important cause of visual impairment among those < 60 years old
ft .,::.roPathY: in the United States. However, the prevalence is related to the duration of
I -..:sition tf gly.og.tt to the glomerular the disease.r
F t : : :rictening5 diabeticglomerulosclerosis .
& -::nuria ) progressive renal destruction/ Clinical Course/Progression of Diabetic Retinopathy:
Hyperglycemia induce microvascular disease ) microaneurysms )
r ' ::sease and failure red blood cells (RBCs) extravasation ) blot hemorrhages ) leaked
with serous fluid will form hard exudates (Nonproliferative Retinopathy) )
ls .-:.rallv appeat tn30-40o/o of patients progressive occlusion of retinal vessels ) retinal ischemia and infarction
disease
d -, ::.: leading cause of end stage renal with development of cotton wool exudates (Preproliferatrive Retinopathy)
L - . , r renal iailure in type 1 diabetes mellitus ) compensatory neovascularization in the retinal surface and vitreous
,1tr ,:.: t)'pe 2 diabetes mellitus'
space (Proliferative Retinopathy) ) fibrous tissue formation and retraction
) tractional retinal detachment with or without macular edema and
5 . . =:hroPathY:r2
Io ,,.,., retinal/vitreous hemorrhages ) visual impairment and blindness
melliius ) microalbuminuria (30-300
. According the Diabetes Mellitus Prevention Project (2007),8% of those
rr. ::oteinuria (> 300 mg/24 hours) with or
with impaired glucose test and 73% of newly identified diabetes mellitus
r u:: - those destined to have end stage renal have retinopathy.
"g
rr.-.ailure . Almost all of those who become diabetic before 30 years old and/or
duration of the disease is > 20 years have retinopathy.

t2 13 lArlttlA R.|IA9!PAI
'*'iid'ou nnuttc
Lic' I 109&9
 on retinopathy give diverse results:
o Clinically, in the Presence of ,

' Studies on the effects of pregnancy proteinuria, it is diflicult ti

proliferative retinopathy're
a. Klein, et al- Pregnancy worsens by showing superimposition of preeclam;
b. Chaturvedi, et al-Pregnunty t'u"to effect on retinopathy o The perinatal mortaliry rate is
women'20
p;;;;;tt; of-retinopathvi" --rti and nulliparous
the same S-ye'at follow-up of with diabetes mellitus compa.
c. Arun and Taylor - In a p'o'pttiiut postpartum
5gwomenwithtypeldiabetesmeilitusconfirmedthatthebaseline
factor for progression'2l Atherosclerosis and Coronar.r' H
retinopathy was the only indepe"J.n,
ritt
o Coronary heart disease ani
in pregnant diabetics. Affe;:
.Amongthosewithearlyorminimalretinopathybeforeconception,the preclinical cardiomyopathl :
pregnancy is 10%'
chance of progression during o Diabetic patients u'ith long
hypertension and nePhroP a:i
.Hypertensionandpreeclampsiafurtherincreasetheriskofprogressive artery disease.
retinopathy during Pregnancy' o The hemodynamic change-'
myocardial stress.
3. Diabetic NeuroPathY o Epinephrine release in re.P--
mellitus' the risk for myocardial in;u:-,
years from onset of diabetes
' Usually develops after 10-15 o Exaggerated lipid changes :-
is the vascular beds during P:e-:
sensorimotor diabetic neuropathy
' Peripheral 1td symmetrical
uncommon in PregnancY' -,:.rections
in the
Diabetic gastropathy (diabetes
mellitus-rela:t^11ti:*sturbance . Almost 80% of women u ith :.:
' in pregnancy because
gastroinresrir;i;;0 is particularly troublesome
nutritionai'disturbances and during pregnancy comPared i'':
it is associated with nausea' fl"tir
""itiii"g'
*ui u. treated with H2 blockers or mellitus.
difliculty with glucose control.
metocloPramide' ' Most common infections are u:::-
and wound infections follou ing :
.Painfulinsulinneuritis,arenonspecilrcachesfeltsecondarytorapid are increased in diabetic pregrl:
tightening of glycemic control'r5
' -:.:=::ions are risk factors fcr :::
4,CardiovascularComplications(ChronicHypertension,Preeclatttpsia,Atherosclerosis l-ir and progression of r:e::
and CoronarY Heart Disease) :.-.::ric UTI.

. Chronic HYPertension preexisting renal or retinal - : :".:r Endocrine D isturbances

o UsuallY with associated underlying or
preeclampsia, abruptio
. The incidence of thyroid glar::
HrtJ.?13Jtxinrr.^tions: maternal stroke, year postpartum in type 1 diab::
" placenta, intrauterine growth restriction
(IUGR)
of the normal population.

PreeclamPsia diabetes ,1:,crative Delivery

:*Ti:T:ilo n" higher i" Yith "u."'j1o-'^'.?:::""""a1
'lg'.'
mellitus compared"with nondiabetic
pregnan t patient'
forces preterm deliverv ln
The reported cesarean sectio: :.'-
o It is a major *-pri.lii";;;^amorioften 800/o, and reflect medical Jtr e ;s-:
diabetiqP{J€$fllPies'
+.4 q' ,

lr
 ::- :::inopathy give diverse results: o clinically, in the presence of developing hypertension and worsening
i::. :: : liferative retinopathy. re
proteinuria, it is difficult to distinguish whether this is due to
:-'. :--' effbct on retinopathy by showing superimposition of preeclampsia or due to worsening nephropathy.
1 i--.. : multi and nulliparous women.2o o The perinatal mortalify rate is increased 20x from preeclampsia women
nncfnrrfrrm \-trecr
:ry::'.: postpartum fn.llmw-ltn of
S-year follow-up nf with diabetes mellitus compared to those without hypertension.
.:', :.:-iitus confirmed that the baseline
,.-:irt nsk factor for progression.2r . Atherosclerosis and Coronary Heart Disease
o Coronary heart disease and myocardial infarction are rare events
:-,, :::inopathy before conception, the in pregnant diabetics. Affected diabetic pregnant women may have
:: L:,-. is 10%. preclinical cardiomyopathy and autonomic neuropathy.
o Diabetic patients with long standing disease who have developed
lncTease the risk of progressive hypertension and nephropathy are at higher risk to develop coronary
artery disease.
o The hemodynamic changes associated with pregnancy increase
myocardial stress.
o Epinephrine release.in response to hypoglycemia might exacerbate
onset of diabetes mellitus. the risk for myocardial injury.
o Exaggerated lipid changes plus destructive and thrombotic events in
:-,-::::irotor diabetic neuropathy is the vascular beds during pregnancy may accelerate atherosclerosis.

' Infections
*:--::..1s-related nerve disturbance the in
.r-- , :::ublesome in pregnancy because Almost 80% of women with type I diabetes mellitus develop infection
, -..:::q. nutritional disturbances and during pregnancy compared with only 25% in those without diabetes
-'' . :.3) be treated with H2 blockers or mellitus.

Most common infections are urinary tract infections (url), cervicovaginal

aches felt secondary to rapid and wound infections following delivery but almost all types of infections
are increased in diabetic pregnancies.

Pre e c I amp s i a, At h ero sclero sis Infections are risk factors for the development of preterm labor/d,elivery,
DKA and progression of preexisting nephropathy among those with
chronic UTI.

', rng or preexisting renal or retinal Ot her E nd o cr i n e D i sturb ances

-.:::nal stroke, preeclampsia, abruptio The incidence of thyroid gland disorder during pregnancy and the first
"-- :=s:riction (IUGR) year postpartum in type I diabetes mellitus is almost 3x higher than that
of the normal population.

n-ith overt/pregestational diabetes Operative Delivery

'::etic
. pregnant patient.
most often forces preterm delivery in The reported cesarean section rate in women with diabetes mellitus is 20-
80oh, and reflect medical diversities in obstetrical practice. The diagnosis

I 5 ilAnra R' rAclDl'lt'D'

'-'d6-et* ur*rc
-le't totttl
 preterm births, secondary to su:
ofdiabetesmellitusortheknowledgethatthewomen.alebeingtreated
and fetal or maternal conditions
withinsulintriggeranincreaseininterventionamongobstetricians.
macrosomia . Maternal and Fetal Medicine Ur
. common indications for cesarean delivery are prematuriry a. 9oh preterm birth rate amcr:
and other diabetes mellitus-related complications' 4.Soh for nondiabetics
b. 7o/o incidence of indicated pr
8, DKA mellitus versus 2oh for nonc'.
.DKAaffectsonlyl%ofdiabeticpregnanciesbut.is.oneofthemost . Canadian Study (Yang and \\-i-.'.
serious.o-pti*tionswhichsignificantlyaffectsboththemotherandthe births among pregestational diai
fetus with fetal loss rate of > 20%' compared to nondiabetics

. and the following

This complication is unique to type 1 diabetes mellitus - ?olyhydramnios
gravidarum, f3-mimetics for
are the trrown precipitints: hyperemesis
tocolysis,steroidsadministrationforfetallungmaturify,infections . Often associated with diabetes r:
secondary to fetal hyperglvcem::
.PregnantwomenusuallyhaveDKAwithlowerbloodglucoselevels osmotic pressure due to increas;
comPared to nonpregnant women' fluid.

' PathoPhYsiologY of DKA: . Polyhydramions ) uterine ore:;

Inadequate inslunn action at the target tissues
) functional CELLULAR
of glucose but
HypoGLf'CEMIA ) compensatoiy hepatic mobilization - .4.itered Fetal Growth (A4acrosomia c, l'-
stillwithauser'ttissuedisposal)glucose-lackingtissuesSecleteketone D),stocia and Brachial Plexus Injun.,
bodies * Uuifalup of glucose in the*blood (hyperglycemia) ) metabolic
acidosis + osmotic diuresis ) profound vascular
volume depletion' loss . 20-40%of infants of diabetic n,-
ofelectrolytesandfurthertissuehypoglycemia)multipleorgansystem for age of gestation (AOG)
collaPse ) coma and death
. Macrosomia develops from lC ',r

Fetal Complications of Diabetes Mellitus in Pregnancy

. Pathophysiology of fetal macr.!
mellitus:
L Early Pregnancy Losses (Abortions) Pederson Model:
Maternal hyperglycemia ) te:
Early abortion is associated with poor glycemic control' fetal pancreatic ) celis ) fe::.
' glucose deposition to fetal sci: :.
.Pathophysiology:Hyperglycemiaduetofailuretodeliverglucose(insulin of macrosomia with excessi',':
resistance) to Jno-tirr,r.sj cellular hypoglycemia and hypoxia (failure of compared to the head ) mcre :r
oxygen delivery to tissues due tt hyperglycemia-mediated shift of
oxyhemoglobindissociationcurvetotheleft))embryonichypoperfusion Macrosomic fetuses have sien::..
polypeptides (insulin-like grcrr ::
and death (earlY PregnancY loss)
potent stimulators of cell difle:::
2. Preterm Lqp,or and DeliverY
Postprandial blood glucose tFP:
ovtrtl$i€betsgt .tonal diabetes mellitus is undisputedly associated with FBS is correlated with fetal sizt .
t

I
t
1

:::: that the women are being treated preterm births, secondary to susceptibilify to infection, polyhydramnios

- :
-::rvention among obstetricians' and fetal or maternal conditions indicating early pregnancy termination.

-- ::-rvery are prematuriry macrosomia
;::npiications.
- :::gnancies but is one of the most
':':::r'aflects both the mother and the
- : . ::abetes mellitus and the following
: ::::-;sis gravidarum, B-mimetics for
: Polyhydramnios
' '.:-:l lung maturity, infections
-..--- ',iith lower blood
glucose levels
. Maternal and Fetal Medicine Units Network (Sibai, et al)t6 showed a:
a. 9o/o ptetetm birth rate among pregestational diabetes mellitus versus
4.50/o for nondiabetics
b. 7oh incidence of indicated preterm delivery for pregestational diabetes
mellitus versus 2%o for nondiabetics
' canadian study (Yang and willy)'7 showed that the incidence of preterm
births among pregestational diabetes mellitus is 28% with S-fold increase
compared to nondiabetics
' Often associated with diabetes mellitus but cause is unclear but probably
secondary to fetal hyperglycemia with consequent polyuria and increased
osmotic pressure due to increased glucose concentration in the amniotic
fluid.

,-.".:. :-ssues ) functional CELLULAR

' Polyhydramions ) uterine overdistension ) pretem labor and derivery
- .' :.:ratic mobilization of glucose but . Altered Fetal Growth (Il4acrosomia or IUGR) and Associated Birth Trauma (Shoutder
- . -::se-lacking tissues secrete ketone Dystocia and Brachial Plexus Injury)
.': r.r--: (hyperglycemia) ) metabolic
' -::',ascuiar volume dePletion, loss ' 20-40% of infants of diabetic mothers have birth weights > 90th percentile
' : :-,.:e mia ) multiPle organ system for age of gestation (AOG)

Macrosomia develops from 20 weeks AOG onwards

: Fregnancy Pathophysiology of fetal macrosomia associated with maternal diabetes

mellitus:
Pederson Model:
Maternal hyperglycemia ) fetal hyperglycemia ) hyperplasia of the
._ . --e mic control. fetal pancreatic ) cells ) fetal hyperinsulinemia ) increased fat and
) anthropometrically distinct type
glucose deposition to fetal soft tissues
, :r:-:rre to deliver glucose (insulin of macrosomia with excessive growth of the shoulder area and trunk
: :'.:emia and hypoxia (failure of compared to the head ) more prone to shoulder dystocia
:.'. ; erg11'cemia-mediated shift of
-, -=: ) embryonichYPoPerfusion Macrosomic fetuses have significantly increased levels of pro-insulinlike
polypeptides (insulin-like growth factors IIGFI - IGF I and II) which are
potent stimulators of cell differentiation and division

Postprandial blood glucose (PPBG) levels in the 3d trimester rather than

rdisputedly associated with FBS is correlated with fetal size and birth weight.

l'7 *oT[[$-*iiFll'l
Llc. I l00dr'
 . Mean PPBG level of 120 mg/dL or above ) 30% chance of macrosomia b. Richey, et al (1995)e and D:
Hyperglycemia ) osmotic;
. Diabetic pregnancies have 6-times more prone to encounter shoulder placenta ) impaired fetal
dystocia compared to nondiabetic women' death

5. Congenital M alformat io ns
c. Another concept is the pcs,
of the endothelial-denvei
. Incidence of major malformations in those with oYefi/plegestational placenta.r'
diabetes mellitus is Soh andthese account for more than half of
perinatal
deaths in diabetic Pregnancies.r
R eferences
. The incidence of congenital anomalies is increasedby 4-8x in
pregestational
diabetes mellitus coripared to 7-2ohin the general population
with neural l. Sheffreld JS, Butler-Koster EL. C:
diabetes mellitus and infant ma,l::
tube defects increased by 4.2 fold and congenital heart disease by 3'4 30.
fold.t8 2. Johnstone FD, Nasrat AA. Pres:::
diabetes on pregnancy outcorne. i'
. However, diabetes mellitus is not associated with increased risk of fetal
,1. American Diabetes Associatlc:
chromosomal abnormalities. Diab etes Care. 1999 ;23 :Sl 0 .

4. Johnstone FD, Lindsay RS. Steel ,i

. The risk is primarily related to the poorly controlled glucose levels weight over 40 years at a single c-::
preconceptionally and during embryogenesis' 5. Garner P, et al. Type 1 DM in p:e=
5. Evers IM, de Valk HW, Visser GH
. PathophYsiologY:
with type I diabetes: Nation*'::.
2004;328(7445):915.
Maternai hyperglycemia )fetal
hyperglycemia )glucose-induced
:. Salvesen DR, Brudenell \I-I
disturbance in G- metabolism of substrates (inositol, prostaglandins, thrombocytopenia in pregnanc:e s :
oxygen (oz) free radicals) )endothelial destruction and narrowing
of
I Obstet Gynecol 1992;166(4).| )$-' :
vessel caliber )hypoperfusion to the O2-sensitive developing embryonic 8. Salvesen DR, Brudenell I\1. S:.
tissues/ orgatrt > gto.or.-induced embryopathy (congenital abnormalities) plasma erythropoetin in pregna:::
Am J Obstet Gynecol 1993; 168( l P:
6. (Jnexplained Fetal Demise 9. Richey SD, et al. Observatic:,s
pregnancy complicated by diab.::.
. Stillbirths without identifiable cause are a phenomenon relatively unique
10. Daskalakis G, Marinopoulos S Ii
et al. Placental pathology in uc:t:
to pregnancies complicated by overt/ ptegestational diabetes mellitus
S c and 20 08 ;87 (4) : 40 3'7 .

11. Stanek J, Eis AL, Myattt L. \

Possible explanations: increased extracellular matri-r -
a. Salvesen, et al (1992,1993)7,8 did cordocentesis and studied the 200 I ;22(Suppl A) : 55 6 : 562.
acid-base metabolism of these fetuses and found decreased pH and 12. Nathan DM. Long term c!-Iu:.:
increased pCOz in the fetal blood suggesting acidemia secondary 19 9 3 ;3 28 (23) : t 67 6 -8 5 .
to hyperglycemia-related classic observation in inhibiting oz and 1 3. Rossing K, Jacobsen P, Homcrc. .
insulin mediated glucose transport to tissues ("cellular hypoxia and and progression of diabetic ne:::
hypoglycemia,' phenomenon) ) fetal metabolic acidosis ) multiple Frank RN. Diabetic retinopath" -'
.','
Bloomgarden ZT. Neuropath"
orga,r1.{estruction and ultimately failure and death'
diabetes. Diabetes Care 2002'): :
ldry,lo.,,,
Tlt ,'
{r
rlr
18
 ,:or-e ) 30o/ochance of macrosomia Richey, et al (1995)e and Daskalakis, et al (200g)ro
Hyperglycemia ) osmotically-induced villous edema in the diabetic
:iJre prone to encounter shoulder placenta ) impaired fetal oxygen transport ) fetal acidemia and
_-:len. death

c. Another concept is the possible hyperglycemia-mediated disturbance

of the endothelial-derived nitric oxide (vasodilator) in the diabetic
: - : -i those with overt/pregestational placenta.lr
. -: -nt for more than half of perinatal
r

References
,,
- increasedby 4-8x in pregestational
:-<

- : the general population with neural l. sheffreld JS, Butler-Koster EL, Casey BM, Mcintire DD, Leveno KJ. Maternal
-'- : ,:d congenital heart disease by 3.4 diabetes mellitus and infant malformations. Obst€t Gynecol2002;100(5 pr l):925-
30.
2. Johnstone FD, Nasrat AA, Prescott RJ. The effect of established and gestational
diabetes on pregnancy outcome. Br J obstet Gynecol1990;97(rr):1009-15.
',.:crated with increased risk of fetal -
3. American Diabetes Association. Clinical Practice Recommendations 1999.
D iab etes Care. 1999 ;23 :Sl 0,
4. Johnstone FD, Lindsay RS, steel J. Type I diabetes and pregnancy: trends in birth
-:: poorly controlled glucose levels weight over 40 years at a singre clintc, obstet Gynecot 20d6;lol6y:nel-soz.
' -. -:enesis. _
5. Garner P, et al. Type I DM in pregnancy. Lancet 1995;346:157.
6. EversIM, de valk HW, visser GH. Risk of complications of pregnancy in women
with type I diabetes: Nationwide prospective study in the Netherlands. BMr
--. :vperglycemia )glucose-induced 2004;328(7445):915.
.' s.;bstrates (inositol, prostaglandins, 7. salvesen DR, Brudenell MJ, Nicolaides KH. Fetal polycythemia and
thrombocytopenia in pregnancies complicated by maternal diabetes mellitus. Am
- :.--:iial destruction and narrowing of J Obstet Gynecol 1992;166(4):1287 -93 .
,:.: O:-sensitive developing embryonic
: : :1 : n'opathy (congenital abnormalities)
8. Salvesen DR, Brudenell JM, Snijders RJ, Ireland RM, Nicolaides KH.
Fetal
plasma erythropoetin in pregnancies complicated by maternal diabetes
mellitus.
Am J Obstet Gynecol 1993;t61(l pt l):gg-94.
9. Richey sD, et al. observations concerning "unexplained" fetal demise in
pregnancy complicated by diabetes mellitus. r Matern Fetal Med 1995;4:169.
-- j: l:e a phenomenon relatively unique 10. Daskalakis G, Marinopoulos S, Krieresi y,papapanagiotou A, papantoniou N,
: : -. :regestational diabetes mellitus et al. Placental pathology in women with gestational diabetes. Acta Obstet
Gynecoit
S c and 20 08 ;87 @) :40 3 -7 .
ll. stanek I Eis AL, Myattt L. Nitrofyrosine immunostaining correrates with
, .::d cordocentesis and studied the increased extracellular matrix evidence of postplacental ilypoxia. placenta
2001 ;22(Suppl A) 556 : 562.
!f , :::uses and found decreased pH and :

12. Nathan DM. Long term complications

:- :.:-.d suggesting acidemia secondary of diabetes mellitus. N Engt J Med
19 9 3 ;328(23) : I 6t 6-8 5 .
- * :.r observation in inhibiting 02 and 13. RossingK,JacobsenP,HommerE,MathiesenE,svenningsenA,etal.pregnancy
:'- - i:lrt to tissues ("cellular hypoxia and and progression of diabetic nephropathy. Diabetitogia 200i;ase),J6-ar.
, tetal metabolic acidosis ) multiple 14. Frank RN. Diabetic retinoparhy. N EngtJ MedZOO+;:SO1t;:+A-Sb.
.."" tailure and death. l5' Bloomgarden zr. Neuropathy, womens' health and socioeconomic aspects of
diaberes. Di ab etes C are 2002;2 5 (6) : I 0 g5_ I 094.

19
'*'iH;oflo$,liHlo
t6. Sibai BM, et al. Risk of preeclampsia and adverse neonatal outcomes among r@rr l. .ileorithmic Pathophysiologr : D
women with pregestational diabetes mellitus. Am J Obstet Gynecol2000;182:364.
17. Young and Willy.
18. Reece EA, et al. Pregnancy outcomes among women with and without diabetic \l:ttcrnrl ( omrrl:r-
microvascular disease (White's Classification B to FR) versus nondiabetic
controls. Am J Perinatol 1998;15:549. l'lacerrl:t-drlir utl lrr,r-
t9. Klein BEK, et al. Effect of pregnancy in progression of diabetic retinopathy. csll'(){elts erusc dcer ci:., :
Diabetes Care 1990;13:34.
20. Chaturvedi N, et al. The relationship between pregnancy and long term maternal Sustairreil I lyl,hlt(.i1.\'( l' \l l.\
complications in the EURODIAB IDDM complications study. Diabetic Med
1995;12:494.
I
l__
lvpclglvccrria-indrrced rrre l.rl,,,i,r- .
21. Arun CS, et al. Influence of pregnancy on long term progression of retinopathy in
distrr{rancc: Ir':creirscrl li.cl O, rrrrl:.., .
patients with type I diabetes. Diabetologia 2008;51:1041. r lrsoc0nstrirters.l)lt1cl.t rrlt c!.rt, :.
(llrrurrbcrancs ,-\l i

I I rtrl,rtlrr'li:tl ltttrtr.- Jr':tru. r,' .r'-.

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20
&r:i:. and adverse neonatal outcomes among Figure
b' ::::liirus. Am J Obstet Gynecol2000;182:364.
Er-.:j among women with and without diabetic
h --r'sification B to FR) versus nondiabetic
ff-:
l1::..--,' in progression of diabetic retinopathy.
l. Algorithmic Pathophysiology: DM-Related Maternal And Fetal Complications
llatu'nIl ( irnruliqrlions
l'laerntl-tlerir ctl lxrrrrritrrcs ( hlll., pnrqcslenrnc antl
cslr(uclrs ulru-.e dcercased lisruc sqnsitir.itv ttr thr: t:l li'uts
of insulirr

E: :€s-een pregnancy and long term maternal liustairrcd

- - -.' ------*-*'---1
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l
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I lr'pei *lyccrniu-inrlncctl urctlhll iles

;ni: --. :n long term progression of retinopathy in di:lLrrharrcr': In*relsctl licr: O: r'irdicrlr lrrrd Secrction oi'[,rltrrre lxrtlics liorl
hu;-- --r:: 2008;5 1: 1041. r :rso*(rrrstriclorslplatclcl lggrculrlorr gluc()s*-hck ilrt.r IirsrIs anJ
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 Frlrl ( onttrlitatittns
DIAGNOSIS AND
ffi",*t.'rir art itptnttxtes (lll'l'. l)l(rr'(\lcr{rrte
irrld s:11{r!'ill' !'ritst
Ernesto S. Uichanco, MD anC
' r'l-itt:ulttt ) ln'rt'lll rl
,t..t..,'a,, itr',,. :eit'tlir ttr lr'llre ellitt'
lrlperglrccnril ) lctrl llpcrglleerrrir

-- F1::l f[:j::'*i;:'r;] liabetes mellitus is a grouP .

l :\perglycemia resulting from defe-
Ilrtr.tL'\.rttt'.1 ittlll"l 1r11 1'rlr.l tr'r
.1r,,i,,rh,,,,.., ilr,t,rr"'l li'r t) r'rlie'rls
lr lr'ttl1.'
l-ctrl , .a.,.t,.',, r'r lrl''tld lr')'l i\ lli'll1
rnd \ )-(r)rtill\tf iet{tl \'irlrl'lct
I
tlt utrr ir I 111lrL src trt.l ll r.""-l'trt'lti tlirri\
rrt.l rllafcgJlols (lhlr)llll)r)\illlLs'\-l i !;l#1.
I
?athogenic processes involved rn ::,
t
high
uti'rr -. Autoimmune destruction cf :h.
gl lrterc*:c.l r.i,lrtrti t l ilh 'rcltl lrrt(lr'rle\i
( o trc{:ll. gluco:u lrndolhclt.rl lintug rlc:iruction an'l li:suc tllttt:ltge tl) alr{llls insulin deficiencY
trtt ott lit Abnormalities that resuil in :3s:
il
i

tlr,:
rnrl
tlcpr.rsil iun
ixtrsc(lrlLlll ttrrrtrrl ilt6 0i' I esrcl -
.\l trt I'r'trl soli
tissrtcs
-he American Diabetes Assocla:::
I ltolerance:2

Type I diabetes mellitus: dt;-::

it is thought to be caused b'' ::
pancreas, resulting in deficie:.: I

Diabetic ketoacidosis (Dll{ :,

of diabetes mellitus.

TypeZ diabetes mellitus: ai';-

Patients with type 2 dial'et;s
the disease can often be ccr::
followed diet.

It is thought to result from rns.

rather than their destructi.'n

Gestational diabetes melliru:

during pregnancy.

In most patients, it subsides :,-

subsequent Years occurs nl:::
The diagnostic criteria for ,jl---:.'
pregnant states are tabulated r: -,'-

'*e.*-*rr4 1xg
.:j

1,1 .. 22
 DIAGNOSIS AND CLASSIFICATION
. iilt(i cilflr!clli ci\[sc
in\ulir ) nlit(rnrl S. Uichanco, MD and Ma. Cristina P. Crisologo, MD
! !clril

l'. ':etes mellitus is a group of metabolic disease characterized by

: .:ergJvcemia resulting from defects in insulin secretion, insulin action or

L'
t i:::ogenic processes involved in the development of diabetes mellitus:
- -\utoimmune destruction of the f3-cells of the pancreas, with consequent
insulin deficiency
- .\bnormalities that result in resistance to insulin action on target tissues

-:ie American Diabetes Association (ADA) three forms of glucose

-::clerance:2

Type 1 diabetes mellitus: diabetis mellitus diagnosed in childhood.

It is thought to be caused by immunologic destruction of the cells of the
pancreas, resulting in deficient insulin replacement.
Diabetic ketoacidosis (DKA) is more common in patients type
of diabetes mellitus.

Type 2 diabetes mellitus: adult-onset glucose intolerance.

Patients with type 2 diabetes mellitus are frequently overweight, and
the disease can often be controlled with weight control and a carefully
followed diet.

It is thought to result from insulin resistance and exhaustion of the cells,

rather than their destruction.

3. Gestational diabetes mellitus (GDM): glucose intolerance identified

during pregnancy.

In most patients, it subsides postpartum, although glucose intolerance in

subsequent years occurs more frequently in this group of patients.

The diagnostic criteria for diabetes mellitus in the nonpregnant and the
pregnant states are tabulated in Tables l, 2 and 3.

z) nAYillAL mctoA,lti
O8.CYT JRRtrC
|
LIc. 10ltle
Table 1. Criteria for the diagnosis of diabetes mellitus in the nonpregnant
state3 ::::;mrned to have, in fact. t]?e: c:
Diabetes :-r. tr.res diabetes mellitus because
Normal Impaired fasting
values glucose/ImPaired mellitus :r:'. become normogl)'cmeic on:e
glucose tolerance
'-:.e: ma\- develop diabetes mel-l::,
--: :ancreatitis. Thus, for the cl.:::
110-125 mg/ dL > 126mg/dL
Fasting plasma <100 mgldl- :: ia:el the particular t)-pe oi l:ai
glucose :.:: :_qenesis of the hvperglr'ce:r::.
75 g OGTT
<140m9/dL 140-199 mg/dL > 200 mg/dL
2nd hour plasma

symptoms of diabetes
Fgore I. Disorders of gl1'cemta
mellitus and plasma normoglr'cemla
glucose (without regard
to time of last meal) >
200 mg/dL

TableZ Diagnostic criteria for GDM

75 gram OGTT 75 gram OGTT 100 gram OGTT
(wHo) (IADPG) (Carpenter & Coustan)

95 mg/dL 95 mg/dL 95 mg/dL

Fasting plasma glucose
l-hour 180 mgldl 180 mgldl- 180 mgldl-

2-hour 155 mg/dL 153 mg/dL 155 mg/dL

140 mg/dL
3-hour
* Diagnosis of GDM is made when 2 0r more of the values are elevated
**Diignosis of impaired glucose tolerance is made when t of the values is elevated

Tabte 3. Diagnostic ctiteria for overt diabetes in pregnancya

Fasting plasma glucose > 126mg/dL

-n the recent years, there hare L'ee:
Glycosylated hemoglobin (HbA1C) > 6,50h : Berghella, et. al.5 states rh.r: C-

Random plasma glucose > 200 mg/dL beyond 20th week age of ges::.::
cutoff was assigned for the ,ira:
. In 2010, the International of
Diabetes and Pregnancy Study
Association : Ray, et. al.6 introduced a n:'.,
Groups (IADPG) made its recommendations on diagnostic criteria for ovett/ requires the absence of dta::
p..g.ituiional and GDM, after reviewing result of the Hyperglycemia and presence of blood glucose 1e'.:-
Adverse Pregnancy Outcomes (HAPO) study' that are higher than normal. :u:
criteria for GDM.
. Assigning a type of diabetes mellitus to an individual often depends on the
circumstances present at the time of diagnosis, and many diabetic individuals ',irnator's Note:
do not easily fit into a single class. For example, a woman with GDM may ;'.oid confusion, let it be emplrcs:i: :::.
conrinue to" h*te hyp.prglicemic episodes long after delivery, and may be ,":,t classifcation scheme for GD.! :.
aA
-t
r
I

.-iius in the nonpregnant state3 determined to have, in fact, type 2 diabetes melritus. Alternatively, person
a who
-lc;aired fasting Diabetes acquires diabetes mellitus because of large doses of ."og.rrou,
,teroid intake
;nur,::se /Impaired mellitus may become normoglycmeic once the glucocorticoids ire discontinued,
but
glir,::,ie tolerance t\n may develop diabetes mellitus many y.a., later after recurrent episodes
: mg/dL > 126 mg/dL
of pancreatitis. Thus, for the clinician and the patient, it is less important
to label the particular type of diabetes mellitus than it is to understand
the
pathogenesis of the hyperglycemia, and to treat it effectively.r

) mg/dL > 200 mg/dL

symptoms of diabetes Figure l. Disorders of glycemia: etiologic types and stages.r

mellitus and plasma Types normoglycemia hyperglycemia
glucose (without regard
to time of last meal) >
240 ms./dL
Stages Normal glucose Impaired glucose Diabetes mellitus
regulation tolennce/
Impaired fasting
glucose (pre-
-5 gram OGTT
tr 100 gram OGTT diabetes)
(IADPG) (Carpenter & Coustan)
Not Insulin Insulin
!5 mgldl- 95 mg/dL
requiring requiring requiring
- St-'l mgldL 180 mgldl- for control for survival
Iype I
- 53 mgldL 155 mg/dL
140 mg/dL Type2

I?"- :.res Are elevated

Other specific
n;- :,: 1 of the values is eleyated
rypes

G"r.trrr.l
$u' :regnancya diabetes mellit s

> 126mg/dL
, In the recent years, there have been other definitions proposed:
o Berghella, et. al.s states that GDM is diabetes meil-itus developing at or
> 200 mg/dL beyond 20th week age of gestation, whereas previously, no gestationar
age
cutoff was assigned for the diagnosis of GDM.
!E:.--r of Diabetes and Pregnancy Study o Ray, et. al.6 introduced a new term, "gestational prediabetes,,,
m: ,:rtions on diagnostic criteria for overt/ which
requires the absence of diabetes melliius before prrgnun"y,
!E :.',ing result of the Hyperglycemia and and the
presence of blood glucose levels (or arelated
marker) in early pregnancy
S,":-: I study. thatare higher than normal, but not yet high enough to meet
tne aagnostll
criteria for GDM.
&:-: :o an individual often depends on the
r : ::rgnosis, and many diabetic individuals Coordinator's Note:
rs - -.r example, a woman with GDM may To avoid confusion, Iet it be emphasized that what
was presented ealier in the text is the
c =:,;--des long after delivery, and may be ?resent classif;cation scheme
for GDM (as established- internationalf). There will be
-- 2s *1u11-*ifFflfrJo
Llc. I l00lll
changes/revisionsthatwitlbepresentedinthenextchapteronScreeningandDiagnosis
SCREENING A}
and that
paIticularly HAP7 rrial (se.e table below)
based on the results oy ,rr:rnt itudies
we may not be necessarity foltowing-this interiationally
accepted values locally but base Walfrido W. Sumpaico, \lD
*od, during tlti pocs consensus Meeting' Full
our yalues according ,o"ilrr- ro,ruriu,
witt be discussed in the next chapter
,*ptorotlon, and bises

i.ecommendations on Detection and I

> 92 mg/dL
iJipino Pregnant Women
> mg/dL
125 > 92mg/dL
(5.1 mmol/L) (5.1mmol/L)
(6.9 mmol/L) )abetes mellitus recognized dunn;
::ther gestational diabetes mellitus , (
>180 mgldl.
(10 mmol/L) :lasma glucose levels.r-2 (Level III. C'
>153 mg/dL >140 mg/dL
>I40 mg/dL
(8.5 mmol/L) (7.8 mmol/ml) - - niversal screening for GDM is rec:
(7.8 mmol/L) j,:de B)
xValues are based on outcome datafrom the HAPO study ' -rr the first prenatal visit, determint
*xValues are based on POGS Consensus Meeting
:-storical and pregnancy risk factcrs

- r^11 Filipino gravidas are considert

References ?acific Islander) and should be sc:
:-.rst prenatal visit (fasting blood s
i.AmericanDiabetesAssociation.Diagnosisandclassificationofdiabetesmellitus. "JbAlcl or random blood sugar
[R.:
Diabetes Cate 20ll;34(suppl 1):562-569'
2.AmericanCollegeofobstetriciansandGynecologists.^.^Gestationaldiabetes.
ACOGPracticeiulletinNo'30'ObstetGynecol200i;9S(2):525-538'
' .- diagnosis of overt diabetes mellitr
:-.llorving results in their f,rrst visit :
3.AmericanCollegeofobstetriciu.',--u,,aGynecologistsPracticalBulletin. . FBS > 126 mg/dL (7 mm:.
Pregestationat
pl?Utt"t' Obstet Gynecol 2005 ; I 0 5 675 -84' :

uK
. RBS >200m9/dL (11.1r::
Evidence Based Guidelines. Informa . HbAlc > 6.5oh
i. ft?i$ir3'"itnt. Maternar-Fetal . 2 hour 75 goralglucose tole:.:
Ltd.2007;43-55' prediabetes: a new
Ray JG, n.rg"t H, Lipscombe LL' Sermer
M' Gestational
6. Med Res 2010;132.251'255'
term for.u'fy pt*niiJn? Indian J
Companies Inc, US' ' -. :iagnosis of GDM is made if a:.
7. Cunningham ff.- wittiu-, obstetrics'ilra "a.McGraw-Hi11 =r,-eeded @ased on American Dia':.
2010. .--ssociation of Diabetes and PrrS:..
Group' Hyperglycemia and adverse
8. The HAPO Study Cooperative Research :::eshold):2 (Level III, Grade C)
581991-2002"
pregnancy ot'i"o"ttt' N bngl J Med 2008;3
. FBS > 92mg/dL
. t hour > 180 mgidL
. 2 hour > 153 mgldl
- l,.r Filipino pregnant women. POG
,:ilori'ing cut off values for the J.:-:=
-::normal.3'a (Level III, GPP)

:l t:Nd
' .ji' 26

l: . ,'t'l i
I w : ': next chapter on Screening and Diagnosis SCREENING AND DETECTION
;c"-. :'.'r' HAPO Trial (see table below) and that
fi :*:,":;riorlally accepted values locally but base Walfrido W Sumpaico,.MD and Angelita R. Teotico, MD
s;, :iritg the POGS Consensus Meeting' Full
b: -, ':itt chapter.
IADPSG/ADA POGS-CPG
Consensus* Consensus** il.ccommendations on Detection and Diagnosis of Diabetes Mellitus Among
> 92 mg/dL > 92me/dL Iilipino Pregnant Women
(5.1mmol/L) (5.1mmol/L)
Diabetes mellitus recognizedduring pregnancy should now be classified as
either gestational diabetes mellitus (GDM) or overt diabetes mellitus based on
plasma glucose levels.r-2 (Level III Grade C)
>140 mg/dL
J (8.5 mmol/L) (7.8 mmol/mL) - , niversal screening for GDM is recommended for Filipino gravidas. (Level III,
Grade B)
s.: , 7.4PO study
3 - :.a::rig --rr the first prenatal visit, determine if the gravida is high risk or not based on
:istorical andpregnancy risk factors. (Level III, Grade B)

I - .=:sis and classification of diabetes mellitus'
E; - , :nd Gynecologists. Gestational diabetes'
E. -,-:et Gynecol 2001;98(2):525-538.
ff,- :..: and Gynecologists Practical Bulletin'
[ ]' - =,-:l 2005;105:675-84.
:',idence Based Guidelines. Informa UK
LF".
: - - Sermer M. Gestational prediabetes: a new
bn l.'-:J Res 2010;132:251-255.
!r: --. l,lrd ed. McGraw-Hill Companies Inc, US.
ir :.;:arch Group. Hyperglycemia and adverse
! ],i. : - -108;358: 1991 -2002..
- -l,ll Filipino gravidas are considered "high risk" by race or ethnic group
Pacific Islander) and should be screened for type 2 diabetes mellitus in the
ilrst prenatal visit (fasting blood sugar [FBS] or glycosylated hemoglobin
iHbAlcl or random blood sugar IRBS)]. (Letel III, Grade C)
: .{ diagnosis of overt diabetes mellitus is given among women with any of the
following results in their first visit:2 (Level III, Grade B)
. FBS > 126 mg/dL (7 mmol/L)
. RBS >200mg/dL (11.1mmol/L)
. HbAlc > 6.5oh
. 2 hour 75 goral glucose tolerance test (OGTT) > 200mg/dL (11.1 mmol/L)
: A diagnosis of GDM is made if any one of the following plasma values are
exceeded (based on American Diabetes Association [ADA] and International
Association of Diabetes and Pregnancy Study Group [IADPSGI consensus
threshold):2 (Level III, Grade C)
. FBS > 92 mg/dL
' I hour > 180 mg/dL
. 2 hour > 153 mg/dL
- For Filipino pregnant women, POGS CPG Consensus Panel recommends the
following cut off values for the diagnosis of GDM. Any value is considered
abnormal.3-a (Leuel III, GPP)

27 ill+llAR ilAetDA,lr.D,
08.0Yr lRRiltc
th. I legile
 . FBS > 92 mg/dL (adapted from ADA and iADPSGP consensus .-. diagnosis of overt diaberes mellin
threshold) or 2 hour >140 mg/dl (adapted from World Health :' :e following criteria at their initial pr
Or ganization [WHO] recommendation) . FBS > 126 mg/dL (7.0 mmol L
* These values will be used as cut off to minimize underdiagnosis until . lIbAlc > 65% using a srandard:
recommendations from results of local clinical studies to validate these values . RBS > 200 mg/dL (11.1 mn:
can be made. elevated FBS or HbAlc.
lhese thresholds were chosen beca
8. For Filipino gravidas with no other risk factors aside flom race or ethnicity i.:.::se vascular events, such as retinopa
and the initial test (FBS, HbAlc or RBS) is normal, screening for GDM .-.. diagnosis of GDM can be made in
should be done at 24-28 weeks using a 2 hout 75 g OGTT. If there are other ::::::a::
risk factors identified, screening should proceed immediately to 2 how 75 g . FBS > 92 mg/dL (5.1 mmol L
OGTT at first consult. (Level III, Grade C) gestational age (FBS 2 126 mg .
diabetes mellitus)
9. If the OGTT at24-28 weeks is normal, the woman should be re-tested at 32 . At 24-28 weeks of gestarion: i
weeks or earlier if clinical signs and symptoms of hyperglycemia ale present abnormal result: FBS > 92 rn_s ;
both in the mother and the fetus (e.g. polyphagia, polyhydramnios, accelerated mmol/L) or one hour > 180 ng
fetal growth , etc). (Lettel II-2, Grade B) dL (8.5 mmol/L)
lhe rationale for these thresholis
10. The OGTT should be performed in the morning after an overnight fast of 8 -,-'.::se Pregnancy Outcome GI{PC
hours following the generalinstructions for the test. (Level III, Grade B)
-.--.me even in plasma glucose values b
. To preparc for the OGTT, the patient is advised to: :cr Filipino pregnant women. PC(
. Observe an overnight (at least 8 hours, but not more than 14 hours) ": . :ne of the following cut off r'alues ::
fast prior to the testing . FBS > 92 mg/dL (adapted fro:
. Have an unrestricted diet e 150 grams of carbohydrates per day) for or 2 hour >140 mg/dL (adaple:
at least 3 days Prior to the testing * These values will be used ;,
. Remain seated and should not smoke during the test
recommendationsfrom resuks c€ ":-
made.

Summary of Evidence

New Terminologies
7 4 Screen?
Since the beginning, the objective o:
The term "gestational diabetes mellitus" has been used in the past to define
women with onset or first recognition of abnormal glucose tolerance during :-:-term type 2 diabetes mellitus anJ :t
- : .i :hat the focus has shifted to the pe:::
pregnancy. However, in 2010, the IADPSG, an international consensus gloup
with representatives from multiple obstetrical and diabetes mellitus organizations,
recommended a change to this terminology. They recommended that diabetes ?roponents for screening have pur ::l
mellitus diagnosed during pregnancy should be classified as overt or gestational.
The rationale for this change is because of an increasing proportion of young \lDM is one of the most common :r:.
women with unreco gnized Wpe 2 diabetes mellitus due to the increasing prevalence srgnificant maternal, fetal and nec.:
of obesity and lack of routine glucose screening/testing in this age group.'In ieral Complications)
January 2011, the ADA endorsed this recommendation.2 The American College
of Obstetricians and Gynecologists (ACOG) has not yet taken a position on the - rdverse outcome associated ri'ith ;:::
proposed change. .-..ntinuously as maternal FBS lere- :

, '1 ,'".;Jt;
'i,. ,, .: 2g
4 )l
,.-, i
r
I
i
::n ADA and iADPSGP consensus
-g dL (adapted from World Health
-.:.Jation)
.'..: c_f to minimize underdiagnosis until
' .:;. clinical studies to validate these values
-:!\ iactors aside from race or ethnicity
- :-3S) is normal, screening for GDM
. I hour 75 g OGTT. If there are other
-_ aro...O immediatelY to 2 hour 75 g
,:
-,, :he rvoman should be re-tested at 32
: .:::proms of hyperglycemia are present
; - -'. phagia, polyhydramnios, accelerated
-,=norning after an overnight fast of
: - -. :rr the test. (Level III, Grade B)
- .:-: is advised to:
-, . S nours, but not more than 14 hours)
: - grams of carbohydrates per day) for
: .-noke during the test
.-. has been used in the past to define
-: abnormal glucose tolerance during
: iG. an international consensus group
- ::l and diabetes mellitus organizations,
-:'. They recommended that diabetes
, -.: be classified as overt or gestational.
:: an increasing proportion of young
', ::;llitus
due to the increasingprevalence
,--:eening/testing in this age group.' In
, :, nmendation.2 The American College
- J r has not yet taken a position on the
A diagnosis of overt diabetes mellitus can be made in women who meet any
: i rhe following criteria at their initial prenatal visit:2
. FBS > 126 mg/dL (7.0 mmol/L), or
. lIbAlc 2 6.5o/o using a standardized assay, or
. RBS > 200 mg/dL (11.1 mmol/L) that is subsequently conflrmed by
elevated FBS or HbAlc.
These thresholds were chosen because they correlate with development of
r.
"''erse vascular events, such as retinopathy and coronary artery disease.
A diagnosis of GDM can be made in women who meet either of the following
:::eria:2
. FBS > 92 mg/ dL (5. I mmol/L), bur < 126 mg/ dL (7 .O mmol/L) ar any
gestational age (FBS > 726 mg/dL 17.0 mmol/Ll is consistenr with overt
diabetes mellitus)
' At 24-28 weeks of gestation: 2 hour 75 gram OGTT with at reast one
abnormal result: FBS : 92 mg/dL (5.1 mmol/L), but < 126 mg/dL (7.0
mmol/L) or one hour > 180 mgldl- (10.0 mmol /L) or 2 hour 2153 mg/
dL (8.5 mmol/L)
The rationale for these thresholds was based on the Hyperglycemia and
8
--:\'erse Pregnancy outcome (HAPO) study, which showed adverse perinatal
: -:come even in plasma glucose values below the known normal cut off levels.3
For Filipino pregnant women, POGS CpG consensus paner recommends
i:i' one of the following cut off values for the diagnosis of GDM.a
' FBS > 92 mg/dL (adapted from ADA and IADSp consensus threshold)
or 2 hour >140 mg/dL (adapted from WHO recommendarion)
* These values will be used as cut off to minimize underdiagnosis until
recommendationsfrom results of local clinical study to validate these values can be
made.
Ihv Screen?
since the beginning, the objective of screening rested mainly on prediction of
---.9-term type 2 diabetes mellitus and its maternal complications and it is only
::'.i'rhat the focus has shifted to the perinatal risks of GDM.
Proponents for screening have put forth the following arguments:
GDM is one of the most common medicar problems in pregnancy (3-5%) with
significant maternal, fetal and neonatal risks. (Refer to chapter on Maternal and
Fetal Complications)
- Adverse outcome associated with diabetes mellitus during pregnancy increases
continuously as maternal FBS level and OGTT value increases. This relation
29
$wllA R IAC,EDA' tl'D
oB.GYl lRRlilllc
Ln, I l0t{1!
 is reported in the IIAPO Study wherein adverse perinatal outcome were also "- : lr€\'dl€nce of GDM in log--nsk
observed in patients with plasma glucose values below the previously set --- l"I in the high-riskgroups, the higi
normal cut off levels. :-:i :'.nce rate statistics alone argues :
-- -::--:,sk groups (Table 2) among Filip:
3. There is an increasing prevalence of diabetes mellitus worldwide. The number :: =:.:-:ned medical risks of GD\I an.i
of people with diabetes mellirus is increasing due to population growth, aging, '-: :"ipinos seems more tenable ncr
urbanization and increasing prevalence of obesity and physical inactivity. " .--.:lin' and cost of testing. The -{::
- -::::tr)' favor universal screening.

4. Type 2 diabetes mellitus now outnumbers type I diabetes mellitus at a 4:l -: l-< our consensus that u.e locall'
ratio. In view of the severity and long-term complications of this disease, the J-:::o gravidas are considered h::
health consequences of this disease threaten to overwhelm the health care
, '::er) and should be screened for r
"i -:
systems of vulnerable countries. The Asia-Pacific region which includes our
country is at the forefront of the current epidemic of diabetes mellitus.
l&nc l. Identihcation of High Risk Gr;;:
Whom To Screen: Universal or Selective Screening?
' :{lstorical risk factors
' Fast pregnancy - ab:;::r
congen:::
Opinion is currently divided as to whether universal or selective screening
for GDM should be done. Proponents for selective screening state that screening unexpl::
should be limited to women with any of the risk factors listed in Table 1.
'?resent pregnancy faml', :.-=
Table 1. Risk Factors for Diabetes Mellitus during Pregnancy mater::a-
drugs a:
Pregnant women with any of the following appear to be at increased risk of developing (sterc::
GDM.5'6 '.
age -1 I ,::
> 25 years of age racia.:::.
< 25 years of age and obese (> 20o over desired body weight or body mass index
Jbstetric risk factors polr h.,'J::
[BMI] >27 kg/m'z)
Pre-pregnant weight > 110% of ideal body weight or BMI > 30 kg/m2 or significant macris _-:
weight gain in early adulthood and befween pregnancies feral ai::
Family history of diabetes mellitus in first-degree relatives Iecuare:.:
Previous delivery of a baby greater than 9 pounds (4.1 kg)
Personal history of abnormal glucose intolerance
Member of an ethnic / racial group with a high prevalence of diabetes mellitus (Hispanic' 7'-cn To Screen?
American, Native American, Asian-American, African American, or Pacif;c Islander)
Previous unexplained perinatal loss or birth of a malformed child
Maternal birth weight greater than 9 pounds (4.1 kg) or less than 6 pounds (2.7 kg)
.':: trllorving are based on IADPSG r,
Glycosuria at the first prenatal visit : .:)-{:
Polycystic ovary syndrome . For women without the afore::
Current use of corticosteroids be performed berween the l{::
Essential hypertension or pregnancy related hypertension . For women with risk facrors :
prenatal visit. If initial resl :ts
ACOG, the American Academy of Pediatrics (AAP) and the 4th International
at 24-28 weeks and again ia:c:
Workshop on Gestational Diabetes Mellitus (4th FIW-GDM) favor selective
sensitivity as pregnanc\. prog:::
screening. The Association of South East Asian Nations (ASEAN) Study
Group on Dtabe.tbpinrk6gnancy (ASGODIP) lists the Philippines as having a
"ol\r
trr.;, *lii
"'" '--*
30
f
I
i

I
t

*:
-:- adverse perinatal outcome were also
: -::se values below the previously set
:
= :i obesity and physical inactivity.
-r:rs rype 1 diabetes mellitus at a 4:7
-.'::::n complications of this disease, the
.:-:iaten to overwhelm the health care
--s:a-Pacific region which includes our
, -: :pidemic of diabetes mellitus.
-'-[oh prevalence of GDM in low-risk patients but has a 38% prevalence rate of
]DM in the high-risk groups, the highest among its member countries. This high
:revalence rate statistics alone argues for mandatory or universal identification of
:igh-risk groups (Table 2) amongFilipino gravidas. Add to this statistic the above-
:rentioned medical risks of GDM and the proposal for universal GDM screening
rr Filipinos seems more tenable not withstanding the problems of technology
:vailability and cost of testing. The American College of physicians and the ADA
:urrently favor universal screening.
It is our consensus that we locally advocate LTNIVERSAL screening. ALL
lilipino gravidas are considered "high risk" by race or ethnic group (pacific
-:lander) and should be screened for type 2 diabetes mellitus in the first prenatal
'.'rsit.

Table 2.Identihcation of High Risk Groups for GDM

* Historical risk factors
5:'::zing? * Past pregnancy
abnormal glucose tolerance macrosomia (birthweight = 8 lbs)
-=:her universal or selective screening congenital malformations
recurrent abortions
==-:ctive screening state that screening unexplained intrauterine death
:' -- : ::sk factors listed in Table 1.
* Present pregnancy family history (first degree relation)
--:-: Pregnancy maternal obesity (> l80lbs or BMI >27 kg/m2)
drugs affecting carbohydrate metabolism
(steroids, betamimetics, etc.)
age 30 years
racial predilection
:=s:red body weight or body mass index * Obstetric risk factors polyhydramnios
.'::ght or BMI > 30 kg/r* or significant macrosomic fetus
-.,.::n pregnancies fetal abnormality
:.::ee relatives recurrent genital tract infections
: - ::rJs (a.1 kg)

" . ' :.:.,:lence of diabetes mellitus (Hispanic- When To Screen?

- ' ;:: .4flican American, or Pacif;c Islander)
- -- -: amalformedchild
lhe following are based on IADPSG recommendations which was later adapted.
-' :' l.1 kg) or less than 6 pounds (2.7 kg)
:1'ADA:
' For women without the aforementioned risk variables, screening should
be performed befween the 24th and 28th weeks of gestation.
' For women with risk factors, they are immediately screened at the first
prenatal visit. If initial test results are normal, repeat tests are in order
:.rtrics (AAP) and the 4th International
at 24-28 weeks and again later at 32-34 weeks due to increasing glucose
:.rs (4th FIW-GDM) favor selective
sensitivity as pregnancy progresses.
:.st Asian Nations (ASEAN) Study
3lP) lists the Philippines as having a

3l
h*rFtu B. HCIDA, tD
O8.GVT JRRITC
Lis. i lo9ll9
During the POGS CPG Consensus Meeting, the following have been agreed upon: -":,-Siep Testing / Normql Vqlues
. The Filipinos are among the high risk groups for developing type 2 diabetes
mellitus, prevalence rates have been estimated to be between 8-100/0.t6-t8 Certain quarrers WHO, ASE.{\
. Because of this data, the following is recommended: :":::ng scheme. Basically, the anhrdr:
o All Filipino gravidas are considered "high risk" by race or ethnic , ,::r value measured 2 hours after gi;
group and should be screened for fype 2 diabetes mellitus in the first .\ value > 140 mg/dL is conside:e
prenatal visit (FBS or HbAlc or RBS).

How To Screen? Screening vs Diagnostic Testing -":,-S:ep Testing / Normal Value: C,;.,,. F
. There is no worldwide standard for screening and diagnosis of diabetes
mellitus in pregnancy. 3ecause of increasing incidence :
: j:.:tg rvhen routine initial prenata. ..,
. Screening is usually performed as a fwo-step procedure where step I identifies :--.: convenient.
individuals at risk for the disease followed by step 2 which is a diagnostic L\DPSG and ADA recommenci'::
testing that will establish the disease. Step 2 is more complicated and costly i :S or FBS at the initial visit and dc::
requiring two elevated values for diagnosis. Doing a two-step approach will :"j-*i are normal. (Refer to Algorithn
exclude low risk individuals. The fwo-step test is the one recommended by
' his recommendation has not b,e e :
ACOG. -, ::agnosis of overt diabetes melli::s
. Another approach is doing the one-step procedure which is a diagnostic test to -.:le -1):

all individuals proposed by the IADPSG and endorsed by the ADA.

- FBS > 126 mg/dl (7 mmot ;_
- HbAlc > 6.5o/o using a sranc,::
. The one-step diagnostic test was simplified by giving a2-hour 75 g OGTT and - RBS > 200 mg/dL (11.1 mn:,.
requiring only a single elevated value for diagnosis.1,2 elevated FBS or HbA l c.
..' diagnosis of GDM is made ii :.:
Two-Step Testing / Normal Values (ACOG Recommendation)ta , FBS > 92 mg/dL bur less tha:
- l-hour 75 g OGTT 2 lg0 me .
The screening test consists of a 50 g oral anhydrous glucose load (oral glucose - 2-hour 75 g OGTT > 153 mg .
challenge test [OGCT]) followed by a plasma glucose determination I hour later.
The patient need not be fasting before the glucose load.
These recommendations are sup:.
A value of either >140 mg/dL (7.8 mmol/L) or > 130 mg/dL (7.5 mmol/L) :.,-h evaluated more than 23,000 p:;,
t hour after the 50 g load, indicates the need for a full diagnostic 3-hour 100 g - , :srigators found a continuum of incr.
OGTT performed in the fasting state. -:=;' (l'asting, 1-hour, and 2-hour) plas:.
The diagnosis of GDM requires any two of the four plasma glucose values
obtained during the test to meet or exceed the values. (Table 3) -:,--ames included macrosomia. ces :::
:: j blood C-peptide elevations, as .,,,:-.

Table 3. Normal values for OGCT / OGTT During the POGS CpG Consens..
Carpenter and Coustan O'Sullivan and Mahan / NDDG : : .\LL Filipino pregnanr parier::: :
bv requesting FBS, FIbAlc or R3S
GCT 130 mg/dL 140 mg/dL '.:
.\ diagnosis of overt diabetes rne ...:.
OGTT ..-.ri ing results in their first visit:
Fasting 95 mg/dL 105 mgldl. FBS Z 126 mg/dL (7 mmoi .-
t hour 180 mg/dL 190 mg/dL
."1 lr RBS Z 200 mg/ dL (1 t. 1 nrrl:.
2 hour l55lng/dL 165 mg/dL
3 hour l-40 mg/dL 145 mg/dL
- HbAlc > 6.soh
- 2-hour 75 g OGTT > 200 nrq :-
.i r1i

32
l{e:ting, the following have been agreed upon:
hg:.h risk groups for developing type 2 diabetes
n';':een estimated to be befween
[c-.r -:rg is recommended:
rc :onsidered "high risk" by race or ethnic
r*:.:d for type 2 diabetes mellitus in the first
b.- -: or RBS).
)ne-Step Testing / Normal Values
8-10%.16-t8 Certain quarters WHO, ASEAN, ADA, IADSPG) are advocating a one-step
:esting scheme. Basically, the anhydrous glucose load is 75 g, and only l blood
;ugar value measured 2 hours after glucose loading is taken.
A value > 140 mg/ dL is considered abnorm al and treatment is began.

ct Testing
c: ::r screening and diagnosis of diabetes
!s :
:r' o-step procedure where step I identifies
uc :: lorved by step 2 which is a diagnostic
cr-,- Step 2 is more complicated and costly
r :.'3nosis. Doing a two-step approach will
h :.'. -.-step test is the one recommended by
-,te-Step Testing / Normal Values New Recommendationit'2
Because of increasing incidence of type 2 diabetes mellitus universal early
::sting when routine initial prenatal laboratory tests are drawn is both desirable
,:d convenient.
IADPSG and ADA recommend universal early testing by obtaining FIbAl c or
.'-3s or FBS at the initial visit and doing a 75 g oGTT at24-28 weeks if the early
:rl5 are normal. (Refer to Algorithm)
This recommendation has not been validated by randomized trials yet.
-- :iagnosis of overt diabetes mellitus is made if any of the following is present

E-::-: procedure which is a diagnostic test to

lP- - SG and endorsed by the ADA.
rs-:::..ied by giving a Z-hour
n--= ::r diagnosis.r,2
En -' .:. : -' : mmendation)la
ro -::. anhydrous glucose load (oral glucose
ra ..:la glucose determination t hour later.
:- . Jucose load.
W -::ci'L) or > 130 mg/dL (7.5 mmol/L)
t::. :-:ed for a full diagnostic 3-hour 100 g
I : -,'' -'.sting, 1-hour, and 2-hour) plasma glucose values increased. These adverse
: L- :.i'o of the four plasma glucose values
F: - ::e r-alues. (Table 3)
l.:le 4):
- FBS > 126 mg/dL (7 mmol/dl), or
- FIbAlc > 6.5oh using a standard assay, or
75 g OGTT and - RBS > 200 mg/ dL ( I I . 1 mmol/L) that is subsequently confirmed by
elevated FBS or lIbAlc.
-{ diagnosis of GDM is made if any of the following are present:
- FBS > 92 mg/dLbutless than126 mg/dL
- 1-hour 75 g OGTT > 180 mgldl- (10.0 mmol/L) or
- 2-hour 75 g OGTT ) 153 mgldl (8.5 mmol/L)
-rese recommendations are supported by results from the HApO study3,
r - --: e'aluated more than 23,000 pregnancies using a 2-hour 75 g OGTT. The
1- :'i:::ators found a continuum of increasing risk of adverse outcome as each of the
-"-.:ris included macrosomia, cesarean delivery, neonatal hypoglycemia, and
-: :.:cd C-peptide elevations, as well as preeclampsia.

-rng the POGS CPG Consensus Meeting, the following have been agreed
O'Sullivan and Nlahan / NDDG i
-iLL Filipino pregnant patients must be screened during the first prenatal
, requesting FBS, FIbAlc or RBS.
140 mg/dL
Jiagnosis of overt diabetes mellitus is given among women with any of the
:ng results in their first visit:
105 mg/dL FBS: 126 mg/dL (7 mmol/L)
190 mg/dL RBS > 200 mg/ dL(l 1.1 mmol/L)
165 mg/dL
FibAl c >- 6.50/o
145 mg/dL
2-hour 75 g OGTT .200 mg/dL (11.1 mmol/I.)

JJ "[u[l-TlFh,'
 AdiagnosisofGDMisgivenbasedonthefollowingcutoffvalues* -^: :'.. rator! Instructions
Anhydrous glucose should be prep
- FBS > 2 mg/ dL @{aptedfrom ADA and IADPSGP consensus threshold)
9

- or 2 hour > 140 mg/dL(adapted from WHO recommendation) - Timing of glucose measure is base
recommendations
*These values will be usedis cut off to minimize under diagnosis until .. Sample should be venous plasma 5
validate these values can be made. - Sample should be assayed bv an
from results of local clinical studies to rexokinase or dehydrogenase.
.FBSvalue-primarilypredictiveofperinataloutcomes(HAPOStudy)
.2hourT5goGTTvalue-primarilypredictiveofmaternaloutcome : Glucose testing for the purpose of
(WHO data) Stlucose meters.

Ifthe result of initial test (FBS, HbAlc or RBS) is normal and

with no other
be done at .4lurnative Testsfor Patients Unable to i
risk factors aside from race or ethnicity, a 2 hour 75 g oGTT
should
should proceed
24-28 weeks. If there are other risk factors identified, screening Some women may not tolerate the :
immediately to 2 hour 75 g OGTT' ::.1 gastrointestinal osmotic imbalan;
If the OGTT at24-28 weeks is normal, the woman should be re-tested at 32 -.:rs of glucose testing have been prc:
are present both
weeks or earlier if clinical signs and symptoms of hyperglycemia
polyhydramnios, accelerated fetal --. -arge studies nor endorsed by the --l
in the mother and the fetus"(e.g. poiyphagia,
growth, etc).
l:: following can be done:
Periodic monitoring by randorn an
Table 4. Criteria for a Positive 75 g OGTT for the Diagnosis of
GDM Intravenous (iV) glucose tolerance
POGS-CPG llbAlc
wHo TADPSG/ADA
consensus* consensus**

>125 mg/dL > 92mg/dL > 92mg/dL

FBS F:..EFERENCES
(6.9mmol/L) (5.1mmol/L) (5.1 mmol/L)

OR International Association of D:':=:

1-hour >180 mgldl- Metzger BE, Gabbe SG, et al I:.:=:
(10 mmol/L) Study Groups recommendations -:.
OR in pregnancy. Diabetes Care i,-'' I - -:
. .

>140 mg/dL >153 mg/dL > l40mg/dL American Diabetes Associatr.-:: l

2-hour
(7.8 mmol/L) (8.5 mmol/L) (7.8mmol/L) Diabetic Care2011;34 Suppl l.--'-
HAPO Study Cooperative Resea:;:
*Values are based on outcome datafrom the HAPO study and adverse pregnancy outcones )i
**Values are based on POGS Consensus Opinion POGS CPG on Diabetes Conser.s -,
Society
Metzger BE, Coustan DR (EJ-i i:
General Instructions for OGTT

Patient Instructions
t. fn" patient should be on at least 3 days of normal unrestricted diet containing
minimum of 150 mg carbohydrate per day prior to the test'
a
Z. Testing should not b; done while the patient is sick or under stress or on
medications that can increase blood glucose level'
J. No smoking is permitted during the test.
4. The patient should remain at rest during the test'
5. Glucose solution should be consumed in less than 5 minutes'

34
'"ltii!'::'
j' - - ::e following cut off values* -;!': rator! Instructions

l": :- and IADPSGP consensus threshold) -\nhydrous glucose should be prepared according to directions.
Timing of glucose measure is based on start time of glucose ingestion.
tlr: ':: n WHO recommendation)
'tr,r"' Sample should be venous plasma glucose.
until
recommendations
-., r,rder diagnosis
Sample should be assayed by an enzyme method, such as glucose oxidase,
h .' :rrinatal outcomes (HAPO Study) hexokinase or dehydrogenase.
i!r'- i:-rv predictive of maternal outcome : Glucose testing for the purpose of diagnosing should not be done using home
giucose meters.

lb.'-: : r RBS) is normal and with no other

r - :our 75 g OGTT should be done at t:ernative Testsfor Patients Unable to Tolerate Orsl Glucose
Iq
r-
}- :, :Jentified, screening should proceed Some women may not tolerate the oral glucose solution due to gastric irritation
;-:-': gastrointestinal osmotic imbalance resulting to nausea and vomiting. Other
F :. --he rvoman should bearere-tested at 32
both
*,:es of glucose testing have been proposed but none of these have been validated
f,mr: rs of hyperglycemia
, present

;r' .:-:- polyhydramnios, accelerated fetal : -arge studies nor endorsed by the ADA and ACOG.'e-2t
i
lie following can be done:
Periodic monitoring by random and 2 hour postprandial glucose test
'- of GDM Intravenous (IV) glucose tolerance test using 25gIY glucose
= Diagnosis
POGS-CPG F{bA1c
1{PSGi ADA
: : tgnsus* consensus**

-- ng dL > 92 mg/dL B.IFERENCES

' :.r'ol/L) (5.1 mmol/L)
i. International Association of Diabetes and Pregnancy Study Groups Consensus Panel,
Metzger BE, Gabbe SG, et al. International Association of Diabetes and Pregnancy
Study Groups recommendations on the diagnosis and classification of hyperglycemia
in pregnancy. Diabetes Care 2010;33:67 6.
: -' :rg'dL > 140 mg/dL 2. American Diabetes Association. Diagnosis and classification of diabetes mellitus.
t ::;:rol./L) (7.8mmol/L) Diabetic Care 2017;34 Suppl 1:652
3. HAPO Study Cooperative Research Group, MetzgerBE, Lowe LR et al. Hyperglycemia
and adverse pregnancy outcomes. N Engl J Med 2008;358:1991.
1. POGS CPG on Diabetes Consensus Panel, 201 l, Philippine Obstetrics and Gynecology
Society
5. Metzger BE, Coustan DR (Eds.). Proceedings of the Fourth International Workshop-

,-i normal unrestricted diet containing

'
::: day Prior to the test.
-: patient is sick or under stress or on
-:cose level.
: - -,:-E the test.
: .n less than 5 minutes'
35
AYll'n
+,rttffiN|o'
 RECOMMENDATIONS FOR FIII
ALGORITHMS FOR DIAGNOSIS OF CONSBNSUS ON DIABETES
DIABETES MELLTTUS IN PR-EGNANCY PROTOCOL FOR TIIE EYAILI
FILIPT
IADPSG Protocol for the evaltratiorl of diabetes itl pregnallcy

Draw blood for FB$, RBG or A1C in wornet'l

at nigh risk fol diabetes

FBS > 126 IngldL i7 !nr*ol'Li or

FBS < tl2 rngldl {5. 1 rt":rrrolr'L) or AIC > 6.5o6 cr < 92 mg/dL (5.1 mmol/L) or
AIC <6 5?c or RBG r ?O0 mgrdL (11 1 mmol.'L) thal is < 210 mg/dl (11.1 mmol/L) or
RBG <?00 mgldl- ill.lrrrnrollLJ sutlsequently continled bv eievaied a < 6.5%
FGB ot AIC

FBs > 3: illgjdL i5 1 nlmol/'L)

ancl < 1?6 mgr'dl (7 mtno|'L)

75E GTT
(. UlYt Oted DM.
no furllrel tesling no further lesting
at 24-28 weeks

IADPSG Protocol for the evaluatiorl of diabetes in pregnancy

Pregrrancies ? 24 weeks of gestatior-t

Draw blood for FBS. RBG or A'1 C in women

-l r'cceed immediately to 2 h 75
IGTT if with other risk factors
g

At high risk for diabetes

FBS < 126 mgldL i5 1 rlnrolll) or FBS > 1:6 m$idL {7 mrr-}oliL) or
AIC > 6.5')b or
AIC <5.So/q or
RBG:. ?0O mgidl (11 .l mmol,'L) that is
RBG ';2OO rrrgldL (1 l.l rlrrrolll*) subseqltently confimed by ele\'3led
FGB or AIC

Overt DM
no further testlng

Groups Consensus
Adapted from: International Association of Diabetes and Pregnancy Study
of Diabetes and Pregnancy Study Groups recommendations on the
Panel. International,Afsociation
diagnosis in pregnancy. Diabetes Care 2010; 33:676'
and ctassif;cdtton,'oSltyffillcemia
,1rr.l I ,1,

36
 RECOMMENDATIONS FOR FILIPINO WOMEN BASED ON POGS CPG
TR DL\GNOSIS OF CONSENSUS ON DIABETES MELLITUS IN PREGNANCY, 2OII
tns s PREGNANCY PROTO COL FOR THE EVAIUATION OF DIABETES IN PREGNANT
FILIPINO WOMEN
!r"; of diabetes in PregnancY

of gestatiotl
FIRST PRENATAL VISIT

-
-. I L-
Draw blood for FBS, HbAlc or RBS
a aat"t

:l:. . 1:6 rngldL (7 lnmolili or

-l:-65"6or
: - 3 ' lOO nrg;ciL {11 1 nrmol"L) that is
: :::aquenily cnnftnrecl tlv elevsted
: -:? cr AIC
FBS < 92 mg/dl (5.1 mmol/L) or FBS > 126 mg/dl (7mmol/L) or
RBS < 200 mg/dL (1 1 . 1 mmol/L) or RBS > 200 mg/dl (1 1 .1 mmol/L) or
HbAIC < 6.50l" HbAIC > 6.5%
FBS > 92 mg/dL (5.1mmol/L)
and < 126 mg/ dL (7mmol/L)

0rert DM.
rro further testing

cf diabetes itr PregnatrcY

3f gestatioll
-J Proceed immediately to 2 h 75 g 2 h 75 g OGTT at 24-28 weeks
OGTT if with other risk factors if with NO other risk factors

_t
r.ronr',rnL
::q . 1:€, tngldL (7 mrrlolr'Ll or
I lJ
-.;i5';o' Repeat 2-h 75 g OGTT at 32 weeks or anytime rn the
= _:_: , 2OO mgrdL i11.1 mmol',L) thal
rs presence of maternal/fetal signs of diabetes mellitus
s-: s"qirerrtly confinred by elevaled (polyhydramnios, macrosomia, polyphagia, etc)
_ :', )l qlL

L)ved DM.
no fLirther t*stinq

3',l
Atilr'1^t'ttlllhJr'D
 ConlerenceonGestationalDiabetesMellitus.DiabetesCarelggg;21(suppl'2):Bl-
\ANAGEMENT ISST
8167. AND GESTATIONAI
6.SolomonCG.Aprospectivestudyolpregraviddeterminantsofgestationaldiabetes.
JAMA 1997;278:1078. diug"osis and
committee
7. American Diabetes Aisociation: Report of the expert -o.nil:
g.
classification or aiateies m"ttirur.
piuo.res Care 1999;22(Suppl. 1):S5-S19.
mellitus: controversies and
\. PRECONCEPTION E\'A
Khandelwal M, uo-to C'n"... Ba. C.tru,ional diabetes
-165'
.u...rr, opinions. Curr Opinion Obstet Gynecol 1999;11l.57
Marjorie I. Santos, \ID a:
g.NaylorcD,etal.selectivescreeninglorgestationaldiabetesmellitus'NEnglJMed
1997;337 l59l-1596.
gestational diabetes: relationships
10. Weiss pAM, et al. ioward universal criteria lor and venous glucose
between 15 and roog."- gi,r.or. loads between capillary lrneralizations for Pregestational D
concentrations. Am J dbtttt Gynttol 1998;178:830-835'
11. K; C, Liu T, et al. Does frank iiabetes in the hrst-degree
relativ_es of pregnant woman . :Ibmen with type I and type 2 dra:
affect the likelihood o"f h., a.u"topi.,g gestational
diibetes mellitus or nongestational
morbidity and perinatal morbidin
DM? Am J Obstet Gynecol 2009.201576sl' have poor glucose control and r a-..
12. Toulis KA, Goulis;a,; "i-iirr. "r gestational diabetes mellitus in women with
polycysticovarysyndrome:asystematicreviewandameta-analysis.FertilSteril2009:
92-661.
' . he leading cause of perinatal rnir
index.and-weight gain prior to .nJ tvpe 2 diabetes mellitus is the
13. Hedderson MM, Williams MA, et al' Body mass Gynecol 2008;409:e1'
pregnancy ana rirr. oi g;,tutional diabetes -tilitut'
Am J Obstet :e prevented by excellent conrci
ER al. Gestational weight gain and risk of gestational
14. Hedderson MM, Cu''z"rro" et ;uring the critical weeks of orgar'.:
diabetes mellitus. Obstet Gynecol 2010; 115:597 ' period).2
management guidelines for
15. ACOG practice sril.ti.'. 6estational diabetes: Ciinical
Obstet Gynecol 200 1 ;30 :98-525'
obstetrician-gynecologists'
16. Guelinckx I, Devlieher R. Reproductive outcome after
bariafic surgery: A critical . The glycosylated hemoglobin ler e
review. Human Reprod Update 2009;15:189' control over the past 2 to 3 months
the year 2000 and projections
17. Bchir WS. Global p.."uf.ir". of diabetes. Estimates for of anomalies.s
for 2030. Diabetes Care 2004;27
1g. Cuasay rc. preualence and determinants of type 2
"1047-1053' diabetes among Filipino-
. Finally, the goal of our education
Ameritans. Diabetes Care 2001;24:2054'2058'
Asia Pacific region' HKMJ pregnancy outcome but also tc
19. Cockram CS. The .piJ".niofogyof diabetes mellitus in the
2000;6(1). affected women for the rest of the
glucose beverage for gestational
20. Lamar ME. Jelly beans as an alternative to a f,lfty-gram
diabetes screening. Am J Obstet Gynecol i999;181:1154
test. J Reprod Med
21. posner NA. Simplifying the intiavenous glucose tolerance G eneralizations for Gestatio nal D i al
1982;27:633.
22.silverstoneFA.Applicationoftheintravenousandoralglucosetolerancetestsin
pregnancy. Diabetes 197 1 ;20:47 6'
. The detection of GDM requires a
women with GDM will responC t'
in such cases is fetal macrosomia
of cesarean delivery.8
. Women with GDM are at cons:.
diabetes mellitus later in life anj '.

. GDM is characterized in ntost cai

from impaired insulin release a:
seen in normal pregnancies. Th.:
and have not been found to be a: :

38
 .- ,i Diabetes Care 1999;21(Supp1. 2):Bl- \I{NAGEMENT ISSUES : PREGESTATIONAL
::. -,: jeterminants of gestational diabetes. AND GESTATIONAL DIABETES MELLITUS
-: :\pert committee on the diagnosis and
.:: 1999;22(Supp1. 1):S5-S19.
- .{. PRECONCEPTION EVALUATION AND PREVENTION
'..: : ::l diabetes mellitus: controversies and
-'::. 1999;11:57-165.
-::'-:r-r:'r3l diabetes mellitus. N Engl J Med Marjorie I. Santos, MD and Ma. Victoria V. Torres, MD

:-. :rr gestational diabetes: relationships

- :E:.r.een capillary and venous glucose
-r S30-835. i3eneralizations for Pregestational Diabetes Mellitus
- .- '-:s:-degree relatives of pregnant woman
,: .-- ,---r- diabetes mellitus or nongestational
= ' Women with type I and type 2 diabetes mellitus are atgreater risk for maternal
.: morbidity and perinatal morbidity and mortalify, especially among those who
- -.-*::al diabetes mellitus in women with have poor glucose control and vasculopathy.'
" '.' . ::d a meta-analysis. Fertil Steril 2009:
. The leading cause of perinatal mortality in pregnancies complicated by type I
: : ::ass index and weight gain prior to and type 2 diabetes mellitus is the major congenital malformation, which can
- : . :,s .{m J Obstet Gynecol 2008;409:e1.
be prevented by excellent control of maternal gfycemia before gestation and
:: ::.:l seight gain and risk of gestational
during the critical weeks of organogenesis (5-8 weeks after the last menstrual
- ":: :'j Ciinical management guidelines for period).2
- . -:-':98-525.
- : -:i3 after bariatric surgery: A critical . The glycosylated hemoglobin level (HbAlc), which reflects average glucose
control over the pastz to 3 months, can be closely correlated with the frequency
I : --.::s lor the year 2000 and projections of anomalies.5
" : :'.'pe 2 diabetes among Filipino-
-, " t: . Finally, the goal of our educational programs should be not only to improve
. - . .-:::s in the Asia Pacific region. HKMJ pregnancy outcome but also to promote healthy lifestyle changes for the
- affected women for the rest of their lives after delivery.2
- - -;:3nl glucose beverage for gestational
-:':.Sl:1154
- :-:rse tolerance test. J Reprod Med
Jeneralizations for Gestational Diabetes Mellitus (GDM)
: and oral glucose tolerance tests in
" The detection of GDM requires a carefully developed plan for screening. Most
\\'omen with GDM will respond to dietary therapy. The greatest perinatal risk
in such cases is fetal macrosomia, which has been associated with a higher rate
of cesarean delivery.s

' women with GDM are at considerable risk for the development of type 2
diabetes mellitus later in life and will require careful follow-up.a

' GDM is characterizedin most cases by postprandial hyperglycemia, resulting

from impaired insulin release and an exaggeration of the insulin resistance
seen in normal pregnancies. These patients can be treated with diet therapy
and have not been found to be at increased risk for intrauterine fetal death.s

39
$rowtI'
 will were significant risk factors flc:
when fasting glucose levels in women with GDM are elevated, not only
birth was not.26
insulintherapyberequired,butsuchhyperglycemiaalsoplacesthesewomen . The presence and the severin
at greater risk for a stillbirth.e
glycemic control.io
. The rapid institution of strict g.
been associated with short-terr
Prevention of Maternal and Fetal Complications
retinopathy is also more likeh'
prevention of, maternal and fetal complications in the periconception period ' Active proliferative retinoPsli
is based on understanding of the nature and effects of these
complications to the ideally be controlled with lase:
mother and fetus. CompTete explanations of these complications
may be seen in . All patients should be schedule .
chapter IV. Listed below u.. ,o.n. of the preventive mea_sures that
may be done first prenatal visit. If retinopa:l
in the periconception period of patients with diabetes mellitus. during pregnancy and postpa::
. Serial f,undoscopic examinatr,':
1. Abortion mellitus is highly recommenJ:,
.AccordingtoDiabeticControlandComplicationTrial,intensive
the rate of ^.:f hropathy
therapy for blood glucose control prior to pregnancy' reduces
spontaneous abortion.
7 . -\ccording to the Diabetes C--:
. only those with F{bA1c of > l2ohand persistently high fastingblood
sugar
rs a 250/o decrease in the ralc --

for abortion'
€Bb) of > 120 mg/ dL are at increased risk lIbAlc levels.T
. All patients with a historr ,-:
2. Congenital Anomalies mellitus of greater than 10 '. ::
. Eotn major malformations and spontaneous abortion can be
reduced
hour urine collection for tota. :
whenexcellentprepregnancyandearlypostconceptionaldiabeticcontrol at the initial prenatal visit.
diabetes mellitus .
is achieved. rt ii, therefore, imperative that patients with Decreased creatinine clearar.:
6
be encouraged to seek preconceptional care of poor perinatal outCofitc :
. Meta analysis of 7 studies conilud"d that preconceptionally controlled gestation, most studies have :,'.:
glucose levels with lower HbAlc is associated with lower risk
for
in pregnancy.
congenital malformations with a rate of 5o/o amon$those with
optimized .
who presented after
In a small subset of rronrcl
control before pregnancy as compared to 9ok in those
r6
serum creatinine exceeding
comPletion of organogenesis' progression to end-stage rcna
. HbAlc of < 8.5% in the first trimester has a congenital auomaly rate of
3.40/o compared with 22'4%o if HgbAlc is > 8 5%'i8 Cardiovascular Complications
. For a woman with diabetes mellitus, an1' visit to a health care provider Artery Disease)
shouldbe used as an opportunity to revierv ihe patient's plans forpregnancy' . Preeclampsia was related tr .
The discussion should focus on obtainir.g excellent glucose control and starting at 24 weeks age of gts
achieving a healthy lifeswle befoie coticcption. Glucose levels should
be
. Preeclampsia is predicted r:
stabilized and an uirat.'. l% abc,ve the normal range achieved.s
. be proteinuria, uric acid of > 6 ::-.
Patients with type 2 diabetes mellitus rvtro are usirlg oral agents should
low platelet (HELLP) parai-1.
converted to insutin. In addition, an evaluation for vasculopathy shouldbe . Renal function tests must hi
accomplished.8
pregestational diabetes meil::
diabetes mellitus of > 10 r:
3. Retinopathy . ".e
Little evidence of progressic:.
. Accordlng to the EURODIAB Prospective Complication Study (2005)'
the {ilra.tlon ofr.{iabetes mellitus and high HbAlc levels at recruitment
pregnancy.2'"
irit,, ,

. ,i,, r9,
40
 .:. GDM are elevated, not onlY will
. :::\cemia also Places these women
lL,i.flloos
r ' -:,iJlls in the periconception period
.' , , .-:ts of these complications to the
i ' -:-ise complications may be seen in
r: . -: sntive measures that may be done
h ::,-.betes mellitus.
Complication Trial, intensive
1.. p..gnancy, reduces the rate of
: :srstently high fasting blood sugar
lisk lor abortion.
:,iuc-ous abortion can be reduced
'-'
-rs tconceptional diabetic control
::rr patients with diabetes mellitus
::rat preconceptionally .6n11elled
:ssociated with lower risk for
: 5I o amon$ those with oPtimized
: -- 9r,: in those who Presented
after
of
:ras a congenital anomalY rate
:. > E 5olo.rs
.-::'. i'isit to a health care provider
: ,, :l't ':atient's plans for pregnancy'
; 'e txcellent glucose control and
.-,'t,,iot.t. Glucose levels should be
.:.' iormal range achieved'S
.. rro are using oral agents should be
be
.'. ',ratiou for vasculopathy should
,'t;tive Complication Study (2005),
: ligh HbAlc levels at recruitment
*'ere significant risk factors for retinopathy progression, rvhereas, giving
birth was not.26
. The presence and the severity of retinopathy can be attributed to poor
glycemic control.ro
. The rapid institution of strict glycemic control during pregnancy has also
been associated with short-term progression of retinopathy. Worsening of
retinopathy is also more likely to occur in hypertensive patients.rr
. Active proliferative retinopathy might worsen in pregnancy and should
ideally be controlled with laser therapy before conception.rr
. All patients should be scheduled for screening retinal examinations at their
first prenatal visit. If retinopathy is present, then follow-up examinations
during pregnancy and postpartum are recommended.r2
. Serial fundoscopic examinations among those with pregestational diabetes
mellitus is highly recommended.20
Nephropathy
. According to the Diabetes Control and Complication Trial (2002), there
is a25oh decrease in the rate of nephropathy for every 10% decrease in
llbA1c levels.7
. All patients with a history of microalbuminuria or those with diabetes
mellitus of greater than 10 years duration should be screened with a24-
hour urine collection for total protein and creatinine before pregnancy or
at the initial prenatal visit.
. Decreased creatinine clearance and proteinuria are the best predictors
of poor perinatal outcome. Although proteinuria will increase during
gestation, most studies have failed to demonstrate apermanent worsening
in pregnancy.
. In a small subset of women with advanced renal disease, those with a
serum creatinine exceeding 1.5 mg/ dL, pregnancy might accelerate
progression to end-stage renal disease.
Cardiovascular Complications (Hypertension, Preeclampsia, Coronary
Artery Disease)
. Preeclampsia was related to glucose control based on lIbAlc monitoring
starting at 24 weeks age of gestation (AOG).2?
. Preeclampsia is predicted if there is any of the following: progressive
proteinuria, uric acid of > 6 mg/dl, (+) hemolysis, elevated liver enzymes,
low platelet (HELLP) parameters.
. Renal function tests must be performed in each trimester in those with
pregestational diabetes mellitus with vascular disease and in those with
diabetes mellitus of > 10 years duration.
. Little evidence of progression of peripheral arterial disease is seen during
pregnancy.2T
4t
 . Coronary heart disease and myocardial infarction are rare events in . Hypertension:
pregnant diabetics.l3 o A goal of systolic blood rr
. In patients with diabetes mellitus-related cardiac involvement, pregnancy most patients with diabe:r
outcome is dismal with maternal mortality rate of > 50oh and perinatal o Patients with diabetes me
mortality rate of > 300/0, making it a potential contraindication to of < 80 mmHg. (Let'el II-_
pregnancy. These patients should undergo preconception counseling and
Le informed of these risks before attempting pregnancy. Therefore, it is
. Nephropathy:
prudent to obtain detailed cardiovascular history and cardiac clearance o To reduce the risk or slor
among those who are > 30 years old with type I diabetes mellitus of > 10 glucose and blood pressul
years duration. o Perform test to assess un
in type I diabetes melliru:
more and in all type 2 d:e
6. Neuropathy
III,
. eeiiptreral neuropathy should be assessed at the preconception visit or
(Level Grade C)

early in gestation by a careful examination of the patient's feet for sensory . Retinopathy:
loss. Instructions on safe foot care should be provided for all women with
diabetes mellitus.2l
o To reduce the risk or sl:.
glycemic and blood press _

o Women with preexis:::

pregnancy or who har.e L,:.
Recommendations by the American Diabetes Association2e
eye examination and L,e
retinopathy. Eye examina
. HbAlc levels should be as close to normal as possible (< 7oh) in an
close follow-up through-.
individual patient before conception is attempted. (Level II-2, Grade B) (Level II-2, Grade B)
. Staring at puberty, preconception counseling should be incorporated in
the routine diabetes mellitus clinic visit for all women of childbearing R eferences
potential. (Level III, Grade C)
1. Kitzmiller JL, Buchanan TA. K.:
. women who are diabetic and contemplating pregnancy should be of diabetes, congenital malforr::
evaluated, and if indicated, should be treated for retinopathy, nephropathy 1996;19:514-40.
and cardiovascular disease. (Lettel III, Grade C) 2. Lauenborg J, Mathiesen E. O-",
Pedersen L, et al. Audit on stillb::--
Diabetes Care 2003; 26:1385 -9.
Medications taken by such women should be evaluated prior to conception
3. Metzger BE, Coustan DR. a:.:
since drugs commonly used to treat diabetes mellitus and its complications
recommendations of the 4th In:e
may be contraindicated or not recommended in pregnancy, including diabetes. Diabetes Care 1998:21 t S.:
statins, angiotension converting enzyme (ACE) inhibitors, angiotensin 4. American College of Obstetri--.:
receptor blockers (ARB) and most non-insulin therapies. (Let'el III, Grade Bulletins-Obstetrics, Coustan DR
c) #30. Washington: American C;--,
). US Preventive Services Task F::,
Since many pregnancies are unplanned, consider the potential risks and Recommendations and rationale
benefits of medications which are contraindicated in pregnancy in all 6. American Diabetes Associar:.- :.
2003;26(Suppl 1):S 1 03-5.
women of childbearing potential, and counsel women using medications
EastmanRC, VinicorF, The Expe:
accordingly. (Level III, Grade C) of Diabetes Mellitus. Repon ::
classification of diabetes mellr:;s
-- -..&g',
-*= -&i i 42

it. t Ir I
It r , --.rdial infarction are tare events in
t o
b" ':
-l:ed cardiac involvement, pregnancy
*,:rtaliry rate of > 50oh and perinatal
-. rt a potential contraindication to
- :. Jergo preconception counseling and
Therefore, it is
'::empting pregnancy.
..--ular history and cardiac clearance
: ..i rth q'pe I diabetes mellitus of > 10
:,.:ssed at the preconception visit or
* - -i::cn of the patient's feet for sensory
- -::-J be provided for all women with
:e: -\ssociation2e
'. :.:rmal as possible (< 7oh) in an
- : ::tempted. (Level II-2, Grade B)
-, -:.seling should be incorporated in
- .:s-: for all women of childbearing
. -::nplating pregnancY should be
',: :-:ted for retinopathy, nephropathy
--.:;i C)
- - , - .1 b e evaluated prior to conception
: ::::es mellitus and its comPlications
, :.:rended in pregnancy, including
r- ::- (\CE) inhibitors, angiotensin
- I6
- :.--rsulin therapies. (Letel III, Grade
- -.: consider the potential risks and
: - ,:.::aindicated in pregnancY in all
. - : ----unsel women using medications
Hypertension:
A goal of systolic blood pressure (BP) < 130 mmHg is appropriate for
most patients with diabetes mellitus. (Level III, Grade C)
o Patients with diabetes mellitus should be treated with a diastolic Bp
of < 80 mmHg. (Level II-2, Grade B)
. Nephropathy:
o To reduce the risk or slow the progression of nephropathy, optimize
glucose and blood pressure control. (Level I, Grade A)
o Perform test to assess urine albumin excretion and serum creatinine
in type I diabetes mellitus patient with disease duration of 5 years or
more and in all type 2 diabetes mellitus patients starting at diagnosis.
(Level III, Grade C)
. Retinopathy:
o To reduce the risk or slow the progression of retinopathy, optimize
glycemic and blood pressure control. (Leuel I, Grade A)
o Women with preexisting diabetes mellitus who are planning
pregnancy or who have become pregnant should have a comprehensive
eye examination and be counseled on the risk of progression of
retinopathy. Eye examination should occur in the first trimester with
close follow-up throughout pregnancy and for I year postpartum.
(Level II-2, Grade B)
S.cferences
l. Kitzmiller JL, Buchanan TA, Kjos S, Combs CA, Ratner RE. pre-conception care
of diabetes, congenital malformations, and spontaneous abortions. Diabetes care
1996;19:514-40.
Lauenborg J, Mathiesen E, Ovesen P, Westergaard JG, Ekbom p, Molsted-
Pedersen L, et al. Audit on stillbirths in women with pregestational type I diabetes.
Diabetes Care 2003; 26:1385 -9.
3. Metzger BE, Coustan DR, and the Organizing Committee. Summary and
recommendations of the 4th International workshop Conference on gestational
diabetes. Diabetes Care 1998;21(Suppl 2):B l-7.
4. American college of obstetricians and Gynecologists committee on practice
Bulletins-obstetrics, Coustan DR. Gestational diabetes ACOG practice bulletin
#30. washington: American college of obstetricians and Gynecologists, 2001.
5. uS Preventive services Task Force. Screening for gestational diabetes mellitus:
Recommendations and rationale. Obstet Gynecot 2003;l0l (2):393 -4.
6. American Diabetes Association. Gestational diabetes mellitus. Diabetes Care
2003;26(Suppl l):S103-5.
7. Eastman RC, vinicorF, The Expert Committee on the Diagnosis and Classification
of Diabetes Mellitus. Report of the expert committee on the diagnosis and
classification of diabetes mellitus. Diabetes Care 1997:20:llg3-gl .
43
*HA-llllfl1'
8. American Diabetes Association. Evidence-based nutrition principles and
recommendations for the treatment and prevention of diabetes and related Temple RC, et. ai. Glycemic c:::
complication s. Diab et es C are 2003 ;26(Supp1 I rn women with type I diabetes.
): S 5 I -6 I . -:
9. Gordon M, Landon MB, Samuels P, Hissrich S, Gabbe SG. Perinatal outcome Stamler ER et. al. High inlectr: ..
and long-term follow-up associated with modern management of diabetic dependent DM: An understarer :
nephropathy. Obstet Gynecol 1996;87 :401 -9. American Diabetes Associari.- :
10. Gordon MC, Landon MB, Boyle J, Stewart K, Gabbe SG. Coronary artery Diaberes Care 2011 ;34(S I ): S I 1 -S :
disease in insulin-dependent diabetes mellitus of pregnancy (Class H): A review
of the literature. Obstet Gynecol Surv 1996;51:437 -44.
ll. Airaksinei KEJ, Anttila LM, Linnaluoto MK, Jouppila PI, Takkunen Jl
Salmela PL Autonomic influence on pregnancy outcome in IDDM. Diabetes Care
1990;13:7 56-61.
12. Landon MB, Catalano PM, Gabbe SG. Diabetes mellitus. In: Gabbe SG, Niebyl
JR, Simpson JL, eds. Obstetrics: Normal and problem pregnancies. Philadelphia:
Churchill Livingstone, 2002:1099-100.
13. Diabetes Control and Complications Trial. Research Group: The eflects of
intensive treatment of diabetes on the development and progression of long term
complications in insulin dependent diabetes mellitus. N Engl J Med 1993;329:977 .

14. Sibai BM, et. al. Risk of preeclampsia and adverse neonatal outcomes among
women with pregestational diabetes mellitus. Am J Obstet Gynecol 2000;182:.364.
15. Yang J, et. al. Fetal and neonatal outcomes of diabetic pregnancies. Obstet Gynecol
2006:108:644.
16. Ray JG, et. al. Preconception care and the risk of congenital anomalies in the
offspring of women with diabetes. A Meta-analysrs. QJ Med 200L;94:435.
17. Reece EA, et. al. Pregnancy outcomes among women with and without diabetic
microvascular disease (White's Classes B to FR) versus non-diabetic controls. Am
J Perinatol 1998;1 5 :549.
18. Miller E, et. al. Elevated maternal HgbAlc in early pregnancy and major
congenitalanomaliesininfantsof diabeticmothers. NEnglJMed l98l;304:1331.
19. Diabetes Prevention Project: The prevalence of retinopathy in impaired glucose
tolerance and recent - onset diabetes in the Diabetes Prevention Program. Diabetic
Med2001;24:451.
20. Ferris FL, et. al. Treatment of diabetic retinopathy. N Engl J Med 1999;667-668.
21. Klein BEK, et al. Effect of pregnancy on progression of diabetic retinopathy.
Diabetes Care 1990;13 :34.
22. Chaturvedi N, et. al. The relationhip befween pregnancy and long term maternal
complications in the EUPODIAB IDDM complications study. Diabetic Med
1995;12:494.
23. Arun CS, et. al, Influence of pregnancy on long term progression of retinopath)'
in patients with type I diabetes. Diabetologia 2008;51:1041.
24. Chew EY, et al. Metabolic control and progression of retinopathy: The diabetes
in early pregnancy study. Diabetes Care 1995;18:631-637.
25. Lovestram-Adrian M, et. al. Preeclampsia is a potent risk factor for deterioration
of retinopathy in type I diabetic patients. Diabetic Med 1997;14:1059-1065.
26. Yerier MO, et. al. Is pregnancy a risk factor for microvascular complicationsl
The EURO DIAB prospective complicarions study. Diabetic Med 2005;22:1503.
1509.
.j,]r
. ,ir:, .-.
.;".
-a , ' '\l
,Jr, 44
bnn ..::rce-based nutrition principles anc
Fllr,: ::: prevention of diabetes and relatec
3-' --:. i):551-61.
- ri
.--. '.;. rmen with type I diabetes. Br J Obstet Gynecol 2006;113:1329.
!::::rler EF, et. al. High infectious morbidity in pregnant women with i n s u I in
E ..--..:rch S, Gabbe SG. Perinatal outcome
:::'::rdent DM: An understated complication. Am J Obstet Gynecol 1990163:I2L
b- .,..:: modern management of diabetic
-- i::erican Diabetes Association. Standards of Medical care in Diabetes - 2011.
.

:.i'
:'.'.art K, Gabbe SG. Coronary arter\ l-:':::es Care 201l;34(S l):Sl l-561.
bp','
b"" .-::;s of pregnancy (Class H): A revieu
b' -- : -.+Ji-44.
l,:,' -,:: MK, Jouppila PI, Takkunen JT.
':"::.incy outcome in IDDM. Diabetes Cari

l.:betes mellitus. In: Gabbe SG, Nieby'l

... r:J problem pregnancies. Philadelphia:

- l:.:.1. Research Group: The effects of

' :..:.:rment and progression of long term
: :t:=s n-rellitus. N Engl J Med 1993;329:977 .

: ::: adverse neonatal outcomes among

* : r,i. ,{tn J Obstet Gynecol 2000;182:364.
-:. :: diabetic pregnancies. Obstet Gynecol
: :-:: risk of congenital anomalies in the
:::-r.ah'sis. QJ Med 2001;94:435.
,:-.,::: \\'omen with and without diabetic
: :, r R) r.ersus non-diabetic controls. Am

--::.1^-c rn early pregnancy and major

:' :'.,ithers. N Engl J Med 1981;304:1331.
--
, cf retinopathy in impaired glucose
'-.=:,-r
lrabetes Prevention Program. Diabetic

-::,:- riathy. N Engl J Med 1999;667-668.

-:. :rogression of diabetic retinopathy.
*,.:.n pregnancy and long term maternal
- I'l complications study. Diabetic Med
" :. -,.n9 term progression of retinopathy
: :1.108;51:1041.
: - . ::ession of retinopathy: The diabetes
::,' -8:631-637.
: :i a potent risk factor for deterioration
-- : i e ric
: Med 1997 ;14:1059 -1065.
-:, : :rr microvascular complications?
.: ::s study. Diabetic Med 2005;22:1503-

rAl'uA.lgliu}!
45
 B. ANTEPARTUM MANAGEMENT Summarlt of Eyidence

. Provision of MNT as parr cl

1. Blood Glucose Management of preeclampsia, macroso n: l-
bone fracture and nerve pa-r
a. Nutritional Management
associated with higher rares :
Cecilia C. Santos-Acuin, MD
It is recommended that ii g:1r'
of MNT then insulin rherar',

Introduction The use of MNT for GD\I re

of patients requiring insuiin , -
. In antepartum nutritional management, the goal is to achieve and maintain of insulin therapy for those '.
normal blood glucose levels during pregnancy as safely as possible. hemoglobin (HbAlc) u'as ..-
smaller but nonsignificanr ::
. Outcomes include: had FIbAlc above normal ' -
l. glucose and ketone levels
2. maternal weight change MNT has been shou,n ro d..-:
3. fetal size and other adverse neonatal outcomes (neonatal hypoglycemia, 0.25% to 2.9% at 3-6 nr. r:.:::
respiratory distress syndrome, stillbirths, mortaliry congenital mal- (ranging from monthly ro -i ::
formations, etc)
-'\
eight management and eners-.
::egnancy, especially for u'omen '
Recommendations
: :,'ttmaryt o.f Evidence
1. Medical Nutrition Therapy (MNT) should be an integral part of gestational
diabetes mellitus (GDM) management. It should be provided for all diabetics Pregnancy weight gain recc:
and for all women with GDM by a nutrition professional. had normal weight or \\'ere '-:
. MNT consists of an assessment of food intake, physical activity and women without GDM.: fI,:,.
medication history and intake, as well as weight status, during and aftet
plegnancy. Energy intake for overlveighr :
. it -uy be administered as a sole management approach, if sufficient restricted as long as weighr s
to maintain normal glycemic control or it may be combined with BMI) while minimizing the n,
pharmacologic treatment and other ancillary measures to achieve normal
glycemia.' (Level I, Grade A) More than weight gain. ir
. It is a consensus that nutrition requirements are the same for pregnant birthweight.s
women with and without GDM.2
. The characteristics of the GDM diet are: Maternal weight reduction iu:
a. it meets the dietary principles for diabetes mellitus management induced hypertension or pre.
b. it provides for the nutritional requirements of pregnancy (resulting in low birthu'eigl:
c. it is individualized for maternal pre-gravid body mass index (BMI) sometimes resorted to in atie:
and weight gain goals was associated with a signiti;:
d. it is culturally accePtable age (SGA) babies.6 (Lereli. C,
"
n'i"t t''*
^
"..,., '
.'a.,ii..,,
:"".. 46
TL}T }IANAGEMENT
xc \fanagement
ld \Ianagement
fu- ',--\cuin, MD
. :he goal is to achieve and maintain
::-rnc)' as safely as possible.
-i- rutcomes (neonatal hypoglycemia,
.---:irths, mortality, congenital mal-
, --: be an integral part of gestational
-: should be provided for all diabetics
- :- -- n professional.
-. :-.od intake, physical activity and
,:-- as ri'eight status, during and after
-:l:ragement approach, if sufficient
--:--. or it may be combined with
- .:.::liary measures to achieve normal
: ---::nents are the same for pregnant
. : ::-:
. - :::betes mellitus management
: - -.r3rre rtS of pregnancy
- :, ::e-gravid body mass index (BMD
jitttmary o_f Eyidence
Provision of MNT as part of intensive therapy for GDM reduces the risk
of preeclampsia, macrosomia and perinatal morbidity (shoulder dystocia,
bone fracture and nerve palsy), although such intensive therapy is also
associated with higher rates of labor induction.3 (Level I, Grade ))
It is recommended that if glycemic control is not achieved within 2 weeks
of MNT then insulin therapy should be started.2 (Level lil, Grade c).
The use of MNT for GDM results in a significant reduction in the number
of patients requiring insulin (24.6%vs.3l.7oh;p 0.05), andalater initiation
of insulin therapy for those who need it (31.6% vs 30.4%). Glycosylated
hemoglobin (HbAlc) was lower during delivery (5.0 vs. 5.2o/o) and, a
smaller but nonsignificant proportion of women (g.1% vs 13.6oh, p 0.25)
had HbAlc above normal.a (Lewl I, Grade A)
MNT has been shown to decrease lIbArc in rype 2 diabeticpatients from
025% to 2.90/o at 3-6 months, with follow-up from a registered dietician
(ranging from monthly to 3 times a year).
'r eight management and energy intake need to be monitored throughout
rregnancy, especially for women with GDM.
S:tlnmary qf Evidence
' Pregnancy weight gain recommendations for women with GDM who
had normal weight or were underweight prepregnancy is the same as for
women without GDM.2 (Level III, Grade C).
' Energy intake for overweight or obese women with GDM may be modestly
restricted as long as weight gain is appropriate (relative to ih. pregravii
BMi) while minimizing the risk of maternal ketosis.2 (Leuel III, Grade c)
' More than weight gain, it is glycemic control that is predictive of
birthweight.5
Maternal weight reduction during pregnancy had no effect on pregnancy-
induced hypertension or preeclampsia and may be harmful io the fetus
(resulting in low birthweight). High prorein supplementation (which
is
sometimes resorted to in attempts to adhere to a i,iow-carbohydrate diet',)
was associated with a significantly increased risk of small foi gestational
age (SGA) babies.6 (Level I, Grade A)
47
*H,t-qffi[]'
 with low instead Evidences on smoking cessa:
3. Carbohydrate consumptron: Consumption of carbohydrates for pregnancy in general.
of high glycemic index (GI) is recommended.l (Level II'1, Grade C)

Summar! o.f Evidence i-Cerences

. to blood
Monitoring of carbohydrates @eing the primary contrib^utor - American Diabetes Associatic:
glucose), by strategies such as carbohydrate counting' food exchange
to achieving - Canadian Diabetes Associarri:
choices, or experieice-based estimation, is a key strategy Gestational diabetes mellitus J:
glycemic control.r (Level I, Grade A) -: Alwan N, Tuffnell DJ, \les: -'
Database Syst Revs 2009, Issue -.

. The type and amount of carbohydrates can bp individualized'

depending I Reader, etal,2006.

o,'gl.u.o,.and/orketonelevelresponse,gestationalweightgain,and
r The HAPO Study Cooperari'.:
pregnancy outcomes. N Engi -'
s..u- triglycerides .2 (Level III, Grade C) r Kramer MS, Kakuma R. E:e:
-',!

Database Syst Revs 2003, Issue -i

o I study with evidence -
recent systematic reviewT cites only 1 intervention Louie JC, Brand-Miller JC. \1::
the need for
that a low Ct vs trigtr GI diet in GDM significantly 1ed-uce.d and pregnancy: A systematlc .::e
no significant differences in fetal and obstetric
insulin by half, UuifounO 3 Colberg SR, AlbrightAL, Biiss::r:
prepregnancy high GI
outcomes. One epidemiologic itudy found that type 2 diabetes: American C,-.1.e:
intakes increased the risk for GDM' Association: Joint position stat::

.Intakeofsugarsubstitutessuchasacesulfamepotassium,aspartameand
sucraloseareacceptableduringpregnancyandlactationwithinacceptable
more nutritious
daily intake limiti. These substances should not replace
opti,ons. Saccharin and cyclamates are not recommended
during
pregnancY.2 (Level III' Grade C)

4. Lifestyle changes:
cessation is
a. Oflering advice tegatding alcohol consumption and smoking
recommended.t (Level IIL Grade C)

b.Intheabsenceofcontraindications,maintainasufficientlevelofphysical
activity and exercise to improve glucose control' reduce cardiovascular
goals' and overall
disease (CVD) risk, contribute to weight management
wellbeing. (Level I, Grade B)

Summaryt o.f Evidence

. Epidemiological evidence suggests higher levels of physical activity

may
II-2, B)
reduce the risk of developing GDM's (Level Grade

. Moderate exercise has been shown in randomized controlled

trials (RCTs)
tolowermaternalbloodglucoselevelsinGDM.8(LevelI,GradeB)
, I'.',.t .,'.
fttai
r?ir
g1-#.*,
r.i, ""'
48
 Evidences on smoking cessation and alcohol consumption are
F:' :. of carbohydrates with low instead
for pregnancy in general.
the same
Er- -::ed.r (Level II-1, Grade C)

fl.-cfcrences

rilh., -i :he primary contributor to blood

x , .::--hvdrate counting, food exchange - American Diabetes Association. 201l Crinical practice Recommendations.

Irn-,:.,-n. is a key strategy to achieving - Canadian Diabetes Association Clinical Practice Guidelines Expert
Committee.
Gestational diabetes meilitus. can J Diabetes 20a3;27:s99-sr05 .
a- -: Alwan N, Tuffnelr DJ, west J. Treatments for gestationar diabetes.
cochrane
Database Syst Revs 2009, issue 3.
l,: ::S Can be individualized, depending -l Reader, et a|,2006.
t' tnse, gestational weight gain, and i rhe HAPO Study Cooperative Research Group. Hypergrycemia and adverse
',|f,''" pregnancy outcomes. N Engl J Med 2009;359:1991-2002.
: Kramer MS, Kakuma R. Energy and protein intake in pregnancy. cochrane
b- I intervention study with evidence -
Database Syst Reus 2003, Issue 4
Louie JC, Brand-Miller JC, Markovic Tp, Ross Gp, Moses RG. Glycemic
L- .1 signihcantly reduced the need for index
and pregnancy: A systematic riterature review. J Nutr Metab 2010;2010:2g2464.
*' :rt diffbrences in fetal and obstetric i Colberg SR, AlbrightAL, BlissmerBJ, Braun B, chasan-TaberL, et al. Exercise
il.-- tound that prepregnancy high GI type2 diabetes; American College of Sports Medicine and the American Diabetes
and
ET Association: Joint position statement. Med sci sports Exerc 2010;42(12):22g2-8a3.

il: :s'r.lilame potassium, aspartame and

Ji' :- .:: l- and lactation within acceptable
F&' ., .lould not replace more nutritious
jtu- : are not recommended during
p

ft :umption and smoking cessation is

*
l:" -:airrtain a suflicient level of physical
!,e. - ---ose control, reduce cardiovascular
: i,' =::ht management goals, and overall

]''' :her levels of physical activiry may'

G:: Level II-2, Grade B)

b*,, :andomized controlled trials (RCTs)

E s rn GDM.8 (Leuel I, Grade B)

$f,YllilA-R"-$rm{'D
tF. I ic$ll
 b. Blood Glucose Management Treatment of Hyperglycemia in pr
. The optimal therapy for u _-
Nemesio A. Nicodemus, MD who are not able to ma::
restricted diet is insulin.

. Insulin administration sho..;l

goals stated above.
Introduction
. Human regular insulin or ra:
Randomized controlled trials (RCTs) and a meta-analysis show that treating treatment for postprandial h-.
gestational diabetes mellitus (GDM) signihcantly reduces the likelihood of
ierious maternal-fetal andneonatal morbidity compared with routine prenatal . Basal insulin needs can be l:
care.l-3 (NPH) insulin.
Treatment in these studies included individualized medical nutrition therapy
(MNT), daily self-monitoring of blood glucose (SMBG), and pharmacologic
. The initial insulin dose for p:,
therapy with insulin, if necessary. be calculated by the follou::
needs:
A randomi zed trial showed that using a low glycemic index (GI) diet for . 0.7- 0.8U/kg acual boJ',
women with GDM effectively halved the number needing to use insulin, with . 1.0 U /kg actual bodr. u:.
no compromise of obstetric or fetal outcomes.a . |.2 U /kg actual bodr- u-::
Pharmacologic therapy is most commonly instituted once diet and exercise
have failed ai evidenced by abnormality in more than half of self:monitored . However, clinical judgmen: :
glucose values or an abnormal value in those women tested weekly. the starting dose of insulin
Traditionally, insulin has been the drug of choice because of its safety in .
pregnancy, lack of significant transplacental passage, and history of use. Most
Once the total daily insulin ::
women can be treated as outpatients.5
is given before breakfast anc
NPH insulin is used. Huma:
best dosed with each meal
Recommendations
. Until more information is obi,
1. Outpatient Glucose Targetsfor Pregnant Women of metformin use in pregnan;
. For GDM, treatment goals are: (Level Grade C) III for treatment of GDM. \\c:
o preprandial glucose concentration of < 95 mg/ dL (5.3 mmol/L) diabetes mellitus are besr c:
o l-hour postmeal glucose value of 1 mmol/L)
140 mg/ dL (7 .8 occurs.
o <
2-hour postmeal glucose value of I20 mg/dL (6,7 mmol/L)
Monitoring
. For women with preexisting type I or type 2 diabetes mellitus who become . Daily SMBG using mete:s
pregnant, glycemic goals are: (Lewl III, Grade C)
monitoring in the clinic for ;.:
o premeal, bedtime, and overnight glucose values of 60'99 mg/ dL (3 '3- warrant intensification of rhe :
5.4 mmol/L)
o peak postprandial glucose value of rc0-129 mg/ dL (5 .4 -7 .1mmo1/1)
a. Women with GDN{ on :
blood glucose levels J lr:::
o HbAlc value of <6.0%
and postprandial bloo,j E- _

. onlv if they cagbe achieved safely

)...r -:;3...:.,,,
.t
,*,,
i,-
.B:-, 50
Fn:e \[anagement ) Treatment of Hyperglycemia in Pregnancy
' The optimal therapy for women with GDM or type 2 diabetes mellitus
f, ' :: jemus, MD who are not able to maintain normoglycemia with a carbchydrate-
restricted diet is insulin.

Insulin administration should be individualized to achieve the glycemic

i' goals stated above.
'I
i:

b.
I
Human regular insulin or rapid-acting insulin analogues are the preferred
.:,.1 a meta-analysis show that treating
treatment for postprandial hyperglycemia in pregnant women.
of
'.:nificantly reduces the likelihood
- -::Jiry compared with routine prenatal
Basal insulin needs can be provided by using neutrar protamin hagenom
G.{PH) insulin.
- ::'' idualized medical nutrition therapy'
r : +ucose (SMBG), and pharmacologic The initial insulin dose for pregnancy is based on maternal weight and can
be calculated by the following guidelines to determine totar daily insulin
needs:
-. : lorv glycemic index (GI) diet for . /kg actual body weight in the first trimester
0.7 - 0.8 U
, .= rlumber needing to use insulin, with . 1.0 U /kg
actual body weight in the second ftimester
-:: I mes.l . l.2U /kgactual body weight in the third rrimester
r instituted
once diet and exercise
.. :r more than half of self:monitored However, clinical judgment and experience must assist in the selection of
- ::--se women tested weekly.
the starting dose of insulin.
, --- :f choice because of its safety in
once the total daily insulin dose is calculated, two-thirds of the daily dose
- .:.:al passage, and history of use. Most
is given before breakfast and the remaining one-third before dinner, if
NPH insulin is used. Human regular insulin and rapid-acting insulin are
best dosed with each meal.

' until more information is obtained regarding long term safety and efficacy
.: w'Jmerl of metformin use in pregnancy, the best approach is to not use metformin
" lil. Grade C)
.. for treatment of GDM. women on metformin for treatment of q!pe 2
',
-::. :,f 195 mg/dL(5.3 mmol/L) diabetes mellitus are best changed to insurin if unexpected pregnancy
,, -: < 110 mg/dL (7.8 mmol/L) occurs.
- , -': < 120 mg/ dL (6.7 mmol/L)
Monitoring
: :;pe 2 diabetes mellitus who become
-
...- Grade C)
' Daily SMBG using meters appears to be superior to less frequent
monitoring in the clinic for detection of glucose concentrations that may
,- : :lucose values of 60-99 mg/ dL (3.3-
warrant intensification of therapy beyond individualized MNT.s
--: 100-129 mg/dL (5.4-7.1mmol/l)
a. women with GDM on diet treatment alone may monitor capillary
" -. blood glucose levels 4 times a day (fasting blood grucose once a day
and postprandial blood glucose thrice a day)

5t
'rNl*r*HffihJD
th. f stfis
 andon MB, Spong CY, Thom i
Women on pharmacological therapy may monitot 4to 6 times a day
1
and Human Development Mate:
and include preprandial values
:linical trial: standard therapl r's
1'Engl J Med 2009;361:1339 {6
urine ketone testing is recommended in GDM patients with severe
Horvath K, Koch K, Jeitler K. ei :
hyperglycemia, weight loss during treatment, or other concerns of
possible
Jiabetes mellirus: systematic rc;.,
"starvation ketosis." \'loses RG, Barker M, Winter 1.1
need for insulin in gestationai :::
. Fingerstick blood ketone testing is more representative of laboratory Pridjian G, Benjamin BD. Up:.
measurements of ketosis ..i,n 20 10;37'.255 -267 .

.{ACE Task Force for Derel::.:.

Committee. Endocrine Pr't::: :: l'!.
.American Diabetes Assoctali.- :.
Summary of Evidence \'letzger BE, Buchanan TA. C :.-
ol the fifth international ric:k::
TheHyperglycemiaandAdversePregnancyoutcome(HAPO)Studyshowed Diabetes Care 2001;3}(Suppi. - >
that there are strong, continuous associations of maternal glucose levels with , Kitzmiller JL, Block IN{. Br--'.':
above the 90th
adverse pregnancy outcomes. The odds ratios for birth weight pregnancy: summary of e" ri-:
percentile, cord-blood serum c-peptide level above the 90th percentile and primary Diabetes Care 2008',31 ,1060- I .
-:
in the fasting plasma i0. Rowan JA, Hague WH. Ga: 'i,
delivery were significantly higher with an increase
".ru..un
glucose level of 6.9 mg/ dL, an increase in the 1-hour plasma glucose level of 30'9 outcomes in the metformln .: .
"mg/ dL' The
dL and an increas=e in the 2-hour plasma glucose level of 23.5 mg/ 16.
1. Cypryk K, Sobczak M, Perr,::r.
odds were computed compared to the following values: fasting blood sugar
1

andperinatal outcome in diar.::.

(FBS) <i5 mg/at, l-houi plasma glucose S 105 mg/dL and 2-hour plasma regular human insulin during ::,
glucose 190 mg/dL. .1. Lapolla A, Dalfra MG, Spez:: !
In an RCT comparing rwo forms of treatment for GDM, fasting capillary patients treated with insulin Ls:
glucose predicted t-t.onutut complications and postprandial glucose predicted Diabetol. 2008;45 :6 I -66.
(LGA) infants' llbAlc values during
ireeclampsia and large for gestational age 13. Masson EA, Patmore JE. Bras:
treatment also predicted LGA infants. mellitus treated with insulin l:.:
The rapid-icting insulin analogups that have been studied in pregnancy include 14. Hod M, Visser GHA, Damm F
lispro and urpurt. An RCT of subjects with rype I diabetes mellitus found similar a randomized trial comparin; .:
with type I diabetes. Diabe:c: |
saiefy in the use of aspart insulin compared with regular human insulin. The
data _

There are still no conclusive 15. Mathiesen ER, Kinsley B. -{:

that detemir is safe in pregnancy are convincing. hypoglycemia in type I diab'e::--
reports on the safety of glargine insulin' versus human insulin in 322 pr:,
Although insuiin ii the preferred treatment approach, metformin and 16. Sciacca L, Marotta V, Insalac: I
glyburide have been shown to be effective alternatives rvithout adverse effects in Nutr Metab Cardiovasc Dis 201i 1
some women.

References

l. Croq'ther CA, Hiller FE. Moss JR, McPhee AJ, Jeffries wS, Robinson FS, for
the Australian Carbohydrate Intolerance Srudy in Pregnant Women (ACHOIS)
Trial Group. Effect of treatment of gestational diabetes mellitus on pregnancy
outcomes. N Engt I Med 2005; 352.2417'2486'
'-a\.',-
ikrr.n ti '-
?irr*a. 52
Ei :-::rapy may monitor 4 to 6 times a day
Jn-..
q,-.:ded in GDM patients with
@. :::atment, or othet concerns of possible
Er: :: more representative of laboratory
2. Landon MB, Spong C\ Thom E, et al. The National Institure of Child Healrir
and Human Development Maternal-Fetal Medicine Units Nen', ork randomized
clinical trial: standard therapy vs. no therapy for mild gestational diabetes meliirus.
N Engl I Med 2009;361:1339-48.
severe
3. Horvath K, Koch K, Jeitler K, et al. Eff'ects of treatment in lvomen u,ith gestatronal
diabetes mellifus: systematic review and meta-analysis. BMJ2010;340:c1395.
4. Moses RG, Barker M, Winter M, et al. Can a low gly'cemic index diet reduce rhe
need for insulin in gestational diabetes mellitus? Diabetes Care 2009;32 .996- 1000.
5. Pridjian G, Benjamin BD. Update on gestarional diaberes. Obstet Gynecol Clin N
Am 2010;37'.255-267 .

Jhe -- .::r' Outcome (HAPO) Study showed
lB:::.,-:ls of maternal glucose levels with
3b -':.:s for birth weight above the 90th
t r: :. :-bove the 90'h percentile and primary
|n ,' .'.:th an increase in the fasting plasma
j - -= 1-hour plasma glucose level of 30'9
rp : -:: glucose level of 23.5 mg/dL.The
ftr ,..:s'ing values: fasting blood sugar
tg.- :: 1 105 mg/dL and 2-hour Plasma
I --::l:ment for GDM, fasting caPillarY
.:rd postprandial glucose predicted
-G.\) infants. FIbAlc values during
- :', e Lreen studied in pregnancy include
- ..;e I diabetes mellitus found similar
: '.,..:h regular human insulin. The data
- .:---::rg. There are still no conclusive
'::,:irleftt approach, metformin and
. '.:.:natives without
adverse effects in
6. AACE Task Force for Developing a Diabetes Comprehensive Care Plan Writing
Committee. Endocrine Prac ric e, Ma rc h. Apri I 20 I 1 ;12 (Suppl 2) : l -5 3.
7. American Diabetes Association. Diabetes Care January 20ll 34 (Suppl 1):1.51.
8. Metzger BE, Buchanan TA, Coustan DR, et al. Summary and recommendations
of the fifth international workshop-conference on gestational diabetes mellitus.
Diabetes Care 2007 ;30(Supp1. 2):S25 I -5260.
9. Kitzmiller JL, Block JM, Brown FM, et al. Managing preexisting diabetes for
pregnancy: summary of evidence and consensus recommendations for care.
Diabetes Care 2008;3 I : I 060- 1 079.
10. Rowan JA, Hague WH, Gao W, Mclntyre HD. Glycemia and its relationship to
outcomes in the metformin in gestational diabetes trial. Diabetes Care 2010;33:9-
16.
1 l.
Cypryk K, Sobczak M, Pertyriska-Marczewska M, et al. Pregnancy complications
and perinatal outcome in diabetic women treated with Humalog (insulin lispro) or
regular human insulin during pregnancy. Med Sci Monit2004;10:PI29-32.
12. Lapolla A, Dalfra MG, Spezia R, et al. Outcome of pregnancy in type 1 diabetic
patients treated with insulin lispro or regular insulin: An Italian experience. Acta
Diabetol. 2008;45 :61 -66.
IJ, Masson EA, Patmore JE, Brash PD, et al. Pregnancy outcome in type 1 diabetes
mellitus treated with insulin lispro (Humalog). Diabet Med 2003;20:46-50.
14. Hod M, Visser GHA, Damm P, et al. Safety and perinatal outcome in pregnancy:
a randomized trial comparing insulin aspart with human insulin in 322 subjects
with type I diabetes. Diabetes2003;53 (Suppl l):A4\7.
.l Mathiesen ER, Kinsley B, Amiel SA, et al. Maternal glycemic control and
hypoglycemia in type I diabetic pregnancy: A randomized trial of insulin aspart
versus human insulin in322 pregnant women. Diabetes Care 2007;30:7il-7i6.
t6. Sciacca L, Marotta V, Insalaco R et al. Use of insulin detemir during pregnancy.
Nutr Metab Cardiovasc Dis 2010;20:el5-e16.

:J-:: AJ, Jeffries WS, Robinson FS, fci

' -. :::Jf in Pregnant Women (ACHOIS
-', :,::,.nal diabetes mellitus on pregnanc\
'-.-:i<

tiAvlt{lA R- ilAGDI' tl"c

53
Lh.I tF{n
 2. Antepartum Fetal Surveillance Techniques of monitoring
L Perceived fetal movemens
Pilar T. Lagman-Dy, MD
2. CST
3. NST
1. Ultrasound evaluation
a. Congenital anomali s:.
b. BPP
c. Fetal growth velocrn r
Introducticn d. Doppler velocimetrr s:

Fetal surveillance can be divided into: 4. Perceived Fetal Movements

1. Screening for congenital anomalies Oldest and simplest meri:.-

. The American Diabetic Association (ADA) recommends screening half of pregnancy.
for congenital anomalies in women with gestational diabetes mellitus
(GDM) who present with evidence of preexisting hyperglycemia Studies have shown a pos:::
(glycosylated hemoglobin [FIbAlc] of > 7o/0, a fasting blood sugar torso and lower extremrt.. :

ultrasound.
[FBS] > 120 mg/dL, or a diagnosis of GDM in the first trimester).r0
" Women with these findings are more likely to have unrecognized
pregestational diabetes mellitus and are at higher risk of fetal The "count to 10" n:c:l :

malformation from exposure to hyperglycemia during organogenesis. commonly used

2. Monitoring for fetal well-being (fetal movement counting, nonstress test Limitations of the merh--;
gestations, and grou'th a'n:..
[NST], contraction stress test [CST], Doppler velocimetry, biophysical .
profile IBPPI) MaternalhypogJvcer:.:-
with decreased fetal n:
3. Ultrasound assessment for estimated fetal weight (macrosomia or
.
activity.
intrauterine growth restriction [IUGR]) With advances in ferai s
the initiation of tesrir:.
is begun at26 to 2E u'e ,
Fetal Monitoring Techniques
B. Contrcction Stress Test
. Monitoring for fetal well-being is generally based on local practice.
CST is a test of fetal u'eil-i
. The frequency of antenatal monitoring is dependent on: contractions.
1 patient's degree of metabolic control
2. type of therapy she is receiving Principle of the test:
3. presence of other risk factors, like hypertension , Myometrial pressure :
spiral arteries and in:::
" Generally, the three important goals of antenatal surveillance are to: villous space decreas::
l. help prevent perinatal morbidity and mortality fetus has a baseline o.r,.
2. detect fetal health compromise as accurately and effectiveh'as possible with the contractions
3. provide appropriate guidance for obstetric intervention or justifiable . CST has the advana:
continuation of pregnancy compromise better. L,'. :

54
 Sun'eillance Techniques of monitoring
PU 1. Perceived fetal movements
i: 2. CST
3. NST
l. Ultrasound evaluation
a. Congenital anomaly scanning (fe tal2D echocardiography if indicated)
b. BPP
c. Fetal growth velocity monitoring
i
d. Doppler velocimetry studies
:

Pe rceived Fetal Moyements

l

i
3.,,
b. : .:.-.n (ADA) recommends screening
| * - .: * ith gestational diabetes mellitus
! : -::ce of preexisting hyperglycemia
!$-, - -:, of > 7oh, a fasting blood sugar
f"+ ':s rf GDM in the hrst trimester).r0
i - - :rore likely to have unrecognized
t -, and are at higher risk of fetal
F .'.:erglycemiaduringorganogenesis.
c Oldest and simplest method of monitoring fetal well-being in the second
half of pregnancy.
c Studies have shown a positrve correlation between the number of combined
torso and lower extremity movements perceived and those confirmed by
ultrasound.
o The "count to 10" method (10 movements in 2 hours) is the most
commonly used

J : -. :rlovement counting, nonstress test
!'[*- , - Doppler velocimetry, biophysical
Gn - .::J letal weight (macrosomia
c Limitations of the method: the inabiliry to detect malformations, multiple
gestations, and growth abnormalities, or to anticipate stillbirths.
. Maternal hypoglycemia, although generally believed to be associated
with decreased fetal movement, has been reported to stimulate fetal
or
.
activity.

s- ': With advances in fetal survival at earlier gestational ages, the timing of
the initiation of testing has changed. Fetal kick-counting monitoring
is begun at 26 to 28 weeks in diabetic pregnancies.

-il Contraction Stress Test

tfi' .--'. L'ased on local practice.
o CST is a test of fetal well-being in response to stress denoted by uterine
jcpendent on: contractions.
|ur: i
E.-.
x
o Principle of the test:
3: -.::rtension . Myometrial pressure during a contraction causes occlusion of the
spiral arteries and interrupts the flow of oxygenated blood into the
! . ' .:.:enatal surveillance are to: villous space decreasing the partial pressure of fetal oxygen. If the
fetus has a baseline oxygen deficit, late decelerations will be apparent
b :'-r:rortality with the contractions.
t& : ::irately and effectively as possible
--

ti '.' :':stetric intervention or justifiable ' CST has the advantage over the NST or BPP of detecting subtle
compromise better, by detecting hypoxia prior to the onset of acidosis.

a* 55

r$N$'
 Interpreting CST findings: a. Nonstress Test
' Negative CST - no late decelerations with adequate uterine contractions
(three contracrions within l0 minutes) o Principle of the resr:
' Positive cST - persistent late decelerations wirh adequate uterine . NST is based on the assr
contractions (three contractions within l0 minutes) depressed fetus vvill prc
- associated rvith higher incidences of abnormal perinatal outcome . Absence of accelerati.
including mortaliry fetal distress in labor, low ApGAR score and mean fetal sleep cvcles :
reduced birth weight nervous system (C\S
- frequency of a positive CST requiring delivery in diabetic . The absence of these a:
pregnancy ranges from 1-10 % of patient tests. may be a sign of feral ;
o Interpreting NST:
Table l. Positive Contraction Stress Test in Diabetic pregnancy . Reactive - (2-15-1-r-:l
Positive Test No. Patients Comments above baseline, lastine
Gabbe t6 242
maybe continued up ::
7 fetal distress
Kitzmiller t2
stimulation of a nona.-:
109 2low APGAR .
Coustan I
Non-reactive - none oi :
72low APGAR
Fadel 2 23
o Its ease of performance ar;
Lavin 5 60 3 SGA, 2 low APGAR a popular antepartum res:

o Studies on CST o Because the predictive valur

. Ray, et al.16 evaluated 3l insulin-dependent and 7 GDM patients with negative CST NST has nc'.,
CST. Eight insulin-dependent patients and one GDM patient with rate test for screening fetal c
severe preeclampsiahad positive CST:2/9 ) fetal death in utero
(FDU) and 3/9 ) low 5 minute APGAR score. o It is recommended that \S
. Gabbe, et alj observed no intrauterine deaths within I week of a diabetics being tested belc:
negative CST in 21 1 insulin-dependent diabetic patients. data from several published
' Four additional studies of 282 insulin-dependent diaberic women
confirmed Table 3. Weekly Reactive NST in lnsu.:
negative cST predicts fetal well-being in metabolically
th at a
stable patients for one week.
3arrett
o A negative csr result in type 2 diabetics predicts fetal well-being in a Lavery
metabolically stable patient for I week. rJp to 50% of positive cST iesults I'f riler and Horger
are ultimately considered false-positive.

. Frequency of Stillbirth in Insulin-Dependent Diabetic Pregnancy (Negative CST) D. Utrasound Examination

T^bk
No. Patients Stillbirth Indications of ultrasound in pre
Gabbe 211 0 - Confirmation of fetal viab:-:
Kitzmiller 134 0 - Accurate dating of pregnar.
Coustan '71
0 - Detection of congenital an:
Fadel 2t 0 - Assessment of fetal grou'r:r
Lavin 55 0 - Monitoring of fetal r,r.ell-L,e::
ari^,i.."
,.'i 56
 r
J. fonstress Test
dc - .:- :ns with adequate uterine contractions
I - . :::nutes) o Principle of rhe rest:
I ....: Jecelerations with adequate uterine ' NST is based on the assumption that a nonacidotic, non-neurologrcally
E.:s rvithin l0 minutes) will produce heart rate accelerations as it movei.
depressed fetus
E -: ---:.nces of abnormal perinatal outcome ' Absence of accelerations associated with fetal movement ) may
lr.- ::slress in labor, low APGAR score and mean fetal sleep cycles or an abnormality, such as fetal acidosis, cenf;l
nervous system (cNS) depression, or congenital abnormalities.
tG : JST requiring delivery in diabetic ' The absence of these accelerations in the resting fetal heart rate (FHR)
I , : ,. of patient tests. may be a sign of fetal compromise.

o Interpreting NST:
Pregnancy ' Reacrive - (2-15-ls-20) two accelerations of the FHR, rising 15 beats
above baseline, lasting 15 seconds within 20 minutes. The tracing
maybe continued up to 40 minutes if criteria are not met. Acoustic
7 fetal distress
stimulation of a nonacidotic fetus may elicit FHR accelerations.
2 low APGAR . Non-reactive - none of the criteria for reactive test was met.
72low APGAR
o Its ease of performance and absence of contraindications make the NST
3 SGA, 2 low APGAR a popular antepartum test.

o Because the predictive values of a reactive NST appears equal to that of a

!;-. :-Jependent and 7 GDM patients with negative csr, NST has now become the preferred antepartum fetal heart
** :atients and one GDM patient with rate test for screening fetal condition in diabetic pregnancies.
lp*-, :.'.e CST: 2/9 ) fetal death in utero
[m-- -:. -\PGAR score.
o It is recommended that NST be done twice weekly in insulin-dependent
diabetics being tested beyond 32 weeks age of gestation (AoG) bised on
r - -:ruterine deaths within I week of a
data from several published series.
h*:.: =rdent diabetic patients.
J ::: insulin-dependent diabetic women
neble 3. Weekly Reacrive NST in Insulin-Dependent Diabetics
f,S I ; :=Jics letal well-beingin metabolically
a 3arrett
No. Patients
426
No. Fetal Deaths
6
I avery
p - :-::erics predicts fetal well-being in a l0
b - =.i Up to 50% of positive CST results \hller and Horger 49 3
l{t- ,.:-.e.

D. WtrasoundExamination
::nt Diabetic Pregnancy (Negative CST)

Indications of ulrrasound in pregnancies complicated by diabetes mellitus:

0 -
0 -
0 -
0 -
0 -
Confirmation of fetal viability
Accurate dating of pregnancy
Detection of congenital anomalies as early as at l8-20 weeks of gestation
Assessment of fetal growth velocity
Monitoring of fetal well-being

57 {A'.So\$ffill
 tests), however, 37.50k hal :

E. BiophYsical Profle study did not demonstrate :i-.

it did establish that rhe Bpp :
o Parameters: unnecessary interventions :
1. NST beyond 37 weeks in mosr ci
30 seconds duration
2. Fetal breathing movements: 3 in body movements
3. Fetal movements: three or more
going from extension to flexion or vice Detecting Macrosomia
4. Fetal tone with an extremiry
VCISA o Obstetricians are motir arei :
5. Amniotic fluid index (AFI) > 5 cm the potential for trauma anJ
as a 0 (does not meet criteria)
or 2
o Each of the 5 components is scored o Definition:
a maximum score of 10' - fetal weight in excess .-:
lmeets criteria), wiitr
- weight above the 90th:r
oTheBPPisameasureoftheprobabilityofacuteandchronicfetal movements' and fetal
hypoxia ;';;;;1;' NST' fetal ureuttring' fetalis the marker for chronic o Predictors:
""d
tone markers monitor acute asphyxia'
whilJFI 1. Landon, et al.e foun:
asPhYxia' was accelerated after -rl
gestational age (LG.{, :t
o The normal fetus will have a score
of 8 or 10. A fetus that maY be 2. An abdominal girth ;::
"
.otnptomised will have a score of 6
or less' with 84% sensitivin' a::
3. Using difference benre e
equally' clinical management
o Although each component is weighted the score diameter (BPD) rirth r
shoutdbe based t;;;il;; the absJlute score' but also on and non-macrosomia i
composition and clinical context' fetuses, with a false-pcs:
4. AC and estimated ferai .

o Modified BPP includes NST and AFI only' . AC values > 90th
predicted in 780 c c:
oGolde,etal'Tobservedthat430of434BPPsdoneafterareactiveNSTina
. EFW > 90th percen
diabeticpopututio.,*'.u''o"iutedwithreassuringscoresof8orgreater' . BothAC and EF\\- :
of25BPPsao,'.un.,unonreactiveNST,2lhadscoresof8;4werebelow correctly in 88c : cf
8'TheBPPdidnotappeartoaddmoreinformationaboutfetalcondition
on ultrasound parameters o
if the NST *u, ,.u"ii*, but a score of 8 based reactive NST.
Of clinical importance. cesa
fetal ourcome as was a
was as reliable J;;#;good predicted to be macrosoml,-
to be macrosomic).
olnastudyofg8insulin-dependentdiabeticpatients,anormalBPPwas o Using the BPD and AC. rh
confirmedaspredictingnormalAPGAR"o"'tn99o/oofpatients';only was: EFW = 0,02597AC -
2.9% of97S BPP;;;re-abnormal' Ten
patients had an
"bt?111T:: ]'::: + 1.2659 which is rhe for::
beforedelivery;in6ofthesecases,neonatalasphyxiaordepressronwas of statistically significanr :
estimation.
Present.

oJohnson,etal.sdescribedtwice-weeklytestson-50insulin-dependent Note: However, even if a.-

diabeticwomenandweeklyBPPsintgscp\4s.Therewerenostillbirths could be identified correc:
BPP was low - 33% (8 of 238
in this series. The incidence of abnormal would be obviated.
144

58

: - seconds duration
: --.Jv movements
:,: fiom extension to flexion or vice
- 's a 0 (does not meet criteria) or
- -:: of 10.
-:::riity of acute and chronic fetal
::=:ihing, fetal movements, and fetal
. .,r hile AFI is the marker for chronic
bi- ,. :i 8 or 10. A fetus that may be
lgr - ::.ess.
I n" , -.::d equally, clinical management
.- ,.-:e score, but also on the score
lr
F.
i
3 -- , -'n]y
k -r: 3PPs done after areactive NST in a
b*. n::h reassuring scores of 8 or greater.
!r', :;ST. 21 hadscores of 8; 4 werebelow
h -,,. Lnformation about fetal condition
tE :: :: E based on ultrasound parameters
':-.- cutcome as was a reactive NST.
T predicted to b'e macrosomic was 28.30h (vs. 10.7% in fetuses predicted not
;!r: ::abetic patients, a normal BPP was
I ,i -l-iR scores in 99% of patients.; only
!u - =: patients had an abnormal BPP just
Fr, :-:onatal asphyxia or depression was
b ==iJy' tests on 50 insulin-dependent
B -- -38 GDMs. There were no stillbirths
I rr' ::nal BPP was low - 3.3o/o (8 of 238
5a
rests), however, 37.Soh had significant neonatat morbidiry. Although this
srudy did not demonstrate the superiority of the Bpp over the NST alone,
it did establish that the BPP may also be used for fetal surveillance with few
unnecessary interventions, thereby allowing prolongation of pregnancy
beyond 37 weeks in most of the patients studied.
i Detecting Macrosomia
obstetricians are motivated to predict macrosomia before birth because of
the potential for trauma and other related morbidity.
2
Definition:
- fetal weight in excess of 4,000 or 4,500 g (incidence of 16-45%)
- weight above the 90th percentile for AOG
Predictors:
l Landon, et al.e found that abdominal circumference (AC) growth
was accelerated after 32 weeks' gestational age in a group of large for
gestational age (LGA) fetuses of diabetic gravidas.
2. An abdominal girth change of > 1.2 cmlweek detected LGA fetuses
with 84To sensitivity and 85oh specificity.
3. using difference between the fetal trunk diameter and the biparietal
diameter (BPD) with 1.4 cm as the threshold befween macrosomia
and non-macrosomia, Elliot, et al. were able to detect 87% of such
fetuses, with a false-positive rate of 390h.s
4. AC and estimated fetal weight (EFW) by ulfrasound
. AC values > 90th percentile - macrosomia can be correctly
predicted in 78% of cases
. EFW > 90th percentile - predicted macrosomia in 74% of cases
. Both AC and EFW > 90th percentile - macrosomia was diagnosed
correctly in 88% of cases
of clinical importance, cesarean delivery rate for disproportion in fetuses
to be macrosomic).
using the BPD and AC, the best-fit equation for estimating fetal weight
was: EFW = 0.02597AC + 0.2t6tBpD - 0.1999 (AC x BpD ) / 1000
+ 7.2659 which is the formula used to target LGA fetuses with reports
of statistically significant reduction in random error of birth wiight
estimation.
Note: However, even if all infants destined to be macrosomic at birth
could be identified correctly, only about 50% of all shoulder dystocias
se -'ftw
would be obviated.
 Iable 4. False-negative and False-pos:
G. Doppler Studies

o Doppler velocimetry of the umbilical artery may be useful in monitoring

pregnancies with vascular complications and poor fetal growth, because
women with insulin-dependent diabetes mellirus are at increased risk for
the development of preeclampsia and fetal growth restriction'

Bracero, et al2, in a study on 25 patients with vasculopathy, found a

significant positive correlation between umbilical artery systolic/diastolic Maternal fetal kick counting is s

(S/D) ratio and serum glucose levels.

Because well-controlled class .:
Landon and Gabber), in 291 studies in 35 insulin-dependent diabetic death, antepartum surveillance :
patients, umbilical artery waveforms were abnormal in 50oh of fetuses
of women with vascular disease compared with l2oh of those without Those with complications like :
class A2, and all pregestationa.
hypertension or nephropathy.
u'eeks, with twice-weekh' \Sl.

Summary
i.eferences
. Antepartum surveillance is the standard of care in diabetic pregnancies, with
either twice-weekly NST or weekly CST.
L Barrett JM, Salyer Sl. Boe:::.
patients. Am J Obstet G1'n;::; '.:

. A study reported 2 Bracero I, Sculman H. Flersc:.

that twice-weekly modified BPP is likewise successful in and pregnancy. Obstet G,. x::. .
'-

preventing stillbirth. 3. Diamond MP, Vaughn \\X

insulin-dependent diabetic p ::.
. Absence of FHR reactivity and the presence of decelerations were predictive -1. Dicker D, Feldberg D, Yeshr'.
of the diagnosis of fetal distress in labor requiring cesarean section delivery. diabetic pregnancy: predicti'. e :
1988;159:800.
. No differences were observed befween various classes of diabetics; 85% of
in diabetic patients. Obsre: G;.,:,
the tests were reactive and l20h had decelerations. No differences in AFI were
seen between diabetic classifications, thus this study does not support the use
6. Gabbe SG, Mestman, Freen::.
in diabetes mellitus, classes i :
of routine amniotic fluid assessment in the well-controlled term diabetic. Since
they commonly have elevated AFI, monitoring those patients for a decline in biophysical profile, and ccn::.
volume is not helpful. insulin-requiring diabetic pr:=
8. Johnson JM, Lange IR. H.:::
. At some institutions, CST is used as primary surveillance because it provides management of the dial.e::: :
a constant marker of uteroplacental reserve. Class R or F diabetic patients 9. Landon MB, Gabbe SG .\::.
with small for gestation al age (SGA) fetuses or a concomitant diagnosis of mellitus. Diabetes 1985:,i{ :.
hypertension may require commencement of testing as early as 26 weeks 10. Landon MB, Gabbe SG i
gestation. However, the incidence of false-positive CST range from 40-60%; velocimetry in pregnancv c :::
Obstet Gynecol 1989;7 3:9 c'-
therefore, intervention in the preterm diabetic should occur when either several
11. Landon MB, Gabbe SG l=::
tests suggest fetal compromise or pulmonary maturation is documented.
diabetes mellitus. Clin C':::::

,. '.1' ', . t'-

It*.,.' 1j'l 60
4

: False-negative
l!r* --' rtery may be useful in monitoring
pl -::-::s and poor fetal growth, because
fc"--:.::s mellirus are atincreased risk for
F .- : =tal growth restriction.
| -: -:::e nts with vasculopathy, found a
l- " , =: umbilical artery systolic/diastolic
[r. ,
I
] x--: =; rn 35 insulin-dependent diabetic
tt "-i .lere abnormal in 50% of fetuses
tr ::.:ared with l2o/o of those without
F
I
I
;
B
r L,dcrences
!r- : - i .are in diabetic pregnancies, with
L:,.
r
p - '::ied BPP is likewise successful in
t
! 3.
b :' ,'; =ice of decelerations
were predictive
b .i: -::equiring cesarean section delivery'
h:-=- '.anous classes of diabetics;85% of
i ;c - = -.rations. No differences in AFI were
ts -- *: lhis study does not support the use
;a : --": *'e1l-controlled term diabetic. Since
l, : , :-,:,-ring those patients for a decline in
t 8.
L r - =...-' surveillance because it provides
E: -:;::re. Class R or F diabetic patients
b- ":rjSes or a concomitant diagnosis of
;r, - =:t of testing as earlY as 26 weeks
ir '.-=e-positive CST range from 40-60%;
p : :::tic should occur when either several
ir"-- . :.rr]'
j
maturation is documented'
l;ft { - :.se-negatrve and False-positive Rates for Antepartum Tests
False-positive
(per 1,000)
0.4 > 50%
3.2 s0%
0.6 40%
" l.l::ernal fetal kick counting is started at 28 weeks for all diabetic gravidas.
- ::-ause well-controlled class Al diabetics are at low risk for in-utero fetal
':ath. antepartum surveillance may begin
at 40 weeks, with weekly NSTs.
- llcse rvith complications
iike hypertension, previous stillbirth, preeclampsia,
:-:-ssA2, and all pregestational diabetics should begin anten atal testing at 32
u:eks, rvith twice-weekly NSTs.
.
Barrett JM, Salyer sl, Boehm FH. The nonstress test: an evaluation of 1,000
patients. Am J Obsret Gynecol l98l;l4l:153.
I Bracero I, Sculman H, Fleischer A, et al. Umbilical artery velocimetry in diabetes
and pregnancy. Obstet Gynecol 1986;68:654.
Diamond MP, vaughn wK, Saiyer s, et al. Antepartum fetal monitoring in
insulin-dependent diabetic pregnancies. Am J obster Gynecor I 985; r53 :52g.
1. Dicker D, Feldberg D, Yeshaya A, et al. Fetal surveillance in insulin-dependent
diabetic pregnancy: predictive value of the biophysical profile. Am J Obstet Gynecol
1988;1 59:800.
5. Elliot JP, Garite TJ, Freeman RK, et al. Ultrasonic prediction of fetal macrosomia
in diabetic patients. Obsret Gynecol l9B2:60:159.
6. Gabbe SG, Mestman, Freeman RK, et al. Management and outcome of pregnancy
in diabetes mellitus, classes B to R. Am J Obster Gynecol 1977;129:723.
;. Golde sH, Montoro M, Good-Anderson B, et al. The role of nonstress tests,
biophysical profile, and contraction stress tests in the outpatient management of
insulin-requiring diabetic pregnancies. Am J obstet Gynecor 19g4;14g:269.
Johnson JM, Lange IR, Harman CR, et al. Biophysical profile scoring in the
management of the diabetic pregnancy. Obstet Gynecol lggg;72:g4l .
9. Landon MB, Gabbe SG. Antepartum fetal surveillance in gestational diabetes
mellitus. Diabetes 1985;34:50.
10. Landon MB, Gabbe sG, Brunner Jp, et al. Dopprer umbilical artery
velocimetry in pregnancy complicated by insulin-dependent diabetes mellitus.
Obstet Gynecol 1989;7 3:961.
11. Landon MB, Gabbe SG. Fetal surveillance in the pregnancy complicated by
diabetes mellitus. Clin Obstet Gynecol l99l;34:535.
61
"{st-tflltJo
t2. LandonMB, Mintz MC, Gabbe
growth: predictor
SG. Sonographic evaluation of fetal abdominal
of the large-for-gestational-age infant in
pregnancies
C. INTRAPA]
complicated by diabetes mellitus. Am J Obstet Gynecol 1989;160:115.
13. Lavery JP. Nonstress fetal heartrate testing. Clin Obstet Gynecol 1982: 25:689. l. Intraparn
14. Miller JM, Horger EQ. Antepartum heart rate testing in diabetic pregnancy.
J Reprod Med 1985:30:515. \ernes
15. Nyland L, Lubell NO. Uteroplacental blood flow in diabetic pregnancy:
measurements with indium I l3 and a computer-linked gamma camera. Am J
Obstet Gynecol 1982;1 44:298.
16. Ray M, Freeman R, Pine S. Clinical experience with the oxytocin challenge
test. Am J Obstet Gynecol 1972;114:I. Recommendations
17. Sabbagha RE, Minogue J, Tamura RK, Hungerford SA. Estimation of
birthweight by use of ultrasonographic formulas targeted to large- approriate- Women with gestational diab:
and small-for-gestational-age fetuses. Am J Obstet Gynecol 1989;160:854' therapy are best managed x rth
18. Spong CY. Antepartum fetal monitoring: when, what, and how Contemp monitoring protocols during labc:
Obstet Gynecol 1998;36'45. nellitus.
Women with very mild GD\i :
:lood glucose assessment dunng .a

)urins Labor

. The last insulin dose is given si-

. Monitor plasma glucose ever',

. Give short-acting insulin r ia --,
plasma glucose above 120 m_s

. of control during lab:

Targets
mmol/L) or capillary glucose -
. Discontinue IV insulin immeJ:

lor Cesarean Section Patients

. The last insulin dose is gir en s -

. Determine random plasma g:1:.;

. Infuse short acting insulin (,l j .

mg/dL.
. Discontinue IV insulin immei:,

'Ql,u... . Check plasma glucose 2 hou:s :

i' T.F
{. t,,l,lt.
.,.,

L,'
"'i 62
r5-' : :rographicevaluationof fetal abdominal C. INTRAPARTUM MANAGEMENT
4r-' :-eestational-age infant in pregnancies
@s - ': I Obstet Gynecol 1989;160:1 15.
@"'- ::sting . Clin Obstet Gynecol 1982; 25:689. l. Intrapartum Glucose Management
r-- - :eart rate testing in diabetic pregnancy.
Nemesio A. Nicodemus, MD
;n: .:.:al blood flow in diabetic pregnancy:
$ ;-: . :omputer-linked gamma cameta. Am J

tu: .. :xperience with the oxytocin challenge

[: - B.ecommendations
hr-, :: RK, Hungerford SA. Estimation of
f[5:: -.:: lormulas targeted to large- approriate- women with gestational diabetes mellitus (GDM) requiring pharmacologic
k-' .. .4.m J Obstet Gynecol 1989;160:854. :::apy are best managed with intravenous (IV) insulin drips and glucose
m: .:,'ring: when, what, and how Contemp ::nitoring protocols during labor similar to women with pregestational diabetes
--ellirus.
women with very mild GDM may not require insulin therapy but should have
:.: od glucose assessment during labor.

l"-..ng Labor

The last insulin dose is given subcutaneously the night before or that morning.

Monitor plasma glucose every 7-4 hours.

Give short-acting insulin via IV infusion at a dose of 0.5-1 unit per hour for
plasma glucose above 120 mg/dL.

of control during labor are: plasma glucose 80-120 mg/dL (4.4-6.7

Targets
mmol/L) or capillary glucose 70- I 1 0 mg/ dL (3.9 -6.1 mmol/L).

Discontinue IV insulin immediately prior to delivery.

: :. Cesarean Section Patients

The last insulin dose is given subcutaneously the night before.

Determine random plasma glucose immediately prior to cesarean section.

Infuse short acting insulin (0.5-1 unit per hour) if plasma glucose is above 120
mg/ dL.

Discontinue IV insulin immediately prior to delivery.

Check plasma glucose 2 hours post cesarean section up to 24 hours.

63
nAro#wt'
 l-1. Hod M, Visser GHA, Dan:
In the Immediate Postpartum Period pregnancy; a randomized tr:a
in 322 subjects with tYPe 1 d::
. Monitor plasma glucose every 4-6 hours for 24 hours' i5. Mathiesen ER, Kinslel' B. .\
hypoglycemia in type 1 diab
. Administer insulin subcutaneously when indicated' aspart versus human i::s -
2001;30:'171-776.
15. Sciacca L, Marotta V. Insa
pregnancy. Nutr Metab Ccr:::
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The National Institute of Child
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4. Moses RG, Barker M, Winter M' et al'
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'
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I 3. Masson EA;i-;;";. JE, Brash
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t..'igeJ;;th
'Aht, i
'r;", 64
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. Monitor plasma glucose every 4-6 hours for 24 hours. in 322 subjecrs with n.pe 1
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. Administer insulin subcutaneously when indicated. hypoglycemia in type I ;:
aspart versus human :
2007;30:771-77 6.
i6. Sciacca L, Marotta \'. In
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gestational diabetes mellitus: systematic review and meta-analysis. BMJ
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the need for insulin in gestational diabetes mellittts? Diabetes Care 2009;32:996-
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Monit 2004;10 :PI29 -32.
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diabetic patients treated with insulin lispro or regular insulin: An Italian
experience. Acta Diabetol. 2008;45:61-66.
13. Masson EA, Patmore JE, Brash PD, et al. Pregnancy outcome in type I diabetes
mellitus tre{fd with insulin lispro (Humalog). Diabet Med 2003:20:46-50.
..l,t,
, t. ;.
'r,-, 64
 Hod M, Visser GHA, Damm P, et al. Safety and perinatal outcome in
pregnancy: a randomized trial comparing insulin aspart with human insulin
in 322 subjects with type I diabetes. Diabetes 2003;53 (Suppl l):A417.
Mathiesen ER, Kinsley B, Amiel sA, et al. Maternal glycemic control and
hypoglycemia in type I diabetic pregnancy: A randomized trial of insulin
aspart versus human insulin in 322 pregnant women. Diabetes care
2007;30:771-776.
16. sciacca L, Marotta v, Insalaco F, et al. use of insulin detemir during
pregnancy. Nutr Metab Cardiovasc Dis 2010;20:el5-e16.

1,, : -:: AJ, Jeffries WS, Robinson FS, for

:::Jv in Pregnant Women (ACHOIS)
ts' -::.-nal diabetes mellitus on pregnancy
t -t,
ts :ll.
.. The National Institute of Child
lE
b', ,-:al-Fetal Medicine Units Network
t:l- ::'. \'s. no therapy for mild gestational
l" , -i39-48.
in women with
,ts - -cts of treatment
F :'.: and meta-analYsis. BMJ
review

[e- ,-:-: a low glycemic index diet reduce

5l-" . ::ellitus? Dlabetes Care 2009;32:996-
'
.,:rtional diabetes. Obstet Gynecol Clin

Fj l:aL,etes Comprehensive Care Plan

b:, '.
!.:,:h-April 20ll;12 (SuPPl 2): I -53'
I; '.- C.;re January 2A134 (SuPPl 1):1-

:E- : .:e1. Summaryandrecommendations

3" , ::rference on gestational diabetes
to: _ s:-i 1-s260.
f, ,: :. \{anaging preexisting diabetes for
t.- -- r:rsensus recommendations for care.
I
pr :: HD. Glycemia and its relationshiP

f'
tLt r l.larczewska M, et al' PregnancY
-: :n diabetic women treated with
F* -::.:n insulin during pregnancy' Med Sct

rff' :. Outcome of PregnancY in tYPe 1

-
b" .:::ro or regular insulin: An Italian
F' -l
lE, :. ?regnancy outcome in type I diabetes
F: ::alog). Diabet Med 2003;2A:46-50.

65
"-.*#s'
 Mode of Delivery . Pregnant women with diabetes
2. Intrapartum Fetal Monitoring, Timing and should be offered elective birth d
if indicated, after 38 completed
Rosa Ninez B. Velante, MD
. The risks of fetal macrosomia. b
due date approaches. Routine u
or before 39'h weeks gestation C
and may reduce the risk of na--
Intrapartum Fetal Surveillance: Recommendations
. If an elective cesarean section
.Diabetesmellitusinpregnancyislistedamongtheintrapartumconditions rather than 38 weeks gestation t
fetal outcome where intrapartum
associated *itf, in.t.usei risk"of adverse
electronic fetal surveillance may be beneficial't . Expectant management bevol:
recommended.s
.Duringlaboranddeliverycontinuouselectronicfetalheartrate(FHR)
monitoringi,,..o-*.,'a.oa.,afetalbloodsamplingshouldbeavailable . After 40 or more weeks, the be:
when requested.3'a are likely to be oufweighed br :

diabetes mellitus labor before 41 weeks gestaJc:

. There are some evidence that uncomplicated .gestati:nalto both mother and
risks regardless of the readiness of:l
(GDM), well_controlled with diet may$ose minihal
a low-risk or normal pregnancy.
fetus and maybe monitored like that of . In the presence of obsteu:c
(vasculopathy, nephropathl'. pc :
delivery should be considered a
Timing and Mode of DeliverY
. Assessment of fetal lung maru
Whenshouldd'eliveryoccurinpregnanciescom2llicatedbydiabetesmellitus? pregnancy is no longer requi::
indicated in well-controlled pa
.Thetimingofthedeliveryshouldbeindividualizeddependingonwhetherthe
maternal and/ or fetal complications.12 labor or cesarean section as lJ
patient has any
"o".o-iiu"t estimation of gestational age. i
.Selectthetimingofdeliverytominimizemorbidityforthemotherandfetus. . Assessment of fetal lung maru:
.TherearenodatasupportingdeliveryofwomenwithGDMbefore38weeks gestation.12 When deliverv is
of maternal or fetal compromise' maternal or fetal reasons. del,"'
gestation in ttre absence of ob-lectlve evidence
(Letel III Grade C) maturify testing.3

. pregnancies is typically on
An optimal time for delivery of most diabetic
diabetes mellitus before 38'h
or after the 3g,h week. Deliver a patient with FIow should delivery occur in pregnan
weeksgestationonlyforcompellingmaternalorfetalindications,without
documJntin g fetal lung maturity'
2 . Vaginal delivery at term is poss:
and good glycemic control.:
. and no complicating factors
Patients with well-controlled diabetes mellitus
mayawaitspontaneouslaborandbeallowedtoproglesstotheirexpecteddate . GDM is not in itself an indica::
and the fetus is not
of delivery l;;;;t ;ni.nurur resting remainsleassuring
", .L..,,'
macrosomic.'
,i,.,,,,
. '''.:'i.1,1:,^ 66
 V

th,: ring, Timing and Mode of DeliverY Pregnant women with diabetes mellitus who have a normally grown
fetus
should be offered elective birth through induction of labor o.
section,
-.':lante, if indicated, after 38 completed weeks.ra (Level III, Grade C) "..ur.u.r
l5 MD
The risks of fetal macrosomia, birth injury, and in-utero demise
increase as the
due date approaches. Routine induction of women with diabetes
mellitus on
or before 39th weeks gestation does not increase the rate of cesarean
a.riueiv
and may reduce the risk of macrosomia.
Feldations
If an elective cesarean section is to be performed, it should be at 39 weeks
1fi5::: lmong the intrapartum conditions rather than 38 weeks gestation to reduce neonatal respiratory morbidify.r,s,rr
lttr .:': fetal outcome where intrapartum
!fr',:: =:--cial.r Expectant management beyond the estimated due date generally is not
recommended.5
b: -, elecffonic fetal heart rate (FHR)
[k: :::od samPling should be available After 40 or more weeks, the benefits of continued conservative management
are likely to be oufweighed by the danger of fetal compromise. Induction
of
labor before 4l weeks gestation in pregnant women with diabetes mellitus,
ts-:..:ated gestational diabetes mellitus regardless of the readiness of the cervix, is prudent.2
!" r -'. minimal risks to both mother and
!: - , .--rl'-risk or normal pregnancy'
In the presence of obstetric or diabetes mellitus related complications
(vasculopathy, nephropathy, poor glucose control, or a prior
stillbirth), erective
l.
delivery should be considered at 38 weeks gestation.3

ts r:iicated by diabetes mellitus? Assessment of fetal lung maturity by means of amniocentesis in a diabetic
pregnancy is no longer required with delivery after 3g weeks.
It is also not
:,.::ualized depending on whether the indicated in well-controlled patients who have indications for induction
of
r:.: or fetal comPlications.r2 labor or cesarean section as long as there is reasonable certainfy
about the
estimation of gestation dl age.rs,ra (Level III, Grade C)
-= ::orbidity for the mother and fetus'
-{ssessment of fetal lung maruriry should rarely be needed even at an earlier
-' '.i'omen with GDM before 38 week gestation.r2 when delivery is necessary at an earlier gestational age for
: - :.:e of maternal or fetal compromise' maternal or fetal reasons, delivery should be effected without regard
to lung
naturify testing.3

4,:r' should delivery occar in pregnancies complicated

by diabetes mellitus?

-.:liitus and no complicating factors
. .i:J to progress to their expected date
: -=::ains reassuring and the fetus is no:
' \-aginal delivery attermis possible if women have documented dating criteria
and good glycemic control.s
. GDM is not in itself an indication for cesarean delivery. u

67
If the estimatedfetalweight (EFW) at the time of delivery is < 4,000 g,vaginal Delivery should be actir.elr. su:
delivery is usually appropriate unless there are other obstetric indications for staff.a
cesarean section.rl
Diabetes mellitus should nor
The risk of macrosomia, shoulder dystocia andfetalinjury in labor is increased attempting vaginal birth after a
3-fold in diabetic pregnancy. These risks should be taken into account when Grade C)
planning mode of delivery.3 (Level I, Grade A)

Using ultrasound EFW or abdominal circumference (AC) to make decisions Table 1. Mode of Delivery Based on !
regarding timing and route of delivery may be associated with a lower rate of < 4000 4000-{1
shoulder dystocia, but larger studies are needed to determine if this approach
affects the rate of neonatal injury. (Level III, Grade C)
Trial of labor Consider pasr :i
clinical pelvi:r:.
body to head :r.
Despite alackof conclusive evidence, it appears that cesarean section may be AL anead o! ::
benificial when fetal overgrowth is suspected. However any benefits must be of labor
carefully weighed against the maternal risks/costs associated with cesarean
section deliveries.

Elective cesarean section should be considered if the fetus is suspected to be Special Circumstances
significantly obese. If fetal weight is estimated to be 4,500 g or more' the risks
and benefits of cesarean delivery should be discussed with the patient. The :. Pre-eclampsia
American College of Obstetricians and Gynecologists (ACOG) recommends
offering cesarean delivery to diabetic patients if the fetal weight is estimated to . Pre-eclampsia is approxinia:
be 4,500 g or more.2 (Level II'1, Grade B) complicated by diabetes me.
(Note: This weight cuhoff may not be applicable in the local setting) . Management should be a_.
eclampsia.
When EFW is 4,000-4,500 g, consider past delivery history, clinical pelvimetry,
ultrasound determined body to head disproportion (fetal AC weeks ahead of
biparietal diameter IBPDI) and progression of labor to determine mode of
delivery.15 (Level I, Grade A) . If preterm labor or delir.er.,
to promote fetal lung marur.
In the event of a planned cesarean section, delivery should be carried out . Antenatal steroids adt,ersei.,.
early in the morning to prevent prolonged fasting and to maintain optimum insulin requirements. The p:
glycemic control.3 intensive insulin therapr. an:
prevent hyperglycemia.r :
Delivery should take place in a hospital with fuIl obstetric and anesthetic . Tocolytic drugs are not coi:l
facilities and with access to neonatal intensive care facilities.3 (Level III, Grade C) drugs should be avoided as ;

glucose intolerance.l
Women do not need to fast for induction of labor.3
: " Analgesia and Anesthesia
Induction of labor with prostaglandins may be undertaken according to the
normal regimen used for non-diabetic patients maintaining a normal diet and . Effective pain relief is imp.-::
the dose of insulin. can be used.12

68
 r
1

@€ --:re of delivery is < 4,000 g, vaginal ' Delivery should be actively supervised by experienced obstetric and pediatric
are other obstetric indications for
a
im.r. staff

' Diabetes mellitus should not in itself be considered a contraindication to

fetal injury in labor is increased attempting vaginal birth after a previous cesarean section (VBAC)., (Level III,
;Ec. :rd
;ir. ;:--'uld be taken into account when Grade C)

3;, t-

decisions Table l. Mode of Delivery Based on Estimated Fetal Weight (ACOG)

itl .*--rnference (AC) to make
t -... :e associated with a lower rate of < 4000 4000-4499 g >/= 4500 g
ft .=:Jed to determine if this approach Trial of labor Consider past delivery history, Cesarean section may
)o. -i-- Grade C) clinical pelvimetry, evidence of be considered
body to head disproportion (fetal
section may be
3 .-- z:?ears that cesareanbenefits must be
AC ahead of BPD) and progression
it*.. ::.,t. However any of labor
F .-.* costs associated with cesarean

rs-,.:::ed if the fetus is suspected to be Special Circumstances

b.s: -.:ed to be 4,500 g or more, the risks
i . ::
- discussed with the patient' The :. Pre-eclamltsia
fu; :-''',recologists (ACOG)isrecommends .
i!, ,...-.,. if the fetal weight estimated to Pre-eclampsia is approximately four times more common in pregnancies
t: .
complicated by diabetes mellitus than in the background population.
fi.., ::.. n the local setting) Management should be as for the nondiabetic population with pre-
eclampsia.
p : . ,: :elivery history, clinical.pelvimelry,
weeks ahead of
i . -,-.pottion (fetal AC
ig,'rt,.n of labor to determine mode of
' If preterm labor or delivery before 36 weeks is indicated, betamethasone
i to promote fetal lung maturity should be administered if possible.5,a,r2
iI ,.=-.rn. delivery should be carried out ' Antenatal steroids adversely affect maternal glycemic control and increase
:.-;.i fasting and to maintain optimum insulin requirements. The patient should be admitted to the antenatal unit;
intensive insulin therapy and frequent glucose monitoring are required to
prevent hyperglycemia.a'12
b: -- *'tth fuIl obstetric and anesthetic ' Tocolytic drugs are not contraindicated in diabetes mellitus but f3-agonist
! ::.:-stve care facilities.3 (Level III, Grade C) drugs should be avoided as they can cause severe insulin resistance and
glucose intolerance.3
k- ..i labor.3
i. Analgesia snd Anesthesia
;l-: :rav be undertaken according to the
b* :::ients maintaining a normal diet and ' Effective pain relief is important and all forms of pain relief used in labor
can be used.12

69
-qififfir'
 ' If general anesthesia is used in women with diabetes mellitus, blood Delaying delivery to as near a-s
glucose should be monitored regularly (every 30 minutes) from induction helps maximize cervical matun
of general anesthesia until after the baby is born and the woman is fully labor and vaginal delivery.
conscious. la
A 2006 study to estimate the ge:
outcomes found that for the dra
Summary of Evidence 4l weeks I day.'
Intrapartum Fetal Survei llance Although delivery as earlv as
dystocia, it increases the likelihc
' Insulin-requiring GDM is listed among current pregnancy conditions pulmonary status. Because fen
associated with increased perinatal morbidity and mortality. The most 150 g/week, the reduction in ::
important aspects of fetal surveillance involve fetal monitoring in an effort by inducing labor 2 weeks ear.
to detect fetal compromise and the risk of stillbirth. However, there is still no setting of GDM, macrosomia
clear evidence or consensus on which method(s) of fetal surveillance are the serves as a surrogate marker c:
most effective in detecting fetal risks.'
The effect of induction or ele ::
' A 2009 reviewof the literature on 14 screening and monitoring interventions In a study in which insulin-tre::
in pregnancy on stillbirth found that there are numerous research gaps and were randomized to labor in;-
Iarge, adequately controlled trials are still needed for most of the interventions difference in cesarean delir.er','
examined. Numerous studies indicated that positive tests were associated of labor induction in prer enri:.:
with increased perinatal mortality, but while some tests had good sensitivity in dystocia.a's Both reviews concl:
detecting distress, false-positive rates were high for most teits, and questircns the beneficial effect of indur
remain about implications of testing. However, induction of labor :
women with insulin-requirin_e ;
' Continuous fetal monitoring is recommended when risk factors for fetal labor induction at approximare l
compromise such as diabetes mellitus are detected during labor. when since it lowered the shoulder c..
combined with fetal scalp blood sampling, rates of cesarean section and
operative vaginal deliveries are reduced compared with cardiotocogram In a 2009 systematic revieu
(CTG) alone. the choice of timing of ind::,
EFW or gestational age in s::
' There is no objective evidence that fetal monitoring in uncomplicated GDM with birth weight greater tha:
affects fetal outcome. A 2006 review and opinion paper (The Australian in the expectant-managemen:
Diabetes in Pregnancy Society-Management Guideline on GDM) on induction). There were no siE:
appropriate fetal surveillance for women with diet-controlled GDM shoulder dystocia, neonatal h',':
concluded
that no evidence clearly supports the practice of increased fetal surveillance
in Dataare not available to indica:r
these pregnancies.r
morbidity/mortality in the i:
if pregnancy is allowed ro pr.
Timing qnd Mode of Delivery it is reasonable to intensifl te:
continue beyond 40 lveeks ges:.
' Preferred method and timing of delivery in women with GDM
are derermined
by expert opinion because of the lack of definitive data. Planned Cesarean Section ,.

Conference on GDM): Straie=

r .r-lr i
'70
 with diabetes mellitus, blood Delaying delivery to as near as possible to the expected date of confinement
[',i -'men
minutes) from induction helps maximize cervical maturify and improves the chances of spontaneous
aE-z ... (every 30
labor and vaginal delivery.
r:-, :abv is born and the woman is fullY
A 2006 study to estimate the gestation al age ranges that result in optimal birth
outcomes found that for the diabetes mellitus group, it was 40 weeks 3 days to
41 weeks 1 day.'

Although delivery as early as 37 weeks might reduce the risk of shoulder

dystocia, it increases the likelihood of failed labor induction and poor neonatal
pulmonary status. Because fetal growth from 37 weeks onward may be 100-
I r--::g current pregnancy conditions 150 g/week, the reduction in net fetal weight and the risk of shoulder dystocia
llr -:rbidity and mortality. The most by inducing labor 2 weeks early may theoretically improve outcome. In the
!c: .:.','oh'e fetal monitoring in an effort
However, there is still no setting of GDM, macrosomia (i.e. estimated fetal weight gteater than 4500 g)
ils* :: stillbirth. serves as a surrogate marker of adverse maternal and neonatal outcomes.6
b *.::rod(s) of fetal surveillance are the
t The effect of induction or elective cesarean section on outcomes is unclear.r0
In a study in which insulin-treated GDM women with nonmacrosomic fetuses
n4 .-.=:ing and monitoring interventions rvere randomized to labor induction at 38 weeks of gestation, there was no
b -.:. are numerous tesearch gaps and difrerence in cesarean delivery. Two cochrane reviews have assessed the role
F , - :.=eded for most of the interventions of labor induction in preventing pregnancy complications, including shoulder
in- , . ::.at positive tests were associated dystocia.a's Both reviews conclude that there is insuflicient evidence regarding
-,; sonle tests had good sensitivity in the beneficial effect of induced labor on shoulder dystocia prevention.
:= :rgh for most tests, and questions However, induction of labor reduces the risk of macrosomia in pregnant
\\'omen with insulin-requiring diabetes mellitus.13 Some authors recommend
Iabor induction at approximately 38-39 weeks in insulin-treated GDM patients,
- --::Jed when risk factors for fetal since it lowered the shoulder dystocia risk from l0 to l4%.
detected during labor. Whert
':e
- . :.-: rates of cesarean section and In a 2009 systematic review (5 studies) to estimate benefits and harms of
-- :: -OmPared with cardiotocogranl rhe choice of timing of induction or elective cesarean derivery based on
FFW or gestational age in women with GDM, the proportion of newborns
rr ith birth weight greater than the 90th percentile was significantly greater
*::iroring in uncomPlicated GD\1 rn the expectant-management group (23% compared with 10% with active
, :-.: cpinion Paper (The Australian :nduction). There were no significant differences in rates of cesarean delivery,
,- :i::rent Guideline on GDM) or' shoulder dystocia, neonatal hypoglycemia or perinatal deaths.
" .:: Jiet-conffolled GDM concludec
: - - .:: cf increased fetal surveillance i:l D ata are not available to indicate whether or not there is greater risk of perinatal
rrorbidity/rnortalify in the infants of women with well-controlled GDM
:f pregnancy is allowed to proceed past 40 weeks gestation. Nevertheless,
:t is reasonable to intensifi' fetal surveillance when pregnancy is allowed to
:ontinue beyond 40 weeks gestation.rT

- '.t -rmen with GDM are determine: ?lanned Cesarean Section Guidelines (Fifth International workshop-
:.:-:ritive data. Conference on GDM): Strategies to reduce the risk of birth injury include a

7t rA$r$A^tlllll,hl'D
liberal policy toward cesarean delivery when fetal overgrowth is suspected. o There is insufficient e\-r,ir
However, no controlled trials are available to support this approach. In planning would mandate cesarean
the timing and route of delivery, consideration of fetal size using clinical such as the ACOG, ackr.
and ultrasound estimation of fetal weight, despite inherent inaccuracies, is shoulder dystocia pre\.enti:
frequently used.18 Clinicians should be aware that the accuracy of fetal weight pregnancies with suspecre,
estimation is + 20oh in term babies and that accuracy decreases with increasing than 4500 g in a woman *-:
birth weight.3
. A retrospective cohort srud',.
Prevention of shoulder dystocia: diet-controlled GDM ,r..r. u, ,
o In a study, this complication occurred in 31o/o of neonates weighing women who did not have diabr
more than 4000 g who were delivered vaginally by mothers with diabetes not an independent risk fact.-
mellitus of any fype. A study found a 3oh prevalence in GDM women VBAC among women u'ithou:
versus 1% in normoglycemic women (p < 0.001). Clinical estimation of
weighing more than 4000 gra
fetal size through ulffasonography is used to detect fetal macrosomia,
Logistic regression analysis sh:
which can be identified by increased AC. The l3o/o error rate (+ 2 standard
rnduced labor, augmented laL,c:
deviation [SD]) in estimating fetal weight through ultrasonography should
be considered. A recent cost-effectiveness analysis showed that overall
of successfirl VBAC, while d:e
were not.la
expectant management is the preferable approach, irrespective of EFW
A randomized controlled trial (RCT) in Israel compared induction of
labor with expectant management in the presence of macrosomia (4000- No clinical studies were iden::
4500 grams). There were no significant differences in the mode of birth anesthesia on perioperatir.e gJr;
befween the groups nor in the mean birthweight. There were five cases of A narrative systematic rer.ie',,,
shoulder dystocia in the induction group compared to six in the expectant surgery and trauma impaus :
management group. Study concluded that EFW befween 4000 and 4500 glucose metabolism. While rh:
grams should notbe considered an indication for inducingbirth. However, women with diabetes mellitus. :
the study was not explicitly conducted on women with diabetes mellitus.ra improved with adminisrrarion c

o The commonly used formulas derived from a multivariate regression

multiply multiple coeflicients together, with the resultant product (EFW) References
typically having an accuracy that is seldom less than within l5%. Fetuses
predicted to weigh 4000-4500 gbased on ultrasonographic findings actually 1. Knowledge to Action Evider.::
weigh that much only 50% of the time. A sensitivity of approxim ately 80% with GDM, May 2010,
is typically associated with a specificity of 50-60%. This means a false- 2. Moore TR, Smith CV. Diabe::,
positive rate of 30-50% occurs even with the more predictive formula, 3. Guidelines for the manage::
possibly requiring an unnecessary cesarean delivery of more than 100 mellitus from pre-concepric: :
fetuses in order to prevent I from having permanent Erb palsy. Current 2010 Dublin,Ireland
data do not support a policy of early induction of labor in cases of possible
4. Dunne F. Clinical practices g:::
May 2009.
lst Edition
fetal macrosomia. If one accepts thatS-20% of infants of diabetic mothers 5. Merck Online Manual, 201--
born weighing 4500 g or more will experience shoulder dystocia, 15-30% 6. Serlin D, Lash R. Diagnosis :::
of these will have recognizable brachial plexus injury, and Sok of these Fam Physician 2009;80(1):-i -:_
injuries will result in permanent deficit, approximately 333-1667 cesarean 7. McElduff A, Cheung N\\' j,:,-.
deliveries would have to be performed for possible macrosomia to prevent Society consensus guidelines :,
I case of permanent injury due to shoulder dystocia. However, if fetal relation to pregnancy. If_1.1 :
weight is estimated to be 4500 g or more, the risks and benefits of cesarean 8. British Columbia Reprodu_-:...
=
delivery shoilld be discussed with the patient.r3 Obstetric Guideline 108. 2 0.'' -

, {"ri
i, , "1... 72
. *'l;n . ., ' ..,
Fi ,::n fetal overgrowth isInsuspected'
fh.,, supportthis approach' planning
G t.tt,ion of fetif size using clinicalis
[;-,t ,lespite inherent inaccuracies,
weight
! , ... thit the accuracy of fetal
l.- ., :;curacy decreases with increasing
o There is insuflicient evidence to establish a threshold of EFW which
would mandate cesarean delivery.6 Some professional organizations,
such as the ACoG, acknowledge that a planned cesarean delivery for
shoulder dystocia prevention may be a reasonable management option in
pregnancies with suspected fetal macrosomia when the EFW is greater
than 4500 g in a woman with diabetes mellitus.'3

A retrospective cohort study (n=25,079) examined whether women with

diet-controlled GDM were at increased risk of failed vBAC compared with
s-*:J in 3l% of neonates weighing
with diabetes
women who did not have diabetes mellitus. The study found that GDM was
F*= t "aginally by mothers not an independent risk factor for vBAC. The success rate for attempted
hr. . io o prevalence in GDM women VBAC among women without diabetes mellitus, and the proportion of babies
[, I ' O.Oot;. Clinical estimation of weighing more than 4000 grams was 18% compared with l3o/o (p<0.05).
.; .:sed to fetal macrosomla'
-r detect
(1 2 standard
Logistic regression analysis showed that age, birthweight, white ethnic origin,
3t '.:.The t3% error rate
should
induced labor, augmented labor and previous vaginal birth were all predictors
f , . *t through ultrasonography
that overall
of successfirl VBAC, while diet-controlled GDM and chronic hypertension
E.-..".rt
-_t=''-'.,
anilysis showed
of EFW'
were not.la
upprouih, irrespective
n-*-= -: in Israel compared
inductio-nof
. No clinical studies were identified in relation to the eflects of analgesia or
; ::e presence of macrosomia (4000- anesthesia on perioperative glycemic control in women with diabetes mellitus.
:i':Xl} A narrative systematic review showed that pain and/ or stress following
B" ;ttftTl'iilxJixf?1lin the expectant surgery and trauma impairs insulin sensitivity by affecting non-oxidative
br ; ,
tp compared to six
and 4500 glucose metabolism. while these observations were not drawn from laboring
il"t=: ii''at Bf'W between 4000 Horvever' \\'omen with diabetes mellitus, the suggestion is that glucose regulation can be
L - :,:ation for inducingbirth' mellltus''" improved with administration of analgesia in stressful states.ra
j.;--: : -ln \\'omen with diabetes

! :::'.'.ed from a multivariate regression

(EFW) Itr"Cerences
fo='-., ri ith the resultant product
Ii ; .-ldom less than within 15%' Fetuses Knowledge to Action Evidence summary: Intrapartum Management of patients
b , : -'r ultrasonographic hndings actually 1.
with GDM, May 2010.
80%
, -= .\ sensitivify of approximately a false- Moore TR, Smith CV. Diabetes mellifus and pregnancy. MEDSCApE April, 201I
fuo, ,.--,n' of 50-60%. This meansformula' Guidelines for the management of pre-gestational and gestational diabetes
J. .. with the more predictive
than 100
mellitus from pre-conception to the postnatal period. Health Seryice Executive J:uly
]r-:- :isarean deliverY of more
palsy' Current
2010 Dublin,Ireland
lr"- .:ting permanent Erb Dunne F. clinical practices guideline for the management of diabetes in pregnancy
lcr-- of possible
,"Auairon of labor in cases lst Edition May 2009.
'- ., of infants of diabetic mothers
S-10% Merck Online Manual, 2010.
- .,'perience shoulder dystocia, l:-?0"/o
i* Serlin D, Lash R. Diagnosis and management of gestational diabetes mellitus. Am

! r-,..ilut plexus injury, and 5of2 of these
I :,--::t. approximately 333-7667 cesarean
rfi:-* =J for possible macrosomia to prevent
lr ,, shoulder dystocia' However,cesareanif fetal
of
f, :' :::re. the risks andbenefits
Jr-- ::.: Patient.r3
Fam Physician 2009 ;80(l):57 -62.
McElduff A, Cheung NW, Mclntyre HD. The Australian Diabetes in pregnancy
Society consensus guidelines for the management of type I and type 2 diabetes in
relation to pregnancy. MJA 2005 ;183(7):3j 3 -37 7 .
British Columbia Reproductive Care Program. DM and pregnancy type r and 2.
Obstetric Guideline l0B, 2001.
73
"\$-W---
9. Lamber RMJ. East Chesthire NHST fetal monitoring guideline 2007. Guidelines
for Intrapartum Care of Diabetic Women.
D. POSTPARTUM N,A\
10. Assessment and screening in gestational diabetes Evidence Report (Pub. TER]\{ C(
No. 08-E004): Evidence-based Practice Center: Johns Hopkins Univ. Topic
Nominator: ACOG. March 2008. Susan P. Nagtalon, II,ID a:
11. Royal Women's Hospital Clinical Practice Guidelines (CPGs), 2006 Victoria,
Australia
t2. Savona-Ventura C. Clinical practice guideline - management of diabetes
during pregnancy. Diabetic Joint Clinic, 2011.
13. Chapter 1; ALSO Syllabus Update, 2010; Evidence Review by Robert Gobbo, Status of Glucose Metabolism
MD & Elizabeth Baxley, MD; Evidence Review completed Oct. 2009 &
published January 2010. Post-delivery
14. NICE Clinical Guideline 63. Diabetes in pregnancy - management of diabetes
and its complications from conception to postpartum period, March, 2008. . Persistent hyperglycemia in rh.
15. Menato G, Bo S. Current management of gestational diabetes mellitus. Expert
Rev Obstet Gynecol MEDSCAPE Posted: 02/ 18 / 2008. excluded by measuring fastir:g :
16. Perinatal Manual of Southwestern Ontario: A collaboration between the discharge from the hospital
Regional Perinatal Outreach Program of Southwestern Ontario & the
Southwestern Ontario Perinatal Partnership (SWOPP) 2007. . Elevated values (diabetes me.
17. Summary and Recommendations of the Fifth International Workshop- measurements of fasting plasm:
Conference on GDM. Diabetes Care, 2007 or postprandial glucose (> ll_ :

. In such patients, medical r.

pharmacological therapl'. sh::
control and provide sufficient ::

All types of insulin, glyburide :

women.

Limited data suggesr that me::

not appear to have harmful ne::
demonstrate the safety to the i::
as well as acarbose and glitazc:

Postpartum

Because some cases of gesta::--

preexisting undiagnosed +pe :
GDM should be screened fc: .':
non-pregnant oral glucose ro1.:i

Women with a historv of GDl.

diabetes mellitus.3

,, 't. l.
,
74
t ::=
i: ? ::-:n.
monitoring guideline 2007. Guidelines D. POSTPARTUM MANAGEMENT: SHoRT AND LONG
;cs;":.:ra1 diabetes Evidence Report (Pub. TERM CONSIDERATIONS
!:-"--: :: Center: Johns Hopkins Univ. Topic
L Susan P. Nagtalon, MD and Brenda Bernadette B. Zamora,MD
I l-. --::ce Guidelines (CPGs), 2006 Victoria,

tr:. - . ;uideline - management of diabetes

Cr- tr1.
E. - - : Evidence Review by Robert Gobbo, Status of Glucose Metabolism
h,: .:::ice Review completed Oct. 2009 &
Post-delivery
s'r:. ' pregnancy - management of diabetes
::'t
Ei .- :o postpartum period, March, 2008. ' Persistent hyperglycemia in the early puerperium is uncommon and can be
F ::: :f gestational diabetes mellitus. Expert excluded by measuring fasting or random capillary blood glucose levels before
fu;.: ,l / 18/2008.
E: lrtario: A collaboration between the discharge from the hospital.
F:.::n of Southwestern Ontario & the
Fr:. .::ship (SWOPP) 2007. ' Elevated values (diabetes mellitus) should be confirmed with laboratory
!m:{ : the Fifth International Workshop- measurements of fasting plasma glucose (FpG) (> 126 mg/dL or 7.0 mmol/L)
or postprandial glucose (> 200 mg/dL or I L 1 mmol/L).

' In such patients, medical nutrition therapy (MNT) and, if necessary

pharmacological therapy, should be continued to maintain good glycemic
control and provide sufficient calories for lactation and infant well-belng.r

' All types of insulin, glyburide, or gripizide can be safely used by breastfeeding
women.

' Limited data suggest that metformin, while excreted into breast milk, does
not appear to have harmful neonatal effects. Larger studies are still needed to
demonstrate the safety to the infant of breastfeeding women using metformin
as well as acarbose and glitazones. I

Fostpartum

Because some cases of gestational diabetes mellitus (GDM) may represent

preexisting undiagnosed type 2 diabetes mellitus, women with a hisiory of
GDM should be screened for diabetes mellitus 6-12 weeks postpartum using
non-pregnant oral glucose tolerance test (OGTT) criteria.2 (Level I, Grade Al

women with a history of GDM have a greatly increased subsequent risk for
diabetes mellitus.3

75

"-w{\iT$v.
 Women with a history of GDM should have lifelong screening for the Table 2, Categories of Increased R-:si
development of diabetes mellitus at least every 3 years.2 (Level III, Grade C)
FpG 100_[i :_
Testing to detect type 2 diabetes mellitus and assess risk for future diabetes 2-hplasmaglucose in the 75-e O.
mellitus in asymptomatic individuals should be considered in adults of any
age who are overweight (body mass index [BMI] > 25 kg/m2) and who have :r
one or more additional risk factors for diabetes mellitus (Table 1). In those
'For all three tests, risk is continuL.;.-,-
without these risk factors, testing should begin at age 45 years.2 (Level II-1, :.:..-
:sproportionately greater at higher;,:; :,
Grade B)

Table l. Criteria for Testing for Diabetes Mellitus in Asymptomatic Adult Individuals2 . In those identified with in,-re.
Testing should be considered in all adults who are overweight (BMl > 25kg/m')- and have and, if appropriate, trear orhe
additional risk factors: (Level II-2, Grade B)
physical inactivity
first-degree relative with diabetes mellitus
high-risk race/ethnicity (e.g. African American, Latino, Native American, Asian American,
Pacific Islander)
women who delivered a baby weighing > 9 lb or were diagnosed with CDM
Long Term Prevention / Delar- of
hypertension (> 140/90 mmHg or on therapy for hypertension)
HDL cholesterol level < 35 mg/dl (0.90 mmol/l) and/or a triglyceride level > 250 mg/dl
. Patients with Impaired Gluccs
(2.82 mmol/l) Fasting Glucose (IFG) (Le.,i. ;^-
women with polycystic ovarian syndrome (PCOS) Grade C) should be referred ro a
glycosylated hemoglobin (HbAlc) > 5.'|yo, impaired glucose tolerance (lGT), or impaired
fasting glucose (IFG) on previous testing
weight loss of 7o/o of bodv ue:,
other clinical conditions associated with insulin resistance (e.g. severe obesity, HAIR-AN 150 minutes /weekof modera:e
syndrome) o Randomized controlled u:a
history of cardiovascular disease (CVD)
risk for developing diaberes
ln the absence ofthe above criteria, testing for diabetes n.rellitus should begin at age 45 years. given interventions that sig:
mslliftr5.s-t t These interr.en:
Ifresults are normal, testing should be repeated at least at 3-year intervals, with consideration programs that have been sh
of more liequent testing depending on initial results and ri.sk status.
*Al risk BMI may be lowar in some ethnic groups
3 years) and use of pha:
inhibitors, orlistat and rhiaz,
. If tests are normal, rcpeat testing shown to decrease incideni
carried out at least at 3-year intervals is
reasonable.2 (Letel III, Grade C) . Follow-up counseling appears ::
o Mathematical modeling studies suggest that screening independent of risk
factors beginning at age 30 or 45 years is highly cost-effective (< $l 1,000
per quality-adjusted life-year gained). The rationale for the 3-year interyal
' Metformin therapy for prere:
considered in those at the highes
is that false negatives will be repeated before substantial time elapses,
those with multiple risk facrors
and there is little likelihood that an individual will develop significant
hyperglycemia (e.g. HbAlc > c:
complications of diabetes mellitus within 3 years of a negative test result.
Grade B)
In the modeling study, repeat screening every 3 or 5 years was cost-
effective.a
. Monitoring for the developme::
mellitus should be performeC :..
' To test for diabetes mellitus or to
assess risk of future diabetes mellitus,
glycosylapd hemoglobin (HbA1c), FPG, or 2hovr 75-g OGTT is appropriate
(Table 2),Y (Level II-2, Grade B)
\,.
'' '1; , 76
 have lifelong screening for the Table 2. Categories of Increased Risk for Diabetes Mellitus (Prediabetes Mellitus)*
J ::: :ld
rI€'.: e\-ery 3 yeats.2 (Level III, Grade C) FPG 100-125 mg/dL(5.6-6.9 mmot/L): IFG
OR
:1,:-s and assess risk for future diabetes 2-h plasma glucose in the 75-g OGTT 140-199 mg/dL (7.8-11.0 mmot/L) : IGT
rls ,::uld be considered in adults of any OR
t:::\ [BMI] > 25kg/m'z) and who have HbAlc 5.6-6.4%
r :,:: ::abetes mellitus (Table 1)' In those 'icr all three tests, risk is continuous, extending below the lower limit of the range and becoming
fr,: -.: L,egin at age 45 years.2 (Level II-1, :::roportionately greater at higher ends of the range.

H. -, r Asymptomatic Adult Individuals2 ' In those identified with increased risk for future diabetes mellitus, identiff
renreight (BMI > 25k and, if appropriate, tteat other cardiovascular disease (CVD) risk factors.2
Q,evel II-2, Grade B)

\ative American, Asian American,

I-ong Term Prevention / Delay of Type 2 Diabetes Mellitus
' - .'=13 diagnosed with GDM
..:e
::
rtension)
or a triglyceride level > 250 mg/dl
' Patients with Impaired Glucose Tolerance (IGT) (Level I, Grade A),Impaired
Fasting Glucose (rFG) (Level III, Grade Q, or anHbAlc of 5.7-6.40/o (Level III,
Grade c) should be referred to an effective ongoing support program targeting
-.: glucose tolerance (lGT), or impaired weight loss of 7% of body weight and increasing physical activity to at least
'::.:iance (e.g. severe obesity, HAIR-AN 150 minutes /week of moderate activity such as walking.2
o Randomized controlled trials (RCTs ) have shown that individuals at high
risk for developing diabetes mellitus (those with IFG, IGT, or both) can be
given interventions that significantly decrease the rate of onset of diabetes
b : - -.:.. :lellitus should begin at age 45 years
mellitus.5-rr These interventions include intensified lifestyle modification
F: :-: at 3-year intervals, with consideration programs that have been shown to be very effective (58% reduction after
lm .-.i risk status. 3 years) and use of pharmacologic agents metformin, cr-grucosidase
inhibitors, orlistat and thiazolidinediones (TZDs), each of which has been
shown to decrease incident diabetes mellitus to various degrees.2
3 :.;:--:J out at least at 3-year intervals is
" Follow-up counseling appears to be important for success.2
b -..-:st that screening independent of risk
,
;'l*' =l:s is highly cost-effective (< $11,000 " \Ietformin therapy for prevention of type 2 diabetes meilitus may be
n:- :: The rationale for the 3-year interval considered in those at the highest risk for developing diabetes mellitus, such as
E -,:.::ed before substantial time elapses' :hose with multiple risk factors, especially if they demonstrate progression of
ifln:: .:. individual will develop significant ryperglycemia (e.g. HbAlc > 6%) despite lifestyle modifications.2 (Level II-2,
F*, '.'.:rhin 3 years of a negative test result' Srade B)
F ,--::ening every 3 or 5 years was cost-
" \Ionitoring for the development of diabetes mellitus in those with prediabetes
nellitus should be performed every year.2 (Lewl III, Grade C)
in .;;.ss risk of future diabetes mellitus'
l5 . .' or 2 hour 75-g OGTT is appropriate
'
*s$-\$s'
Breastfeeding fasting glucose levels in breasrre
effect with lower diabetes mell:
Breastfeeding is recommended by numerous health agencies as the preferred
method of feeding for infants for at least one year because of its multiple . Pending clarification of these
immediate and long term benefits for both mother and child. GDM, should be activeh' encc,
o The American Academy of Pediatrics (AAP) strongly endorses extent possible during the firs: ',
breastfeeding as the primary source of nutrition for infants with a strong
family history of diabetes mellitus.r2
A study on the effect of lactation on glucose metabolism in women with Contraception
recent GDM showed that postpartum glucose values were significantly
lower in the breastfeeding group (p 0.0 I ). Nonlactating women developed l, Barrier Methods
postpartum diabetes mellitus at a 2-foldhigher rate than lactating women. r3
The association befween infant feeding practices and type 2 diabetes . Barrier methods, lvhich :c.
mellitus in later life was examined in alarge longitudinal diabetes mellitus spermicides, are x'elI suiie;
study among a population with avery high prevalence of type 2 diabetes lack of systemic side effec...
mellitus. Type 2 diabetes mellitus was 59o/o less common in exclusively
breastfed people compared with those who were exclusively bottlefed.ta . Strong patient-partner mc::
As part of the same study, the long term effects of diabetes mellitus during contraceptive success.
pregnancy and the influence of early life events on offsprings of both
mothers with diabetes mellitus and those without were also examined. . The use of condoms sho;.:
The researchers found that diabetes mellitus in the next generation was who appear at risk for se::
less common among breastfed children than among bottlefed children. immunodeficiency virus r :i
Therefore, in theory, increased infant breastfeeding rates may lessen or
prevent long term adverse outcomes such as diabetes mellitus during 2, fntuaaterine Devices
pregnancy in the next generation.ls
The association between lactation duration and incidence of the . The intrauterine device
metabolic syndrome among women of reproductive age was assessed contraceptive method ri ir:-
among 1399 women in the Coronary Artery Risk Development in Young ideal contraceptive for u c:
Adults (CARDIA) Study, a multicenter, population-based, prospective o The World Health Org.
observational cohort study conducted in the United States. It was found for Contracepti\,e Use
that longer duration of lactation was associated with lower incidence of contraindication to ILI
the metabolic syndrome years after weaning among women with a history o Their safety is reaffi_in
of GDM and thus, may have persistent favorable eflects on women's 2 diabetes mellitus us::
t6
cardio-metabolic health. increased risk of pel','i:
o Only few studies ha'.:
Better prenatal education and counseling about breastfeeding should be made levonorgestrel-re I eas i :- :
available to pregnant women with GDM or type 2 diabetes mellitus. recent randomized :::.t
mellitus did not shc-.'.
Hospital staff should be knowledgeable with respect to the benefits of daily insulin dose.::
breastfeeding and comfortable assisting higher risk women with initiation.'7
. Based on the available er:;;
The effect of breastfeeding per se on subsequent risk of diabetes mellitus is not IUDs can be used safel', ',',:
clear. Limited studies show lower rates of postpartum diabetes mellitus and prior GDM.'8

78

:-: i: health agencies as the Ptefefied
: r: --ne year because of its multiple
.-- :iother and child.
':-,:rics (AAP) stronglY endorses
: - . :utrition for infants with a strong
: - - icose metabolism in women with
.- giucose values were significantly
---
s -- - - Nonlactating women develoPed
I : : :righer rate than lactating women.13
: : --r-g practices and type 2 diabetes
- -:rge longitudinal diabetes mellitus
'-. of type 2 diabetes
. :iigh prevalence
.'. less common in exclusively
59ou'o
1' ' ,. '.r ho rvere exclusively bottlefed.ta
,:::: effects of diabetes mellitus during
:.'. ,ife events on offsPrings of both
r: : '-:-'rse rvithout were also examined
:', :ellirus in the next generation was
:: :::1'rreastfeeding
than among bottlefed children'
r.. .:,: rates may lessen or
--=; such as diabetes mellitus during
iuration and incidence of the
-,-- --f reproductive age was assessed
*'. -:rt€r! Risk Development in Young
--:::er. population-based, prospective
-:: -n rhe united states. It was founc
,. :-isociated with lower incidence ot
. ::ning among women with a histoq;
:,:-i-iieflt favorable effects on womens
. ,'-:out breastfeeding should be mad"
!- ta-1-^L^^
L-: t]-pe 2^ diabetes *^11:+,,^
mellitus.
h-:.:.: $'ith respect to the benefits c:
r*': :.Sher risk women with initiation.
r of diabetes mellitus is n --
- : : . quent risk
r'' ., --: postpartum diabetes mellitus a::
T
fasting glucose levels in breastfeeding women with prior GDM and a protective
effect with lower diabetes mellitus rates in healthy women who breastfed.
Pending clarification of these issues, all women, including those with prior
GDM, should be actively encouraged to exclusively breastfeed to the greatest
extent possible during the first year of life.t (Level III Grade C)
Contraception
Barrier methods, which include condoms, diaphragm, cervical cap, and
spermicides, are well suited for women with prior GDM because of their
lack of systemic side effects or influence on glucose tolerance.
Strong patient-partner motivation and efTicient patient education improve
contraceptive success.
The use of condoms should be encouraged in atl women with prior GDM
who appear at risk for sexually transmitted diseases (STD) and human
immunodeficiency virus (HIV). 18
: Intrauterine Devices
The intrauterine device (IUD) is a very effective and reversible
contraceptive method without metabolic disturbances and therefore is an
ideal contraceptive for women with prior GDM.'8
o The World Health Organization (WHO) Medical Eligibiliry Criteria
for Contraceptive Use report does not consider prior GDM as a
contraindication to IUD prescription.re
o Their safety is reaffirmed by studies in women with type 1 or type
2 diabetes mellitus using copper releasing IUDs, which showed no
increased risk of pelvic inflammatory disease (PID) or failureJ}-z2
o Only few studies have been published with data on the use of
Ievonorgestrel-releasing IUD in women with a history of GDM. A
recent randomized trial of the use in women with type I diabetes
mellitus did not show any influence on blood glucose, HbAlc, or
daily insulin dose.23
Based on the available evidence, both copper and levonorgestrel-releasing
- IUDs can be used safely without any specific restriction in women with
pnor GDM.'8
79
 T

3, Combination Orsl Contrsceptives

effect of the fype and, or i--,
and maternal age. ta:-
' combination oral contraceptives (cocs) contain estrogen and progestin
o In healthy popularions e
and are the most widely used type of hormonal contraception.rs
COC-users have not esi;
and short term studres
' Generally, ethinyl estradiol has no net effect on glucose tolerance and
effect on lipid metat oli-s:
insulin sensitivify2a but even the lowest ethinyl estradiol dosage may
adversely influence hemostatic and renin-angiotensin systems to increase
o Newer COC formularll:
lipid profiles.25.:5
thrombosis risk and blood pressure.25

. The majority of women u rr:

Ethinyl estradiol affects lipid metabolism, increasing triglycerides and
cholesterol levels and decreased cholesterol.25'26 The metabolic eflects are
absolute risk of cardioras;;
dose COC can be prescnbe ;
dose-dependent with respect to the amount of estrogen used in the COC.
increase with age.:e -'

. Smoking and maternal age > 35 years add risks to these events.27
The magnitude of other ns.r :
. It is important to use the lowest dose hyperlipidemia, coagularir n
possible, or "low-dose COCs" -.'
(presence of Leiden fAcr..r
containing 20-35 Stg doses that have proven sufficient to maintain
arterial and venous thron:b.':
satisfactory cycle control. r8
always be considered. '
. The progestin components most widely used in today's COCs are
A periodic risk assessment -
either "second-generation" (e.g. levonorgestrel or norgestimate), ,,third-
prior GDM should be donr
generation" (e.g. desogestrel or gestoden), or the newest progestin,
drosperinone.
When hypertension or nlli.::
o Speroff and Darney (2005) stated that in general, the effect on glucose it would be most cautious :.::
metabolism is mainly related to dose, potency and chemical structure
of the progestin. . In all cases, the lorvest eth.:.-.
o Less androgenic progestins increase glucose tolerance and insulin prescribed and close attenti--:
sensitivity.2T
and weight.r8
o Older progestins have no influence on blood pressure or clotting factors
although they may modiff the effects of estrogen by mechanisms still . All women should re;ei',e
to be explained.
exercise daily, achieve a he -..:
therapy to control bloo,1 p:::
' current information on the drosperinone-containing cocs shows fail. t8
no increase in blood pressure in those susceptible because of its anti
aldosterone and anti-mineralocorticoid activity.
o Although progestins tend to antagonize the estrogen effect, i.e. 4. Non-oral Combination Hormonal l
lowering of triglycerides and HDL cholesterol and increasing LDL .
cholesterol, Speroff's review illustrated that the use of the less-
Non-oral combination i::::
administered as a monrhl', ,:
androgenic progestins increase HDL, decrease LDL, with little
change in cholesterol, increase triglycerides.25-:s
o Available epidemiol--;---'
and in the absence c: s:...
should be considereJ s-::-
' The metabolic effects of a given coc formulation will depend on the net
, ,,,
lt.
, :Jtl,tr,
, g0

r -- --:s) contain estrogen and progestin
p - .:rmonal contracePtion'r8
and
lsL :.:: effect on glucose tolerance may
h r.,,:st ethinyl estradiol dosage
bt ,..-,.-ungiotensin systems to increase
effect of the type and/ or dosage of each hormonal component, smoking
and maternal age.ra'zt
o In healthy populations, epidemiological studies in current or previous
COC-users have not established an increased risk of diabetes mellitus
and short term studies have found no clinically relevant damaging
effect on lipid metabolism.
o Newer COC formulations actually demonstrate a beneficial effect on
lipid profiles.2s'26

!|l.-
The majoriry of women with prior GDM likely fall in the category of low
absolute risk of cardiovascular and venous thrombotic events and low-
Fr
ls dose COC can be prescribed taking into account that the absolute risks
increase with
!E age.2e'30

. The magnitude of other risk factors, i.e. hypertension, migraine, smoking,

!v* --; :Jd risks to these events'2?
i
i hyperlipidemia, coagulation disorders, and family history of thrombosis
or "low-dose COCs"
F -::;e possible,sufficient (presence of Leiden factor V mutation), which increase the odds ratios for
b ''., Prou.n to maintain arterial and venous thrombotic events by 2 to l2-fold in COC users must
r8
always be considered.

.
'::e1)' used in
todaY's COCs .ar.e A periodic risk assessment of cardiovascular risk factors in women with
- :.--rgestrel or norgestimate), "third- prior GDM should be done.
.=,::den), or the newest Progestm'
. When hypertension or migraines are present in women with prior GDM,
: : :jtat in general, the effect on
glucose it would be most cautious not to prescribe a COC.'8
:--s.. potency and chemical structure
. In all cases, the lowest ethinyl estradiol with newer progestins should be
:::'ie glucose tolerance and insulin prescribed and close attention should be paid to increases in blood pressure
and weight.rs
- -= ,-: blood pressure or clotting factors
: =::5 of estiogen bY mechanisms stiU . All women should receive nutritional counseling, be encouraged to
exercise daily, achieve a healthy weight, and receive appropriate medical
therapy to control blood presstre and/ or lipids if lifestyle interventions
--,:trinone-containing COCs shorr': fail.18
- - r. ,ut..ptible because of its antr-
-: - r: activity. n \tn-orql Combination Hormonsl Methods
::.::gonize the estrogen effect' i e
- --
- iholesterol and increasing LD:- Non-oral combination hormonal methods are available and can be
use of the ies''
-,-strated that the lit::
administered as a monthly injection or an intravaginal ring.
. ;iDL, decrease LDL, with o Available epidemiological data are limited to healthy women only
, ::-- :-','cerides.25'28 and in the absence of spccific datarelatingto GDM, the risks/benefits
should be considered similar to those of COCs.'8
- -- - tbrmulation will depend on the ::
$qs\ssfrl'
8l
5. Progestin-Only Oral Contraceptives
. The Food and Drug Authc
2 years because of the asso,
. Progestin-only oral contraceptives (POCs) are taken continuously and
contain low-dose norethindrone, levonorgestrel or desogestrel.
. Studies examining the effec
o Less epidemiological and clinicaldataare available since POCs are less in women with prior GD),:
widely prescribed than COCs, largely because of their higher actual
failure rates and breakthrough bleeding rates. They are well-suited
. Long-acting progestin meli
for those with type 1 diabetes mellitus where estrogen-containing prior GDM unless compl:a
methods are contraindicated and for women with prior GDM who
often have several cardiovascular risk factors, making non-estrogen-
. If esftogen-containing conc
containing contraception favorable. 2e'30 be the first-choice hormor:.:
o In alarge cohort study, in postpartum Latin women, those who were
breastfeeding and therefore prescribed POCs were found to have an 7. Sargical Steri lization
adjusted three-fold ihcrease in the proportion of development of type
2 diabetes mellitus during their first 2 years compared with low-dose
. Operative sterilization is r:.
COCs and nonhormonal methods. These findings have yet to be desirous of subsequenr ch.
confirmed in women of other ethnic backgrounds but indicate that parous women, especiall', :
POCs should not be the first choice of contraception for these women sterilization can be perfo:;::
during lactation.3r
E. Sumtnary
6. Long-Acting Proges ti ns
Women with prior GDNI hare
. Progestin agents can be administered intramuscularly or subcutaneously use all forms of contraceprion

as an implant to deliver long-acting and efficacious contraceptive only methods during iactation s
protection. They offer the same metabolic advantage as POC with no
effect on maternal coagulation factors or blood pressure.r8 When prescribing hormonal n:r
should always be considered.
. IJse of long-acting progestins in women with diabetes mellitus or women neutral method such as an Ir-l
at high risk of diabetes mellitus is very limited. factors.r8
o In an observational cohort of Hispanic women with prior GDM,
use of depot medroxyprogesterone acetate (DMPA) was associated Women with prior GDill requ
with an increased risk of diabetes mellitus (unadjusted hazard tatio their lifestyle and does nor eni^.
metabolic syndrome, or cardic'.
[HR] 1.5S) compared with women who used COCs. The increased
incidence appeared to be explained by increased baseline diabetes
mellitus risk, weight gain during use, and higher baseline triglycerides Care plans should be indir:.j;
and / or breastfeeding. 32 glucose tolerance and screen::i;
risk factors following standari :
. DMPA should be used with caution in breastfeeding women and those
with elevated triglyceride levels (> 150 mg/dL). Blood pressure and rveighr sll,-
lifestyle should always be rer::,-
. Close attention should be paid to weight gain, which also has been
demonstrated to increase the risk of subsequent diabetes mellitus.33

. .'.,{
82
 r
' The Food and Drug Authoriry (FDA) cautions DMPA use for more than
2 years because of the associated decrease in bone mineral density.

br; ?OCs) are taken continuouslY and

B a -:.:rgestrel or desogestrel. ' Studies examining the effect of implant systems on diabetes mellitus risk
in women with prior GDM are still lacking.'s
hr :, l3t? are available since POCs are less
f .:gely because of their higher actual ' Long-acting progestin methods are not a first-line choice in women with
tg.- :.:eding rates. They are well-suited prior GDM unless compliance with taking daily medication is a problem.
ii,, :ellitus where estrogen-containing
td --: tor women with Prior GDM who ' If estrogen-containing contraceptives are contraindicated, the poc would
I:- :: rsk factors, making non-esftogen-
be the first-choice hormonal method or either type of intrauterine device.18
- .:.: :' ir
br:
nE - :::um Latin women, those who were
S urgical Sterilization
l:-,,-:-bed POCs were found to have an
lt[: --: :roportion of development of type ' operative sterilization is an excellent choice for women who are no longer
Fu --:s. -:st 2 years compared with low-do*se
desirous of subsequent childbearing. The option should be offered to
[m*, These findings have yet to-be
parous women, especially those delivered by cesarean section, where the
F. ' ::-::ic backgrounds but indicate that
sterilization can be performed during the surgical process.18
! - :: L1[ contraception for these women
Summary

with prior GDM have many contraceptive options and generally can
"\bmen
'.rse all forms of contraception. The only significant exception is that progestin-
tu: i : :nfiamuscularly or subcutaneousl-v -.niy methods during lactation should be avoided or used with caution.18
F- -:-:.g and efficacious POC
- contraceptive
with no
advantage as
F,- -.:-.-bolic 'I'hen prescribing hormonal methods, cardiovascular risks
andbaseline health
!&.- . :. -.r blood pressure.ls always be considered. A progestin-only method or a metabolically
'hould
neutral method such as an IUD would be desirable in cases of multiple risk
Ip:
t

l
:.:n u'ith diabetes
::-. limited.
mellitus or women
iactors.ls
women with Prior GDM.
f" : --:spanic with prior GDM require effective and safe contraception that suits
F re acetate (DMPA) was associateC "\bmen
teir lifestyle and does not enhance the risk of developing diabetes mellitus,
l&- ,:=s mellitus (unadjusted hazard rattc :retabolic syndrome, or cardiovascular complications.
::.:r u'ho used COCs. The increased
F'
F:,: ..:ed by increased baseline diabetes Care plans should be individualized and should include surveillance of
F* = ;se. and higherbaseline triglycerides
r
3iucose tolerance and screening for lipid disorders and other cardiovascular
I :rsk factors following standard guidelines.

b. - :. in breastfeeding women and those

3lood pressure and weight should be measured at each visit and a healthy
.: l mgldL).
F -rfesryle should always be reinforced.r8
.

P .
'
*'eight gain, which also has beer
slbsequent diabetes mellitus.33
Fs"
l

S}..WJ'.
i

83
!--
 16. Gunderson EP, JacoL,s Di. , :
Reference of the metabolic syndr--:'.= .:
diabetes mellirus sr.rr:.. :
1. Metzger BE, Buchanan TA, Coustan DR, et al. Summary and recommendations Artery Risk Developnt-:.: .:-.

of the fifth international workshop-conference on gestational diabetes mellitus. t7. Satcher, DS. DHHS :'.'-::
Diabetes Care 2007 ; 30 ; S2 :S25 1 -5260. 2001:116:72 -73.
2. American Diabetes Association. Standards of medical care in diabetes 2011. 18. Damm P, Mathiesen ER !.,,
Diabetes Care 20ll ;34(S 1):S I 1-56 l. diabetes. Diabetes Ct;t: ) . .-
3. Kim C, Newton KM, Knopp RH. Gestational diabetes and the incidence of type 19. World Health Organrz.::. :
2 diabetes'. a systematic review. Diabetes Care 2002;25:1862-1868. 3rd ed.2004. wtvu.u ir.- ::-.: :
4. Kahn R, Alperin P, Eddy D, Borch-Johnsen K, et a1. Age at initiation and 20. Skouby SO, Irlolstc,r-l: I :: .
contraception in diaL.c'r:,-'...
frequency of screening to detect type 2 diabetes: a cost-effectiveness analysis. :

21. Kimmerle R, Hein..n:::'.:: .

Lancet 2010 ;37 5 :l 3 65 -l3l 4.
contraccptives for t', 1., j ;..-,
5. Knowler WC, Barrett-Connor E, Fowler SE, et a1. Diabetes Prevention Program 22. Kjos S, Ballagh S.A. L: - ..
Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intrauterine device in ','.
- :-.-.
intervention or metformin. N Engl J Med2002;346:393-403. 1994:84:1 006-1009. 1 :r'rl
6. Tuomilehto J, Lindstrom J, Eriksson JG, et al. Finnish Diabetes Prevention Study 23. Rogovskaya S. Rircr.i i -':
Group. Prevention of type 2 diabetes mellitus by changes in lifestyle among system on \ onren \'..::'. ..
subjects with impaired glucose tolerance. N Engl J Med 2001;344:1343-1350. 2005;105:811-81-s.
l. Pan XR, Li GW Hu YH, et al. Effects of diet and exercise in preventing NIDDM 24, Spellacy WN. Brrhi \\ - :
in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study. metabolism: glucose . .:'., -
Di ab e tes Care 1997 ;20 : 537 -5 44. SeVenty-One wOnl(ll l:-.-ir. ..
8. Buchanan TA, Xiang AH, Peters RK, et al. Preservation of pancreatic beta-cell months. Am J Ol"r,: 3;.':. .

function and prevention of type 2 diabetes by pharmacological treatment of 25. Petersen KR. PharIl].:- ..
insulin resistance in high-risk Hispanic women. Diabetes 2002;51:2796'2803. biochemical markers i-': ..: .
9. Chiasson JL, Josse RG, Gomis R, et al. STOP-NIDDM Trail Research Group. in women witlr iusL.li::-..-.: .

Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM 2002.

ranciomize d trial. Lan c e t 2002 ;3 5 9 :201 2 -207 7 .
26. Godsland lF, Crook Ir S :- .

10. DR-EAM (Diabetes REduction Assessment with ramipril and rosiglitazone of oral contracelrtive .r!r':-,::
323:1315-1381 ,b I 99tr
Medication) Trial Investigators, Gerstein HC, Yusuf S, Bosch J, et al. Effect of
rosiglitazone on the frequency of diabetes in patients with impaired glucose
21 Oral Conlracetiorr. l:. -..
Infetrility, Lippinc;:: '.!'. :
tolerance or impaired fasting glucose: a randomized controlled trral. Lancet 28. Suthingpongse \\i Ta:-.::'-'.:
2006;368:1096-l 105. study ol oral col ltr,lcci':. . - : :.
ll. Ramachandran A, Snehalatha C, Mary S, et al. Indian Diabetes Prevention microg ethirrylcstarli..l .,::: .
Programme (IDPP). The Indian Diabetes Prevention Programme shows that in Thai women. Cot:::.:-'.:.. :

lifestyle modification and metformin prevent type 2 diabetes in Asian Indian 29. Lrdegaard, Kreiner S. C::-.::,
subjectswithimpairedglucosetolerance(IDPP-1). Diaberologia2006;49:289-297. case-control sltrdl. C ,:: . .: .

12. American Academy of Pediatrics, Work Group on Breastfeeding: Breastfeeding 30. Lidegaard, Edsrro nr 3 i.:. :

and the use of human mtlk. Pediatrics 100 1997;100:1035 -1039. a five-year national c.lj:-. .t
13. Kjos SL, Henry Q Lee RM, Buchanan TA, Mishell DR. The effect of lactation 31. Kjos SL, Peters RK. \:.-.:-- .--
on glucose and lipid metabolism in women with recent gestational drabetes. Obstet mellitus in Latin.i ,', -
Gynecol 1993;82:451 -455. I 998;280;533-538
14. Pettitt DJ, Forman MR, Hanson RL, Knowler WC, Ber.urett PH. Breastfeeding 32. Xiang AH, Kau'akul--- 1.1 :.
and incidence of non-insulin-dependent diabetes mellitus in Pima Indrans. Lancet progestin colrtraceftl :-. ,: :
1997;350 :166 -168. gestational diabetc. :-.: ..- .

15. Pettitt DJ, Knowler WC. Long-term effects of the intrauterine environment, birth JJ. Peters RK, Kjos SL ]^.:-: - i
weight, and breast-feeding in Pima Indians. Diabetes Care 1998,21(Suppl) :8138 - a single pregnancv n '.', :r-.
1996;341 :227 -230
BL4I. .

84

r. Summary and recommendations
-': rn gestational diabetes mellitus.
: medical care in diabetes 2011.
,'6
Gunderson EP, Jacobs DR Jr, Chiang V, et al. Duration of lactation and LnciCence
of the metabolic syndrome in women of reproductive age according to gestatio:la1
diabetes mellirus status: a 2)-Year prospective study in CARDIA (Coronarr
Artery Risk Development in Young Adults). Diabetes 2010 Feb;59(2):-195-50{.
l-
Satcher, DS. DHHS blueprint for action on breastfeeding. Public Heolrh R;p
2001; I 16 :72 -73.
t3 Damm P, Mathiesen ER, Petersen KR and Kjos S. Contraception after gestational
d iabetes. D i ab e t e s C a re 2007 ;30 (2) :523 6 -5241 .

. ::abetes and the incidence of type t9. World Health Organization: Medical Eligibility Criteria for Contraceptive Use.
3 r d ed.2004. www. who. int/reproductive-health
- )'.25 1862-1868. r0 Skouby SO, Molsted-Pedersen L, Kosonen A. Consequences of intrauterine
::-. K. et al. Age at initiation and
contraception in diabetic women. Fertil Sreril 1984;42:568 -572.
r :r:es: a cost-effectiveness analysis.
t1. Kimmede R, Heinemann L, Berger M. Intrauterine devices are safe and effective
contraceptives for type I diabetic women. Diabetes Care 1995;18:1506-1507.
:: al. Diabetes Prevention Program 1? Kjos S, Ballagh SA, La Cour M, Xiang A, Mishekk DR Jr. The copper T380A
:: -li type 2 diabetes with lifestYle
intrauterine device in women with type II diabetes mellitus. Obstet Gynecol
-:lo:393-403. 1994;84:1006-1009, 199 4.
-, Finnish Diabetes Prevention Stud;' 13. Rogovskaya S, Rivera R, Grimes DA, et al. Effect of a levonorgestrel intrauterine
' .:-:s by changes in lifestyle among system on women with type 1 diabetes: a randomised trial. Obstet Gynecol
:' :. .l ]'Ied
: 200 l'J441343-l 350. 2005;105:81 1-815.
- :r ::td exercise in Preventing NIDDM r. I
-i. Spellacy WN, Buhi Wc, Birk SA. The effect of estrogens on carbohydrate
- -: Da Qing IGT and Diabetes StudY metabolism: glucose, insulin and growth hormone sfudies on one hundred
seventy-one women ingesting premarin, mestranol, and ethinyl estradiol for six
. ?:eservation of pancreatic beta-cell months. Am J Obstet Gynecol 1911;114:388-392.
-:: rv pltarmacological treatment of 15. Petersen KR. Pirarmacodynamic effects of oral contraceptive steroids on
-' :, Diabetes 2002;5|:2796-2803. biochemical markers for arterial thrombosis: studies in non-diabetic women and
=
: - IP-NIDDM Trail Research GrouP. in women with insulin-dependent diabetes mellitus. Dan Med Bull 2002;49:.43- 60,
2002.
- ::::es mellitus: the STOP-NIDDM
16. Godsland IF, Crook D, Simpson R, et al. The effects of diflerent formulations
-'.:-.: n'ith ramipril and rosiglitazone of oral contraceptive agents on lipid and carbohydrate metabolism. N Engl J Med
323:1 375- I 38 i,b 1990.
.-ll. Yusuf S, Bosch J, et al. Effect of Oral Contracetion. In: Speroff and Fritz: Clinical Gynecologic Endocrinology and
21
. -, in patients with impaired glucose I nJb r ri I i ty, L ipp in c o t t 14/i I I i ams & Wi I kins, 200 5 :86 I -9 42.
. :rndomized controlled ttial. Lancet 28. Suthingpongse W, Taneepanichskul S. An open label randomized comparative
study of oral contraceptives between medications containing 3 mg drospirenone/ 40
>- S et al. Indian Diabetes Prevention
microg ethinylestadiol and 150 microg levonorgestrel/30 microg ethinylestradiol
rr :.:: Prevention Programme shows that
-:.int type 2 diabetes in Asian Indian in Thai women. Contraception 2004;69:23-26.
!"-- 29. Lidegaard, Kreiner S. Contraceptives and cerebral thrombosis: a five-year national
!t-- -lPP-l ). Diabetologia 2006;49:289-29i .
case-control study. Contraception 2002;65 :197 -205.
p'il, 3:oup on Breastfeeding: Breastfeeding 30 Lidegaard, Edstro"m B, Kreiner S. Contraceptives and venous thromboembolism:
hr -99,;100:1035 -1039. a five-year national case-control stvdy. Contraception 2002;65:181 -196.
b - -. \{ishel1 DR. The effect of lactation 31. Kjos SL, Peters RK, Xiang A, et al. Contraception and the risk of type 2 diabetes
la :-- '.i itl.r recent gestational diabetes . Obstet mellitus in Latina women with prior gestational diabetes mellitus. JAMA
I 998;280:533-538.
m_. -:.ruler WC, Bennett PH. Breastfeeding 32. Xiang AH, Kawakubo M, Kjos SL and Br.rchanan TA. Long-acting injectable
@..1 :- ::rbetes mellitus in Pima Indians. Lancet progestin contraception and risk of type 2 diabetes in Latino women with prior
gestational diabetes mellitus. Diabetes Care 2006;29(3):613-617 .
:ts of the intrauterine environment, birth J3 Peters RK, Kjos SL, Xiang A, Buchanan TA. Long term diabetogenic effect of
@.'
a single pregnancy in women with previous gestational diabetes mellitus. Lancet
n, ..:',ts. Diabetes Care 1998,21(Suppl) :8138 - 1996;341:227 -230.

tt$t$"nf$l$tct'D
85
 '-
CIinicsl Presentation
INFANT OF A DIABETIC MOTHER l. Typical somatic features
. Large for gestational ae,
Jose B. Salazar,MD . Head circumference ap:
Hepatomegaly
Cardiomegaly
. Excessivesubcutaneous
Introduction Z. Other features
. Infants often alternate
. The strict control of maternal glucose levels may limit or ameliorate the risk necessarily correlated rr
of certain complications in the newborn, especially those associated with fetal
. Infants may feed poorl"
macrosomia. Strict control of maternal glucose levels, may also reduce the
incidence of congenital malformation.
\{orbidities Seen in Infants of Dia
. Diagnosis of an infant of a diabetec mother (IDM) is made by maternal
history, including an abnormal glucose tolerance test. .. Macrosomia (> 4 kg, some > 1.5 '
. At risk for birth injuries. s';.
o Clavicle fractures
Care of the Infant of a Diabetic Mother o llumerus fractures
o Brachial plexus injur"
A. Review Maternal History o Cephalhematoma
. Type of diabetes mellitus o Subdural hemorrhaees
. Degree of maternal control o Phrenic nerve injurr. :
. Prior obstetric history o Increased risk of adre:
. Other pregnancy complications o Instrumentdeliveries
. Maternal medications, especially insulin or oral hypoglycemic agents
. lncreased risk for c
. Intrapartum medications, glucose drip, insulin, etc. newborn (TT\l
. Fetal assessment
. Asphyxia

B. In the Delivery Room (DR), assessfor: 2, Intrauterine growth restriction I

. Essential Newborn Care . Increased incidence of p:e
- Skin-to-skin contact at birth, breastfeeding within the first hour
. Severe diabetic nephropa::
(unless the neonate requires transfer to the nursery intensive care
. Diabetic vascular disease

unity [NICU]) uteroplacental insuffren;.'

- Skin-to-skin contact aids in thermoregulation and promotes
breastfeeding 3. Hypoglycemia
- Teach mothers to recognize and respond to feeding cues . Blood glucose level < -i'j :
. Macrosomia (4 kg, some > 4.5 kg)
. May develop 1 to 2 ho'.:rs
. Birth injury first 48 hours with or \\:::
. Anomalies (cardiac, musculosketetal, central nervous system [CNS])
. Blood glucose levels sho;l
. Respiratory distress
4, Respiratory distress syndrome (.t
. Occurs 5.6 times higher ::

86
 C. ClinicalPresentation
BETIC MOTHER l. Typical somatic features
. Large for gestational age (LGA)
rz::. \lD . Head circumference appropriate for gestational age
. Hepatomegaly
. Cardiomegaly
. Excessive subcutaneous fat tissue
Z. Other features
. Infants often alternate between lethargic and irritable states, not
necessarily correlated with serum glucose levels
c -. .=ls may limit or ameliorate the risk . Infants may feed poorly during the first days of life
r: . those associated with fetal
':ecially
nL :'ucose levels, may also reduce the
L
Morbidities Seen in Infants of Diabetic Mothers
!c ::--:her (IDM) is made bY maternal )
1. Macrosomia (> 4 kg, some a.5 kg) and LGA
f :: -:ranCe teSt.
. At risk for birth injuries, such as:
o Clavicle fractures
r
o Humerus fractures
o Brachial plexus injury
o Cephalhematoma
o Subdural hemorrhages
o Phrenic nerve injury, i.e. diaphragmatic paralysis
o Increased risk of adrenal hemorrhage (organomegaly)
o Instrumentdeliveries
. Increased risk for cesarean section, i.e. transient tachypnea of the
pr, --:n or oral hypoglycemic agents newborn (TTN)
! ::: insulin, etc. . Asphyxia
Intusuterine growth restriction (UGR)
. Increased incidence of preeclampsia
. Severe diabetic nephropathy (White's Class F), protein/ amino acid loss
fr ::eastfeeding within the first hour . Diabetic vascular disease > decreased uterine attery blood flow and
I -:.:.sfer to the nursery intensive care uteroplacental insuffiency
, ,- :hermoregulation and promotes
3. Hypoglycemia
. Blood glucose level < 40 mg/dL
r: ::spond to feeding cues
. May develop 1 to 2 hours after birth and may persist or recur during the
E,
first 48 hours with or without symptoms (itteriness, lethargy)
:., central nervous system [CNS])
. Blood glucose levels should be taken at 1, 2, 3, 6, 12, 24, 26and 48 hours
me

4, Respiratory distress syndrome (RDS)

. Occurs 5.6 times higher in the IDM

]t 81 tnTl[$*1filfiftl'
[h,l t0lln
 . Insulin antagonizescortisol-inducedlecithin synthesis 10. Cardisc anomalies
. Decreased surfactant production by insulin . Cardiomyopathl'
. May occur in the first hours or days - Septal hypemoph..
- Ventricular irvperrr_-::
5. Hypocalcemia - May cause outlet ::,.-.
. During pregnancy, a mother in a hyperparathyroid state > transferred and essentiallr. res:l: -
calcium to fetus (against a concentration gradient) - May present as he a:: :.
. Parathyroid hormone (PTH) and calcitonin do not cross placenta output state)
. In the neonate, decreased PTH and 1,25 dihydroxy vitamin D at -24hrs - Initial managenteir J:
after birth - Long-term manag-n_
' Occurs in -77% (50% historically) of infants born to insulin-dependent - Usually transienr a.:.: :
mothers, and in those with poor control and longer duration; may be . Truncus arteriosus 1ri i:::
potentiated by prematurity or asphyxia . Double outlet dghr veu::::
_-

. Hypocalcemia develops usually between 48-72 hours after birth . Ventricular septal dete;:
. Transient(2-3 days),improves spontaneously dextrocardia
. Plasma calcium often < 7 mg/dL; iCa2+ < 1.1 mmol/L
. Jitteriness (also with greater risk for apnea, irritabiliry seizures, tetany, I 1. Congenital anomalies
prolonged QT) . 2-3x higher compared .,,,.::-.
. Most susceptible peric; :
6. Hypomagnesemia (improved glycemic cor.:: .

. May occur in -10% of IDM (33% historically) of congenital anomahes

. Correlates with maternal magnesium levels (increased urine magnesium . Correlates with poor co:t::.
losses) glycosylated hemoglob,rn :
. Pathophysiologyunknown
a. Small left colon s1'ndronl.
7. Ilyperbilirubinemia - Obstruction and fee;::.
. Pathophysiologyunknown - Usually resolres rii:i:::
. No change in red blood cell (RBC) lifespan, osmotic fragility
. Delayed clearance and increased RBC mass suggested b. Caudal regression,'sacr.:- ::
- Complcte or parria. .l_:_
8. Polycythemia - Rib anomalies occur
. Seen in -29% of IDM (vs 6% controls) - Femoral hypoplasia :-
. Elevated umbilical cord erythropoietin concentrations in some extremity
. IDM suggests relative hypoxemia - Often associated an:::
. Increased erythropoietin and reticulocyte count tract and heart and r:r-.;:
- May be identified (.-: : *
9. Renal vein thrombosis - Most cases are sp\\:t*.-
. Severe, life-threatening, but rare - Correlates with pc:: :
. Fathophysiology pregnancy
- Polycythemia >hyperviscosity coupled with (possible) decreased
car diac output from cardiomyopathy c. Neural tube dcfects
- Imbalance of pro and anti-aggregatory prostaglandins - 10-fold increase in -ll. j
- Anencephaly. holop: _-.:

B8
lr :.::tin synthesis 10. Csrdiac snomalies
h
-
-,--:n . Cardiomyopathy
t - Septal hypertrophy
- Ventricular hypertrophy (bi or uni-)
- May cause outlet tract obstruction or hypertrophy may be so se'ere
l' - ::rparathyroid state > transferred and essentially result in hypoplastic left heart syndrome physiology
- May present as heart failure (congested lung fields, hepatomegaly, low
lri' :. gradient)
!c3- - .,:in do not cross Placenta output state)
rr -: dihydroxY vitamin D at -24hts - Initial management dependent on physiology (pressors, volume)
- Long-term management may include digoxin and/or p-blocker
- Usually transient and resolves spontaneously by 6 months after birth
I ' .:iants born to insulin-dependent . Truncus arteriosus (with or without aortic arch anomalies)
lr: -:::l and longer duration; maY be . Double outlet right ventricle (DORV)
F a

' ventricular septal defect (vsD), transposition of great arteries (TGA),

b .:.18-12 hours after birth
- - :usl-v dextrocardia
pn,
t-
l;
-- <
'.::'lea,
i.lmmol/L
irritabiliry, seizures, tetany, I 1, Congenital anomslies
. 2-3x higher compared with population without diabetes mellitus
' Most susceptible period during fetal development: 3,8 weeks gestation
(improved glycemic control after 1st trimester has no impact on incidence
lh ' :.;a11Y) of congenital anomalies)
Bi* -- :',els (increased urine magnesium ' correlates with poor control in early pregnancy as evidenced by elevated
glycosylated hemoglobin (HbAlc)

a. Small left colon syndrome

- Obstruction and feeding difficulties; may require surgery
- Usually resolves with time
: -,-n. osmotic fragilitY
: b. Caudal regression/sacral agenesis (caudal dysplasia sequence)
F -- :'.ass suggested
- Complete or partial agenesis of sacrum and lumbar vertebrae
- Rib anomalies occur
- Femoral hypoplasia, clubbed feet, and flexion contractures of left
--f ncentrations in some
exffemity
- often associated anomalies of gastrointestinal tract, genitourinary
.: count tract and heart and neural tube defects
- May be identified (or suggested) very early with 9-10 week ultrasound
- Most cases are sporadic, some with genetic component
- Correlates with poor glycemic control (elevated HbAlc) in early
pregnancy
*qlec1 with (Possible) decreasei
t', Neural tube defects
:-irv prostaglandins
- lO-fold increase in IDM
- Anencephaly, holoprosencephaly, hydrocephalus
*'$-:il'iilili;
89
Management sugar in ,1.
q30 minu:
A, Hypoglycemia allou' for
glucose) sc

' Glucose blood sugar monitoring protocol:

o Testing: check blood sugar within 30 minutes of delivery, at t hour B.IY Glucose Weaning
of life, at 2 hours of life, and thereafter. Infant will need 4 stable blood
sugars prior to discontinuing blood sugar checks. . Continue or initiate q3 hcl
o Treatment: . If blood sugar >45 mg Ji
Blood sugar > 45 mg/dL to decrease IV rate b1' 1 rr,1
- If blood sugar is normal on 4 consecutive blood sugar testing, dL. Some very severe hvpt
no further testing is required slowly.
- If blood sugar 30-45 mg/dL and baby is asymptomatic, . Once IV glucose is disc::
initiate aPProPriate feeding: values> 45 mg/ dL indica:e

Breastfeeding
i. If > 45 mg/dL, continue blood sugar testing and age
Summaly
appropriate feeding
ii. ti < +S mg/dL, or baby not breastfeeding well give 10-15 ml . Maternal hyperglycemia can l
standard term formulaby cup/dropper feeding and repeat
events resulting in neonaral :;
blood sugar in 30 minutes
If < 45 mg/ dL after formula, transfer infant to NICQ begin periconceptually and / or dur:r.,
iii.
intravenous (IV) glucose infusion of D10W at 4 ml/kg/ anomalies in the fetus can occl
hr (7 mg/kg/min of glucose) and repeat blood sugar in 30
minutes
. Improved diabetes mellitus coi
in the IDM, including improve
Not Breastfeeding
i. Give 10-15 ml standard term formula by bottle and repeat . High risk neonates should be s
blood sugar in 30 minutes appropriately.
ii. If > 45 mg/dL, continue blood sugar testing and age
appropriate feeding
iii. If < 45 mg/dL, transfer infant to NICU begin IV glucose References
infusion of D10W at 4 mg/kg/hr (7 mg/kglmin of glucose),
and repeat blood sugar in 30 minutes 1. Cornblath M, Hawdon J. el
hypoglycemia. Suggesred c:e:
Blood sugar < 30 mg/ dL, or < 45 mg/ dL and baby is symptomatic 2. Hernandez E, DagdagA. S::
- Transfer infant to NICU Soc Newborn Med and Phl. P
- Administere IV glucose bolus of 2 mg/kgof D 10W, and begin 3. Korones SS, Bada-Elizev H
IV glucose intusion of D10W at 4 mg/kg/ht (7 mg/kg/min 1993.
of glucose) 4. Merenstein GB, Gardner SI
- Recheck blood sugar in 30 minutes (after bolus) 5.
Mosby,2010
o If bloodsugar>45 mg/dL,re-checkin I hourandresume Polin R, Yoder MC. \\'ork::
2007.
q3 hour testing
'' -, o If blood sugar < 45 mg/dL, repeat 2 mg/kgDl0W bolus
7 ',". and increase D10W IV rate by I ml/kg/hr, repeat blood
90
E_--
sugar in 30 minutes and continue bolus/IV increase with
q30 minutes or the placement of a central catheter (to
allow for the infusion of an elevated concentration of
glucose) so as to avoid fluid overload

B.IY Glucose Weaning

#, fr l*ff il
:'"J"#,T#: gar
ff:Irffii J'H; . Continue or initiate q3 hour feeds until infant is feeding well.
che cks'
su
' If blood sugar 245 mg/dL, decrease IV rate by r mr/kg/hr and continue
":"'; "ffifiiood to decrease IV rate by I ml/kg/hr thereafter for each blood sugar >45 mg/
blood sugar testing dL. Some very severe hypoglycemic infants may need to be weaned more
on 4 consecutive
Hlilt"'tal
t.9uill9rr
slowly.
T*rg il cr- and baby is
asymptomatic ' once IV glucose is discontinued, continue testing until 3 blood sugar
<rroar 30-45 rng/ values >45 mg/ dL indicate infant is ready to come off treatment protocol.
feeding:
irJptiutt
and ugso--nry
continue blood sugar testing
mg/dL,
-- rt F"dine 'Tfi,ffl:l',#l;*;T#Hl'
"' ^r habV y::::?ili,',"?fl.:l'1"::ifj,1,?*f:",iT:l:x'#T#ffij.l1f:::ll:
rccur"6 *'
nOt Dl
cup/dropper
"i.t"*'r"ttturu uy
*' initiar 7-8 weeks or gestation' congenital
::lf:,H"il',',i'",", ffansrer ,,'!u,'r:? It?t;i,'f,, fi:ffi;fiiig trfjHj::tt
[thit:rutru#*;i#3tH'Jt;;'f:
^"
;;*. .iabetes metitus contror in mother the resurts in rewer morbidities
in IDM, including improved long term the neurodevelopment.
:u
and repr should be screened early for hypoglvcemia and managed
formula by bottle lrtfi;Tffi:nares
i-r; ,,.,t standard terrn
.ugut i" 3.9 *i"*,t:^,,e
and e
blood sugar tesdng
l:" mgzdl-, contrnu(
prior. ieeaing IV gluc6.t.o..t
", :rfant to NICU, begln of gluco:
lfr*t;lil1{ilji', a't''eutglmin
rr*.*'""
r. cornblath M, Hawdon J, et al. Controversies regarding derinition or neonatar
sugar m JU hypoglycemia. Suggested operational thresholds. Pediatr 2000;105:1 14 l-ll41.
epeat blood

*t***,'*;;;;;;'ffil
iu;ose) '- ":r1i:::.f.1i',lTi'lrrandresr' il:'lt*:?foo..
il:;;#{flf:'$l#' :
t". workbok in practicar neonarorogv. phladerphia Saunders,

T'J'i::".,1;:g;l;
-:3 hour testing
I
ru! f-Jif#3' Ii
"""'"X
rY ll;
il:,: :3:;1 ;i'iti
;
"',' s' *AIM\I$$I'
eo
 sugar in 30 minutes and continue bolus/IV increase with
q30 minutes or the placement of a central catheter (to
allow for the infusion of an elevated concentration of
glucose) so as to avoid fluid overload

of deliverY, at t hour
r'^inutes B. IV Glucose Weaning
Infant will need 4 stable blood
: -:3r checks.
j . Continue or initiate q3 hour feeds until infant is feeding well.
' If blood sugar >45 mg/ dL, decrease IV rate by I ml/kg/hr and continue
to decrease IV rate by 7 ml/kg/hr thereafter for each blood sugar >45 mg/
- - -JrlS€cutive blood sugar testing' dL. Some very severe hypoglycemic infants may need to be weaned more
a: slowly.
: :- and babY is asymptomatlc' ' once IV glucose is discontinued, continue testing until 3 blood sugar
values >45 mg/ dL indicate infant is ready to come off treatment protocol.

blood sugar and age

Summary

: ::eastfeeding well give 10-15 ml ' Maternal hyperglycemia can lead to fetal hyperinsulinemia and pathogenic
:up droPPer feeding and tePeat events resulting in neonatal morbidities. If maternal hyperglycemia occurs
periconcepttally and/or during the initial 7-8 weeks of gestation, congenital
- -.i ransfer infant to NICU,
4
begin
ml/kg/ anomalies in the fetus can occur.
: .:.:usion of D10W at
: -:-ie) and rePeat blood sugar in 30 Improved diabetes mellitus control in the mother results in fewer morbidities
in the IDM, including improved long term neurodevelopment.

formula bY bottle and rePeat High risk neonates should be screened early for hypoglycemia and managed
- :::m appropriately.
blood sugar and age

,: ::fant to NICU, begin IV glucose References

- ,; kg/hr (7 mg/kg/min of glucose)'
75 mg/ dL anil babY is sYmPtomatic
l. Cornblath M, Hawdon I et al. controversies regarding definition of neonatal
hypoglycemia. suggested operational thresholds. pediatr 2000;105: l l4 l-ll4s.
2. Hernandez E,DagdagA, Santos w. Manual on standards of newborn care. phil
Soc Newborn Med and Phil Pediatr Soc

-,-1us of 2mg/kgof D10W andbegin 3. Korones SS, Bada-Elizey H. Neonatal decision making. Mosky yearbook, Inc,
1993.
I iOW at 4 ig/kg/hr (7 mg/kg/min
4. Merenstein GB, Gardner SL, Handbook of neonatal intensive care. St. Louis
Mosby,2010
F - -'l minutes (after bolus)
in t hour and resume
5. Polin R, Yoder MC. workbok in practical neonatology. philadelphia saunders,
L -: =.g dL, re-check 2007.
I
: ng/ dL, rePeat 2 mg/kgDl0Wbolus
i. - '''.'
b- I!1 rate uy t repeat blood
mtzt<g/hr,

:, 91 ill.rMwsslo
l"
SUMMARY OF REC OMMENDATIONS . If the OGTT at 24-28 u.eeks rs :
weeks or earlier if clinical srgr:s
both in the mother and the fetu.
fetal growth , etc). (Level II-1. C..:.
Diagnosis and Screening

. Diabetes mellitus recognized during pregnancy should now be classified as

' The OGTT shouldbe perforn:::
hours following the general insl:;
either gestational diabetes mellitus (GDM) or overt diabetes mellitus based on
plasma glucose levels. (Level III, Grade C)

. Preconception Counseling and \1an;

Universal screening for GDM is recommended for ALL Filipino gravidas.
As Filipino gravidas are considered "high risk" by race or ethnic group, they . Starting at puberty, precol'r.r.i: ::
should be screened for fype 2 diabetes mellitus in the first prenatal visit (either
routine diabetes mellitus cirr:rc '.:,
using fasting blood sugar [FBS] , glycosylated hemoglobin [HbA 1 c] or random
(Level III Grade C)
blood sugar [RBS]). (Level III, Grade C)
. FIbAlc levels should be as cl..s.. :-
' At the flrst prenatal visit, determine if the gravida has other high risk factors
patient before conception is a:::.:-,
other than by race or ethnicity. (Lewl III, Grade B)

. . Women who are diaberic .t:.,:

A diagnosis of overt diabetes mellitus is given among women with any of the
evaluated, and if indrcated s::,--.
following results in their first visit:
o FBS > 126 mg/dL (7 mmol/L) nephropathy and cardiovasci,l...: :
o RBS > 200mg/dL (11.1 mmol/L) ' Medications taken by such ..r,-::-..
o HbAlc > 6.5% since drugs commonl,v uscd :-- .:
o 2 hour 7 5 goral glucose tolerance test (OGTT) >200 mg/ dL (1 1.1 mmol/L) may be contraindicated or n.: :--
angiotensin converting cl)l\ :--t, :
' A diagnosis of GDM is made if any one of the following plasma values are
blockers (ARBs) and mosr n.:t-.:':
exceeded: (Level III, Grade C)
o FBS > 92 mg/dL ' Since many pregnancies Jrr. ..::
o I hour > 180 mgldl, benefits of medications uhicl :.:-:
o 2 hour > 153 mg/dL of childbearing potential. an; : -- - :

. For Filipino pregnant women, POGS CPG Consensus Panel recommends the
(Level III, Grade C)

following cut off values for the diagnosis of GDM: (Letel III, GPP) , Management of preexistitrg dial,er;s
o FBS > 92 mg/dL
l. Hypertension:
o 2 hour > 740 mg/dL . A goal systolic blooJ r::.
most patients \\'irh di:.:-:::
' For Filipino gravidas with no other risk factors aside from race or ethnicity . Patients with diabe rc.s ::._-
and the initial test (FBS or HbAlc or RBS) is normal, screening for GDM
80 mmHg. (L€t',1 II.: ,-.-.:..
should be repeated at 24-28 weeks using a 2 hour 75 g OGTT. If there are
other risk factors identified, initial screening should proceed immediately to 2
ffi-g OGTT. (LevelIII Grade C)
hour'-71+'.
2. Nephropathy:
. To reduce the risk c: ,. ,.

9,:. glucose and bloo.l l-: .- : r _-: .

92
 fI}DIENDATIONS If the OGTT at 24-28 weeks is normal, the woman should be re-tested at 32
rveeks or earlier if clinical signs and symptoms of hyperglycemia are present
both in the mother and the fetus (e.g. polyphagia, polyhydramnios, accelerated
fetal growth, etc). (Level II-2, Grade B)

The oGTT should be performed in the morning after an overnight fast of

:-::.\' should now be classified as
hours following the general instructions for the test. (Level III, Gtade B)
8

: l\ ert diabetes mellitus based on

Preconception Counseling and Management

*' --:: jed for ALL Filipino gravidas.
: - :'k by race or ethnic group, ther' .
* : ..r*S in the first prenatal visit (either Starting at puberty, preconception counseling should be incorporated in the
routine diabetes mellitus clinic visit for all women of child bearingpotential.
, : remoglobin []IbA I cl or random
"
(Lewl III Grade C)

- .:a'. ida has other high risk factors

' lIbAlc levels should be as close to normal as possible (< 7%) in an individual
patient before conception is attempted. (Level II-2, Grade B)
_--.-":: B)
. Women who are diabetic and are contemplating pregnancy should be
- .::.1 among women with any of the
evaluated, and if indicated, should be screened and treated for retinopathy,
nephropathy and cardiovascular disease (CVD). (Level III, Grade C)

' Medications taken by such women should be evaluated prior to conception

since drugs commonly used to treat diabetes mellitus and its complications
--'GTT) >200 mg/ dL(l 1. 1 mmol/L)
may be contraindicated or not recommended in pregnancy, including statins,
i
angiotensin converting enzymes (ACE) inhibitors, angiotensin II receptor
F ,: the following plasma values are
blockers (ARBs) and most non-insulin therapies. (Level III Grade C)
li

' since many pregnancies are unplanned, consider the potential risks and
benefits of medications which are contraindicated in pregnancy in all women
i of childbearing potential, and counsel women using medications accordingly.
(Level III, Grade C)
T -' Consensus Panel recommends the
F ,: GDM: (Level III, GPP) . Management of preexisting diabetes mellitus-relsted complications:
l. Hypertension:
. A goal systolic blood pressure (BP) < 130 mmHg is appropriate for
most patients with diabetes mellitus. (Letel III, Grade C)
t: . .'.::iors aside from race or ethnicity ' Patients with diabetes mellitus should be treated if diastolic BP falls <
l:' -- : S I is normal, screening for GDM 80 mmHg. (Level II-2, Grade B)
rl}- . r I hour 75 g OGTT. If there are
lDt: - :.: should proceed immediately to 2
Nephropathy:
l . To reduce the risk or slow the progression of nephropathy, optimize
glucose and blood pressure control. (Lo ,,/{ G_dft*Ugtt$*

tr
93
 . Perform test to assess urine albumin excretion and serum creatinine High protein suppler:e :
in type I diabetes mellitus patients with disease duration of 5 years or associated with a s:gr..::
more and in all type 2 diabetes mellirus patients starting at diagnosis. age (SGA). (Leteii. C,-.
(Lewl III, Grade C)
o Carbohydrate consump:i--:.
3. Retinopathy: . Consumption of ca::,-:
. To reduce the risk or slow the progression of retinopathy, optimize index (GI) is recornne :
glycemic and blood pressure control. (Level I, Grade A) . Monitoring of car'a::'
. Women with preexisting diabetes mellitus who arc planning counting, food erchanS.
pregnancy or who have become pregnant should have a comprehensive key strategy to achiei'::,
eye examination and be counseled on the risk of progression of . Intake of sugar suL'siiit:
retinopathy. Eye examination should occur in the first trimester with and sucralose are ac;-:
close follow-up throughout pregnancy and for I year postpartum. acceptable dailv intai: -
(Level II-2, Grade B) . Saccharin and cvclanr::
(Letel III, Grade C)

Antepartum Management o Lifestyle changes

r One must ofler adr'::c :
. Medical Natrition Therapy MNf) cessation. (Letei III C,-:.
o MNT should be an integralpart of GDM management. . In the absence of c:::
. MNT consists of an assessment of food intake, physical activity and physical activin- and r.'.:
medication history and intake, as well as weight status, during and risk, contribute to ue :=--
after pregnancy. (Level I, Grade B)
. It should be provided for diabetic gravidas by a nutrition professional.
. It may be administered as a sole management approach or in Antepartum Blood Glucose Contrt
combination with pharmacologic treatment to achieve normal o Pharmacologic theral.r j; ;1
glycemia. (Level I, Grade A) evidenced by abnormair:.
. Nutrition requirements are the same for pregnant women with and values or an abnormal .' :^ ;;
without GDM.
o Traditionally, insuiin has '::
o Weight management and energy intake need to be monitored throughout pregnancy, lack of signrl-:;..-:
pregnancy, especially for women with GDM. Most women can be tre::;:
' Pregnancy weight gain recommendations for women with GDM who
had normal weight or were underweight pre-pregnancy is the same as o Guidelines lor ourpai:::.: :
for women without GDM. (Level III, Grade C) diabetics:
. Energy intake for overweight or obese women with GDM may be For GDM, treatmenr E-.i.. .
modestly restricted as long as weight gain is appropriate with her pre- . Preprandial glu::',
gravid body mass index (BMI) while minimizing the risk of maternal . 1-hour postmea. i-
ketosis. (Lewl III, Grade C) . 2-hour postmea. :*;
r More than weight gain, it is glycemic control that is predictive of
birthweight.
. Maternal weight reduction during pregnancy had no effect on pre-
e,c.lampsia and may be harmfu I to the fetus (resulting in low birthweigh|.
. .)',

,'*,^
, .r, 94
,",,
,,.
:l&-::in excretion and serum creatinine
rc-.:: *'ith disease duration of 5 years or
E --=^l-rrus patients starting at diagnosis.
&c :::gression of retinopathy, optimtze
!,c:-::,.i. (Level I, Grade A)
,,rr . : : les mellitus who are planning
E :::gnant should have a comprehensive
F.:,..ed on the risk of progression of
! ' - , lld occur in the first trimester with
tE.,-::ancy and for 1 year postpartum.
lc, ---l\I management.
G-. --: food intake, physical activify and
;i: :-' *'eil as weight status' during and
lfr'= - : :.rar-idas by a nutrition professional'
! . .,-1e management aPProach or in
F, , ::J treatment to achieve normal
i evidenced by abnormality in more than half of self-monitored glucose
! :. : j lme for Pregnant women with and
! ,-::r3 need to be monitored throughout
!r ,' .:.GDM.
tr,:. jations for women with GDM who
lur :.:-*.eight pre-pregnancy is the same as
-6i-' ' -il, Grade C)
ii .: obese women with GDM maY be
p .-:ht gain is appropriate with her pre-
lf .',:ile minimizing the risk of maternal
I 2-hour postmeal glucose value of Sl20 mg/dL (6.7 mmol/L)
I: . ',;emic control that is predictive of
! : -:-:rg pregnancy had no effect on pre'
&- - :he fetus (resultinginlowbirthweight)
&_
High protein supplementation (to have "low-carbohydrate diet") was
associated with a significantly increased risk of small for gestational
age (SGA). (Level I, Grade A)
Carbohydrate consumption
r Consumption of carbohydrates with low instead of high glycemic
index (GI) is recommended. (Level II-1, Grade C)
Monitoring of carbohydrates by strategies such as carbohydrate
counting, food exchange choices, or experience-based estimation, is a
key strategy to achieving glycemic control. (Level I, Grade A)
Intake of sugar substitutes such as acesulfame potassium, aspartame
and sucralose are acceptable during pregnancy and lactation within
acceptable daily intake limits.
Saccharin and cyclamates are not recommended during pregnancy.
(Level III, Grade C)
o Lifestyle changes
. One must offer advice regarding alcohol consumption and smoking
cessation. (Level III, Grade C)
. In the absence of contraindications, maintain a suflicient level of
physical activity and exercise to improve glucose control, reduce CVD
risk, contribute to weight management goals, and over-all wellbeing.
(Letel I, Grade B)
Antepartum Blood Glucose Control
o Pharmacologic therapy is instituted once diet and exercise have failed as
values or an abnormal value in those women tested weekly.
o Traditionally, insulin has been the drug of choice because of its safety in
pregnancy, lack of significant transplacental passage, and history of use.
Most women can be treated as outpatients.
o Guidelines for outpatient glucose monitoring and targets for pregnant
diabetics:
For GDM, treatment goals are: (Level lil, Grade C)
. Preprandial glucose concentration of <95 mg/dL (5.3 mmol/L)
'. l-hour postmeal glucose value of 1140 mg/dL (7.8 mmol/L)
95
-'${fliqi$}'
For women with preexisting fype I or type 2 diabetes mellitus who become o Maternal fetal kick ccur-
pregnant, glycemic goals are:
. Premeal, bedtime, and overnight glucose values of 60-99 mg/ dL (3.3- o Becausewell-conrrolle;
5.4mmol/L) antepartum surveillan;e

.'
Peak postprandial glucose value of 100-129 mg/ dL (5.4 -7 .lmmol/L)
FfuAlc value of 56.0% o Those with complica
. only if they can be achieved safely preeclampsia, class -L.
antenatal testing at -11 rr r

o Insulin administration should be individualized to achieve the glycemic

goals stated above. Human regular insulin or rapid-acting insulin o Absence of fetal hearr ra
analogues (if postprandial levels are high) or neutral protamine hagedorm and consistent late dece-
(NPH) insulin may be used for control of basal insulin needs (if FBS levels requiring cesarean secti--
are high).
Total daily insulin needs maybe computed as follows: o Doppler velocimerrv ls
. 0.7 to 0.8 U/kg actual body weight in the first trimester complications, u.hich tr;
. 1.0 U /kg acfial body weight in the second trimester or IUGR.
. 1.2 U /kg actral body weight in the third trimester
o Although insulin is the preferred treatment approach, metlormin and Intrapartum Management
glyburide have been shown to be effective alternatives without adverse
effects in some women. Intrapartum Blood Glucose Ca
o Women with GD\Ion ::
o In women with GDM, metformin (alone or with supplemental insulin) is (IV) insulin drips and g:t'.:
not associated with increased perinatal complications as compared with women with pregestarl::
insulin. The women preferred metformin to insulin treatment. However,
further follow-up data are needed to establish long-term safety. o Women with verv mil,J i
have blood glucose a-<ses,
o Urine or fingerstick ketone testing is recommended in GDM patients with
severe hyperglycemia, weight loss during treatment, or other concerns of o Insulin managemenr c;:
possible " starvation ketosis. " should be handled b,'. ,
modality.
o Patients akeady needing pharmacologic treatment should be referred to a
specialist - Perinatologist or an Endocrinologist who has confidence and o The following are clini::
experience in insulin therapy. . During Labor:
L Moniror:l"s
2. Targers ::' :_-
Antepa r t um Fe tal S ur ve il lance a. pla_.m: :
o Suggested fetal surveillance modalities are: b. Cap:...r:.
1. Screening for congenital anomalies (lst and late 2nd trimesters)
2. Monitoring for fetal well-being (fetal movement counting, nonsffess . For Cesarean Se;::,-:
test [NST], contraction stress test ICST], Doppler velocimetry, 1. Determine rani.:
biophysical profile IBPP]) section
3. . Ultrasound
.. '.. ;'t
assessment for estimated fetal weight (EFW) (macrosomia 2. Plasma glu;lsr :
, oi-inttElLterine growth restriction IIUGR]
"- u: ) 3. Discontinue i-,' r:

.,,11,r 96
i

F :I drabetes mellitus who become Maternal fetal kick counting is started at 28 weeks for all diabetic gravidas.
F

F
:1
- -- --'se values of 60-99 mg/ dL (3.3- Because well-controlled GDMs arc at low risk for in-utero fetal death,
antepartum surveillance may begin at 40 weeks with weekly NSTs.
I* . ) -129 mg/ dL (5.4 -7 .lmmol/L)
Those with complications like hypertension, previous stillbirth,
b

Fx :1
preeclampsia, class A2, and all pregestational diabetics should begin
antenatal testing at 32 weeks with twice-weekly NSTs.
F

lr -
.:ualized to achieve the glycemic
ls -:sulin or rapid-acting insulin Absence of fetal heart rate (FHR) reactivify and the presence of persistent

F
F
:,-. cr neutral protamine hagedorm
- : i.asal insulin needs (if FBS levels
and consistent late decelerations were predictive of fetal distress in labor
requiring cesarean section delivery.
i,
Doppler velocimetry is only useful in diabetes mellitus with vascular
ry- ,..J
.
as follows:
F- ,:. the first trimester complications, which predisposes the patient to develop preeclampsia and
b ..:ond trimester or IUGR.
h .::rd trimester
I
F Intrapartum Management
'.:rent approach, metformin and
l-'
r
: -::',e alternatives without adverse
Intrapartum Blood Glucose Control
o Women with GDM on insulin therapy are best managed with intravenous
:. ,.r u.ith supplemental insulin) is
&r

h (IV) insulin drips and glucose monitoring protocols during labor similar to
f*
F,:
-, :,-.rnplications as compared with
--.: to insulin treatment. However,
women with pregestational diabetes mellitus.

p ,.:lish long-term safety. o Women with very mild GDM may not require insulin therapy but should
have blood glucose assessment during labor.
I
F. .: --:lmended in GDM patients with
!. -
= Ireatment, or other concerns of
o Insulin management during labor, delivery and immediate postpartum
should be handled by a specialist adept in giving such a therapeutic
r.
modalify.
b

F
&:
to a
.. -- ::eatment should be referred
-..:.ologist who has confidence and o The following are clinical strategies that the obstetrician must know:
. During Labor:
F
1. Monitor plasma glucose every 1-4 hours
2. Targets of control during labor:
!
a. Plasma glucose 80-120 mg/ dL (4.4-6.7 mmol/L) or
l

I* ,:fe: b. Capillary glucose 70- 1 1 0 mg/ dL (3 .9-6.1 mmol/L)

F : . st and late 2nd trimesters)

ts- :.i movement counting, nonstress For Cesarean Section Patients and Immediate Postpartum Period:
lr .,: [CST], Doppler velocimetry, 1. Determine random plasma glucose immediately prior to cesarean
section
!r- r: iital weight (EFw) (macrosomia 2. Plasma glucose should be kept below 120 mg/dL
in - - GRI) 3. Discontinue IV insulin immediately prior to delivery

h 97
 o Assessment of fetal lung r
4. Check plasma glucose 2 hours post cesarean section up to 24 pregnancy is no ionger re.
hours (every 4-6 hours) indicated in well-conrr:' r
5.
1

Administer insulin subcutaneously when indicated (for levels labor or cesarean secrr,-:-
>120 mg/dL) estimation of gestation a1

fntapartum Fetal Surveillance and Delivery Mode of Deliver:t

o GDM is not itself an i::.
fntrapartum Fetal Surveillance delivery at term is possrb.t
o Diabetes mellitus in pregnancy is associated with increased risk of adverse good glycemic control.
fetal outcome and thus, intrapartum electronic fetal surveillance may be
beneficial. o The risk of macroscm:-r
increased 3-fold in diaL,e:
o During labor and delivery continuous electronic FHR monitoring account when plannine
=
is recommended and fetal blood sampling should be available when
requested. o Using ultrasound EF',\-
decisions regarding tin.: : :.
o Uncomplicated GDM, well-controlled with diet may pose minimal risks lower rate of shoulder C'.'s
to both mother and fetus and maybe monitored like that of a low-risk or
if this approach affect-. ::,
normal pregnancy.
o If the EFW at the time ,-:
appropriate unless rhe::
Timing of Delivert
section.
o The timing of the delivery should be individualized depending on whether
the patient has any concomitant maternal and/or fetal complications. o Elective cesarean secri::. ,

be significantly obese If
o There are no data supporting delivery of women with GDM before 38 the risks and benefits oi
:

,
weeks gestation in the absence of objective evidence of maternal or fetal patient. The American (
compromise. (Level III, Grade C) (ACOG) recommends c5<
fetal weight is estimareC r.
o If an elective delivery has to be performed among diabetic pregnancies, it
is typically on or after 39 weeks rather than 38 weeks gestation nor earlier o When EFW is -1000--lr _

to reduce neonatal respiratory morbidity. pelvimetry, ultrasound ;::

weeks ahead of biparie t:-
o Patients with well-controlled diabetes mellitus and no complicating determine mode of deli-.e:
factors, may await spontaneous labor and be allowed to progress to their (Note: This weighr dt:-:.-" ',:
expected date of delivery as long as antenatal testing remains reassuring to locally validate rl, e .,t'' ' . ,. ,

and the fetus is not macrosomic. make our own recolt't1:.'t'::"

o However, expectant management beyond the estimated due date generally Delivery should take ;
is not recommended because after 40 or more weeks, the benefits of neonatal intensive care
continued conservative management are likely to be outweighed by the
danger of fetal compromise. Induction of labor before 41 weeks gestation Diabetes mellitus shcu.;
in pregnant women with diabetes mellitus, regardless of the readiness of to attempting a ragr::. :
the cervix, is prudent.
(Level III, Grade C1

. ,,1,' I,.,lti'. 98
11,,
F'*.1,1

-:s post cesarean section vP to
fu-
ra:.:--usly when indicated (for
o Assessment of fetal lung maturity by means of amniocentesis in a diabetic
24 pregnancy is no longer required with delivery after 38 weeks. It is also not
indicated in well-controlled patients who have indications for induction of
levels labor or cesarean section as long as there is reasonable certainty about the
estimation of gestational age. (Level III, Grade C)

lr', Mode of Deliverv

o GDM is not itself an indication for cesarean delivery and that vaginal
delivery at term is possible if women have documented dating criteria and
lss.- --.rted with increased risk of adverse good glycemic control.
E :":cronic fetal surveillance may be o The risk of macrosomia, shoulder dystocia and fetal injury in labor is
increased 3-fold in diabetic pregnancy. These risks should be taken into
account when planning mode of delivery. (Level I, Grade A)
!r-: ---us electronic FHR monitoring
d, :pling should be available when o Using ultrasound EFW or abdominal circumference (AC) to make
decisions regardingtiming and route of delivery may be associated with a
lower rate of shoulder dystocia, but larger studies are needed to determine
E- : $'ith diet may Pose minimal risks
of a low-risk or
if this approach affects the rate of neonatal injury. (Level III, Grade C)
Q.,= :.cnitored like that
o If the EFW at the time of delivery is < 4000 g, vaginal delivery is usually
appropriate unless there are other obstetric indications for cesarean
section.
!ht : jn'idualized depending on whether
::l'a| and/ or fetal comPlications' Elective cesarean section should be considered if the fetus is suspected to
be significantly obese. If fetal weight is estimated to be 4500 g or more,
H '. of women with GDM before 38 the risks and benefits of cesarean delivery should be discussed with the
J- =;tive evidence
of maternal or fetal patient. The American Congress of Obstetricians and Gynecologists
l (ACOG) recommends offering cesarean delivery to diabetic patients if the
fetal weight is estimated to be 4500 g or more. (Level II-1, Grade B)
F ::red among diabetic Pregnancies, it
i&: - : :han 38 weeks gestation nor eadier When EFW is 4000-4500 g, consider past delivery history, clinical
rr: pelvimetry, ultrasound determined body to head disproportion (fetal AC
weeks ahead of biparietal diameter [BPD]) and progression of labor to
.:s mellitus and no comPlicating determine mode of delivery. (Level I, Grade A)
'6- allowed to progress to their (Note: This weight cuhoff ma! not be applicable in the local setting. The urgency
]&a: :nd be
testing remains reassuring to locally validate
the fetal weight-to-risk to dystocia patterns is at hand in order to
lE! ':tenatal make our own recommendations.)
I
Delivery should take place in a hospital with full obstetric, anesthetic and
I]: :nd the estimated due date generalll'
neonatal intensive care facilities. (Leuel III, Grade C)
;!n: j0 or more weeks, the benefits of
bY the
Fr,: : :re likely to be outweighed Diabetes mellitus should notin itself be considered a contraindication
&.u,,-: ,: of labor before 41 weeks gestation
to attemptingavaginal birth after a previous cesarean section (VBAC).
ls- :.litus, regardless of the readiness ol (Level III, Grade C)

99
nN,.s\,il|l$lo
 Special Circumstqnces
In such patients, NA-T a:
Pre-eclqmpsiq be continued to matnni:
o Management should be as for the nondiabetic popuration
with pre-
calories for lactation an.i
eclampsia.
o All types of insulin r
Preterm Labor and Deliver! breastfeeding women
o If preterm labor or delivery before 36 weeks is indicated, betamethasone
to promote fetal lung maturity shourd be administered Limited data suggesr rha:
if possibre. not appear to have harn::-
o Antenatal steroids adversely affect maternal glycemic control
and increase
to demonstrate its safer. :
insulin requirements. patients should be admined to the antenatal
unit;
intensive insulin therapy and frequent glucose monitoring are
prevent hyperglycemia.
required to o Because some cases oi Gl
2 diabetes mellirus. ri om:
o Tocolytic drugs are not contraindicated in diabetes mellitus but f3 for diabetes mellitus 6_.1
agonist criteria.
drugs should be avoided as they can cause severe insulin resistance (Levet I, Gr;.;; .:-
and
glucose intolerance.
Women with a histor,,. ::
Analgesia and Anesthesia development of diaheies :
o years.2 (Level lil, GrcJt C
Effective pain relief is important and all forms of pain relief used
in labor
can be administered.
Testing to detect rr.pe i ;
o Based on the narrativesystematic review thatpainlstress diabetes mellitus in as..::
following surgery in adults of any ag. ,* i_-
and trauma impairs insulin sensitivity by affecting nonoxidative gtulose
metabolism, it might he surmised that glucose regulation can be have one or more addiric:
improved without these risk facr:rs
with administration of analgesia in stressful states.
II-1, Grade B)
o If general aaesthesia is used in women with diabetes meflitus,
blood
glucose should be monitored regularly (every 30 minutes) If tests are normai, repea! :
from induction reasonable.2 (Lelel
of general anesthesia until after the baby is born and the woman III. G,-::
is fully
conscious.
To test for diabetes me1-::-
HbAlc, FPG, or 2 hour -_.
Postpartum Management - FPG 100-125 mg dL 5
(rFG) OR
. Status of Glacose Metabolism
- 2 hour plasma gluc:s;
mmol/L) ) Imparre:,
Post-delivert - lIbAlc 5.6-6.{c:
o Elevated values should be confirmed with fasting plasma glucose
(> 126
mg/dL or 7.0 mmol/L) or postprandiar grucose (> 200 mg/dL In those identified u ith i::r,
or il.1 and, if appropriate. rrc:.: --::
mmol/L).

'il',, '( ,tl *;i'l ''t 100

:,, f,,^ .
l
g
.l
t l: '"i:eks is indicated, betamethasone
l.,r :.3 administered if possible.
Jq'.:::ral glycemic control and increase
l.: :e admitted to the antenatal unit;
Fr-: iucose monitoring are required to
b:=: rn diabetes mellitus but f3 agonist
GL- :luse severe insulin resistance and
nc '-. lorms of pain relief used in labor
F, rhatpain/ stress following surgery
: .,,
li'lr:. rv affecting nonoxidative glucose
ft;: :lucose regulation canbe improved
ir '-::ssful states.
r * --::ren with diabetes mellitus, blood
k.-. revery 30 minutes) from induction
h ::bv is born and the woman is fullY
s; ',r ith fasting plasma glucose (> 126
p'::al glucose (> 200 mg/dL or 11'1
o In such patients, MNT and if necessary pharmacolo gical therapy, should
be continued to maintain good glycemic control and provide sufficient
calories for lactation and infant well-being.
o All rypes of insulin, glyburide, or glipizide can be safely used by
breastfeeding women.
o Limited data suggest that metformin, while excreted into breast milk, does
not appear to have harmful neonatal effects. Larger studies are still needed
to demonstrate its safety to the infant of breastfeeding women.
Po s tp ue rp er a I Re cla s s ifi ca t i o n
o Because some cases of GDM may represent preexisting undiagnosed type
2 diabetes mellitus, women with a history of GDM should be screened
for diabetes mellitus 6-12 weeks postpartum using nonpregnant OGTT
criteria. (Lettel I, Grade A)
o Women with a history of GDM should have lifelong screening for the
development of diabetes mellitus or prediabetes mellitus at least every 3
years.2 (Level III, Grade C)
o Testing to detect type 2 diabetes mellitus and assessing risk for future
diabetes mellitus in asymptomatic individuals should be considered
in adults of any age who are overweight (BMI > 25 kg/m2) and who
have one or more additional risk factors for diabetes mellitus. In those
without these risk factors, testing should begin at age 45 years. (Level
II-1, Grade B)
o If tests are normal, repeat testing carried out at least at 3-year intervals is
reasonable.2 (Level II\ Grade C)
o To test for diabetes mellitus or to assess risk of future diabetes mellitus,
HbAlc, FPG, or 2hour 75 g OGTT is appropriate (Levet II-2, Grade B)
- FPG 100-125 mg/dL(5.6-6.9 mmol/L): ) ImpairedFastingGlucose
(rFG) OR
- 2 hour plasma glucose in the 75 g OGTT 140-199 mg/dL (7.S-11.0
mmol/L) ) Impaired Glucose Tolerance (IGT) OR
- lIbAlc 5.6-6A%
o In those identified with increased risk for future diabetes mellitus, identify
and, if appropriate, treat other CVD risk factors.2 (Level II-2, Grade B)
t0r *q*ttiHl'
Long Term Prevention or Delay of Type ZDiabetes Mellitus for ContracePtive Use reP;
conffaindication to ILD Pres
. Patients with IGT (Level I, Grade A),IFG (Level III, Grade C), or an llbAlc of
5 .7 -6.4% (Level III, Grade C) should be referred to weight management
plogram :
increasing physical activity to
o Based on the available er':Je
targeting weight loss of 7oh of body weight and IUDs can be used saf-elr -'r:::
at least 150 minutes /week of moderate activity such as walking' prior GDM.
. Follow-up counselingappearc to be important for success' Combination Oral Contracelries (

. o Smoking and maternai ag: >

Metformin therapy for prevention of type 2 diabetes mellitus may be
considered in those at the highest risk for developing diabetes mellitus, such as o The metabolic eflects of a g:-.
those with multiple risk factors, especially if they demonstrate progression of effect of the rype and cr ;'-s
hyperglycemia (e.g. llbAlc > 6%) despite lifestyle modifications' (Level II'2, and maternal age.
Grade B)
o In healthy poPulations ::--
. Monitoring for the development of diabetes mellitus in those with prediabetes COC-users have not esI:i:-:s:
melitus should be performed every year. (Level III, Grade C) short term studies ha.'e :--;:
lipid metabolism.
. Breastfeeding
o The direct effect of breastfeeding per se on subsequent risk of diabetes o The majority of u omt:: '.q . -:
mellitus is not clear. Limited studies show lower rates of postpartum absolute risk of cardil.',.-s---
diabetes mellitus and fasting glucose levels in breastfeeding women with dose COC can be F\re:-:.::-
prior GDM and a protective effect with lower diabetes mellitus rates increase with age and ::-'-: ::
in healthy women who breastfed as well as among the oflsprings who factors in women lri:h ::--'-:
breastfed.
o The magnitude oi othe::..'.
o Pending clarification of these issues, all women, including those with hyperlipidemia. coag ':l..:: -- :
prior GDM, should be actively encouraged to exclusively breastfeed to the (presence of Leider, :3.--:l:
-,-

greatest extent possible during the first year of llfe. (Lertel III, Grade C) arterial and venous ::'-:: ::.: :
always be considered

. Contraception o When hypertensicn --: :-..::-

it would be most .a-:: -- *! : :
Barrier Methods (condoms, diaphragm, cervical cap, and spermicides)
o Barrier methods are well suited for women with prior GDM because of o In all cases. the 1c'.i-i:;-:-:
their lack of systemic side eflects or influence on glucose tolerance. prescribed and clcs: l::::.:- - :

and weight.
Intrauterine Device (WD)
o IUD is a very effective and reversible contraceptive method without o All women shoulc ::-:...:
metabolic disturbances and therefore is an ideal contraceptive for women exercise dail1'. achie"i .'. :..:
with prior GDM. therapy to control b.--:: ::
fail.
o The World Health Organizatron (WHO) Medical Eligibilify Criteria
. ./1'.,
.:" ' 102
I

p l--at'etes Mellitus for contraceptive use report does not

t consider prior GDM as a
r contraindication to IUD prescription.
F: -:.:.\il, Grade C), or an FIbAlc of
!,, -. : :c $ eight management program o Based on the available evidence, both copper and levonorgestrel-releasing
ire : ::.J increasing physical activify to
IUDs can be used safely without any specific restriction in women with
.:l
|t i*: such as walking. prior GDM.
I
....., for success.
lpt Combination O ral Contraceptives (C O Cs.)
b
o Smoking and maternal age > 35 years add risks to these events.
i'* . :t 2 diabetes mellitus maY be
F : =.cping diabetes mellitus, such as
=
.
o The metabolic effects of a given Coc formulation will depend on the net
fr-. ' :rer demonstrate progression of efrect of the type and/ or dosage of each hormonal component, smoking
and maternal age.
i
o In healthy populations, epidemiological studies in current or previous
bfr,, ,, :rellitus in those with prediabetes
i COC-users have not established an increased risk of diabetes mellitus and
F -,'.:: III, Grade C) short term studies have found no clinically relevant damaging effect on
I lipid metabolism.
of diabetes
! : '- .: on subsequent risk postpartum o The majority of women with prior GDM rikely fall in the category of low
3: ,, snorv lower rates of absolute risk of cardiovascular and venous thrombotic events and low-
F"i.: =.' ls in breastfeeding women with
e
dose coc can be prescribed taking into account that the absolute risks
p:- '::h lower diabetes mellitus rates increase with age and that periodic risk assessment of cardiovascular risk
! i ,i:il as among the offsPrings who factors in women with prior GDM should be done.
F

i o The magnitude of other risk factors, i.e. hypertension, migraine, smoking,

Lc-, , :il rvomen, including those with hyperlipidemia, coagulation disorders, and family history of thrombosis
;ts: -:,:ed to exclusively breastfeed to the (presence of Leiden factor v mutation), which increase the odds ratios for
L '',: '. ear of life. (Level III, Grade C) arterial and venous thrombotic events by 2- to r2-fold in coc users must
always be considered.

when hypertension or migraines are present in women with prior GDM,

I :=:rical cap, and spermicides)
ft: ,,.omen with prior GDM because
I c: -:fluence on glucose tolerance.
it would be most cautious not to prescribe a COC.
of
In all cases, the lowest ethinyl estradior with newer progestins should be
prescribed and close attention should be paid to increases in blood pressure
and weight.

n::;rble contraceptive method without All women should receive nutritional counsering, be encouraged to
S::e is an ideal contraceptive for women exercise daily, achieve a healthy weight, and receive appropriate medical
therapy to control blood pressure and/or lipids if lifestyle interventions
fail,
!rr: \\'TlO) Medical Eligibiliry Criteria

F:
103 *HsH*'
 o If estrogen-containris ::
Non-oral Combinatiom Hotmonal Methods would be the firsr-ch:::.-
o These products can be administered as a monthly injection or an
intravaginal ring. Surgical S teri li za ti o n
- not yet widely avallable locallY o An excellent choice :::
subsequent childbearir: :
Progestin-only Oral Contraceptives (POCS) those who deliver br' ,-:,,
o POCs are taken continuously and contain low-dose norethindrone,
levonorgestrel or desogestrel.
- Less epidemiological and clinical data available lnfants of Diabetic Mothers
- Less widely prescribed than COCs, largely because of their higher
actual failure rates and breakthrough bleeding rates. . Monitoring and ,nanagefient
- Well-suited for those with type 1 diabetes mellirus where estlogen- .,.

containing methods are contraindicated and for women with prior Blood sugar monitoring prortrc,:
GDM who often have several cardiovascular risk factors, making non-
estrogen-containing contraception favorable.
Testing:

Long Acting Progestins

o Check blood sugar \\ rli::.
and thereafter.
o Long acting progestins can be administered intramuscularly (IM)/ o Infant will need .1 s:a:i:
subcutaneously (SQ) or as an implant to deliver long-acting and eflicacious
sugar checks.
contraceptive, Protection.
Treatment:
o They offer the same metabolic advantage as POC with no effect on
maternal coagulation factors or blood pressure.
Blood sugar > 45 mgi dL ) :
required.
o Use of long-acting progestins in women with diabetes mellitus or If blood sugar 30-45 mg dL S:
sugar levels
women at high risk of diabetes mellitus is very limited.
. In an observational cohort of Hispanic women with prior GDM,
use of depot medroxyprogesterone (DMPA) was associated with 1. Breastfeeding
an increased risk of diabetes mellitus compared with women who
used COCs. 2. Formula feeding L,', :;:

o DMPA should be used with caution in breastfeeding women and those 3. Transfer to nurser', .:.:
with elevated triglyceride levels (> 150 mg/dl). infusion of D10\\' :.: -

o Close attention should be paid to weight gain, which also has been o If blood susar < l:
demonstrated to increase the risk of subsequent diabetes. D12.5 or the :.,--:
infusion of .,:. :-. .

o The Food and Drug Authority (FDA) cautions DMPA use for more fluid overlca:
than 2 years because of the associated decrease in bone mineral
density.

o Long-acting progestin methods are not a first-line choice in women

with prior GDM unless compliance with taking daily medication is a
problem.

104
 o If estrogen-containing contraceptives are contraindicated, the poc
hr-. would be the first-choice hormonal method or either type of IUD.
iL::=: as a monthlY injection or an
S argical S te ri lizati on
D o An excellent choice for women who are no longer desirous of
subseguent childbearing especially among parous women particularry
F those who deliver by cesarean section
rr: -ontain low-dose norethindrone,
,

ic.- :ata available lnfants of Diabetic Mothers

I C - -s. largely because of their higher
lk - -:.h bleeding rates. . Monitoring and ffiqnsgement of hypoglycemia after delivery
ffir - diabetes mellitus wherewith
estrogen-
n-: ::icated and for women Prior
Blood sugar monitoring protocol
l:::::.rvascular risk factors, making non-
Err: : tavorable.
Testing:
o Check blood sugar within 30 minutes of delivery, at l, 2 hours of life,
and thereafter.
k .*ninistered intramuscularly (IM)u o Infant will need 4 stable blood sugars prior to discontinuing brood
flr.--: :-. deliver long-acting and efficacious sugar checks.

Treatment:
I ::.lntage as POC with no effect on Blood sugar > 45 mg/dL ) normal x 4 (consecutively), no further testing
ti':,- : Pressure.
required.
If blood sugar 30-45 mg/ dL: step-by-step procedure is done to increase blood
r .: ,"omen with diabetes mellitus or sugar levels
r:=- itus is verY limited.
t:: --irspanic women with Prior GDM. l. Breastfeeding
!E::::one (DMPA) was associated with
ns -.:llitus compared with women who
2. Formula feeding by cup or dropper

s--- --: in breastfeeding women and those

3. Transfer to nursery intensive care unit (NICU) and give IV glucose
& > 150 mgldl). infusion of Dl0W at 4 ml/kg/ hr and repeatblood sugar in 30 min

ii :: ri-eight gain, which also has been o If blood sugar < 45 mg/ dL repeatedly ) consider switching to
n:,. --f subsequent diabetes. D12.5 or the placement of a central catheter (to allow for the
infusion of an elevated concentration of glucose) so as to avoid
q. : DA) cautions DMPA use for more fluid overload.
r :ssociated decrease in bone mineral

d: :re not a first-linechoice in women

D[:,:ce with taking daily medication is a
sl[tlt*||*ffit}'
r05
L _-
 APPENDIX

LEVELS OF EVIDENCE AND GRADES OF RECOMMENDATION

LEVEL DEFTMTION
I Evidence obtained from at least one properly randomized
controlled trial
II-1 Evidence obtained from well-designed controlled trials without
randomization
II-2 Evidence obtained from well-designed cohort or case-control
analytic studies, preferably from more than one center or research
group
II-3 Evidence obtained from multiple time series with or without the
intervention.
III Opinions of respected authorities, based on clinical experience;
descriptive studies and case reports or reports of expert
committees.

GRADE DEFINITION
A There is good evidence to support the recommendation of the
practice in diabetes mellitus in pregnancy
B There is fair evidence to support the recommendation of the
practice in diabetes mellitus in pregnancy
C There is insuflicient evidence to recommend for or against the
inclusion of the practice in diabetes mellitus in pregnancy
D There is fair evidence to support the recommendation that the
practice be excluded in diabetes mellitus in pregnancy
E There is good evidence to support the recommendation that the
practice be excluded in diabetes mellitus in pregnancy
GPP A good practice point (GPP) is a recommendation for best practice
based on the experience of the Technical Working Group.

106