This document discusses diabetes mellitus and its classification, signs, symptoms, causes, and management during pregnancy. It begins by defining diabetes and describing its four main categories. It then discusses gestational diabetes in detail, including its causes, significance, and effects on both mother and fetus. These effects include complications like macrosomia, birth defects, hypoglycemia, and others. Throughout, it provides information on managing diabetes during pregnancy to minimize risks through glycemic control and monitoring.

1. Dr Shail Kaur
Assist Prof
Dept of Obs & Gynae
PIMS

2. Diabetes
Derived from the verb diabainein, made up of the prefix dia, "across, apart," and the word bainein, "to walk, stand."
Diabetes is first recorded in English, in the form
diabete, in a medical text written around 1425.
A variable disorder of carbohydrate metabolism caused
by a combination of hereditary and environmental factors
and usually characterized by inadequate secretion or
utilization of insulin, by excessive urine production, by
excessive amounts of sugar in the blood and urine, and by
thirst, hunger, and loss of weight

3. American Diabetes Association (ADA)
classified the disease in four categories
 Type 1 diabetes: autoimmune destruction of the pancreatic β cells,
resulting in an inability to produce and secrets insulin.
 Type 2 diabetes: insulin resistance, a relative insulin deficiency as
well, or it may be both.
 Third category: gestational diabetes mellitus (GDM) is defined as
the onset or first recognition of diabetes during pregnancy.
 Fourth category: is associated with genetic disorders, pancreatic
diseases, drug and chemical use, and infections

4. Other causes of diabetes
 Genetic defects of β-cell function
 Maturity onset diabetes of the
young
 Mitochondrial DNA mutations
 Genetic defects in insulin
processing or insulin action
 Defects in proinsulin conversion
 Insulin gene mutations
 Insulin receptor mutations
 Exocrine pancreatic defects
 Chronic pancreatitis
 Pancreatectomy
 Pancreatic neoplasia
 Cystic fibrosis
 Hemochromatosis
 Fibrocalculous pancreatopathy
 Endocrinopathies
 Growth hormone excess
(acromegaly)
 Cushing syndrome
 Hyperthyroidism
 Pheochromocytoma
 Glucagonoma
 Infections
 Cytomegalovirus infection
 Coxsackievirus B
 Drugs
 Glucocorticoids
 Thyroid hormone
 β-adrenergic agonists
 Statins

5. Comparison of type 1 and 2
diabetes
Feature
Onset
Type 1 diabetes
Type 2 diabetes
Sudden
Gradual
Age at onset
Mostly in children
Mostly in adults
Body habitus
Thin or normal
Often obese
Ketoacidosis
Common
Rare
Usually present
Absent
Low or absent
Normal, decreased
or increased
Concordance
in identical twins
50%
90%
Prevalence
~10%
~90%
Autoantibodies
Endogenous insulin

7. Gestational diabetes
 Abnormal maternal glucose regulation occurs in 3-10%
of pregnancies
 Glucose intolerance of variable degree with onset or
first recognition during pregnancy, accounts for 90%
of cases of diabetes mellitus (DM) in pregnancy.
 Renal glycosuria(5-50%)
 diminished renal threshold due to increased glomerular
filtration and impaired tubular reabsorption
 Glycosuria even with blood sugar levels below 180mg/dl
 No treatment required

8. Gestational diabetes mellitus
(GDM)
 Any degree of glucose intolerance with onset or first
recognition during pregnancy
 Women with gestational diabetes have a 35-60%
chance of developing diabetes mellitus over 10-20 years
after pregnancy.
 Hyperglycemia in pregnancy results in both maternal
and fetal complications.

9. Significance
 GDM offers an important opportunity for the
development, testing and implementation of clinical
strategies for diabetes prevention.
 Timely action taken now in screening all pregnant
women for glucose intolerance, achieving euglycemia
in them and ensuring adequate nutrition may prevent
in all probability, the vicious cycle of transmitting
glucose intolerance from one generation to another

10. Maternal complications
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Abortions
Infections
Hypertension
Pre-ecclampsia
Polyhydramnios
Preterm delivery
Increased risk of prolonged labour, injuries,
PPH,cesarean delivery
 Puerperal sepsis, lactation failure
 Development of diabetes mellitus after pregnancy.

11. Fetal complications
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Macrosomia
Neonatal hypoglycemia
Polycythemia
Increased perinatal mortality
Congenital malformation
Hyperbilirubinemia
Respiratory distress
Hypocalcaemia
Long-term consequences of macrosomia include increased
risk of glucose intolerance, diabetes, and obesity in
childhood.

12. Birth defects
 CNS and skeletal
 Neural tube defects
 Anencephaly
 Microcephaly
 Caudal regression
syndrome
 Sacral agenesis
 CVS
 VSD,ASD
 COA
 TGA
 Situs inversus
 TOF
 Renal
 Renal agenesis
 Hydronephrosis
 Double ureter
 Polycystic kidneys
 GI
 Duodenal atresia
 Anorectal atresia
 Omphalocele
 TEF
 Others
 Single umbilical artery

13. Glycosylated Hb

14. Risk factors
 The Western style diet of high fat, high carbohydrate,
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and high sodium(a significant contributor to excessive
weight gain during pregnancy and, thus, a risk factor
for developing diabetes)
Obesity
Age greater than 25 years
prior history of gestational diabetes
first-degree relative with diabetes
history of poor obstetrical outcome
certain ethnic groups

15. Metabolism in Pregnancy
 Each meal sets in motion a complex series of hormonal actions,
including a rise in blood glucose and the secondary secretion of
pancreatic insulin, glucagon, somatomedins, and adrenal
catecholamines. These adjustments ensure that an ample, but not
excessive, supply of glucose is available to the mother and fetus.
 Compared with nonpregnant subjects, pregnant women tend to
develop hypoglycemia between meals and during sleep. This occurs
because the fetus continues to draw glucose across the placenta from
the maternal bloodstream, even during periods of fasting.
Interprandial hypoglycemia becomes increasingly marked as
pregnancy progresses and the glucose demand of the fetus increases.
 Levels of placental steroid and peptide hormones (eg, estrogens,
progesterone, and chorionic somatomammotropin) rise linearly
throughout the second and third trimesters. Because these hormones
confer increasing tissue insulin resistance as their levels rise, the
demand for increased insulin secretion with feeding escalates
progressively during pregnancy. By the third trimester, 24-hour mean
insulin levels are 50% higher than in the nonpregnant state.

16. Physiologic changes of late
pregnancy
 Human placental lactogen, which is structurally
similar to growth hormone, and tumor-necrosis
factor-alpha induce changes in the insulin receptor
and in post-receptor signaling.
 Changes in the beta-subunit of the insulin receptor,
decreased phosphorylation of tyrosine kinase on the
insulin receptor, and alterations in insulin receptor
substrate-1 (IRS-1) and the intracytoplasmic
phosphatidylinositol 3-kinase (PI3K) appear to be
involved in reducing glucose uptake in skeletal muscle
tissue.

18. Metabolism in Diabetes
 If the maternal pancreatic insulin response is inadequate, maternal
and, then, fetal hyperglycemia results. This typically manifests as
recurrent postprandial hyperglycemic episodes. These
postprandial episodes are the most significant source of the accelerated
growth exhibited by the fetus.
 During a healthy pregnancy, mean fasting blood sugar levels decline
progressively to a remarkably low value of 74 ± 2.7 (standard deviations
[SD]) mg/dL. However, peak postprandial blood sugar values rarely
exceed 120 mg/dL.
 Meticulous replication of the normal glycemic profile during
pregnancy has been demonstrated to reduce the macrosomia rate.
 when 2-hour postprandial glucose levels are maintained below 120
mg/dL, approximately 20% of fetuses demonstrate macrosomia.
 If postprandial levels range up to 160 mg/dL, macrosomia rates rise
to 35%.

20.  Surging maternal and fetal glucose levels are accompanied
by episodic fetal hyperinsulinemia.
 excess nutrient storage, resulting in macrosomia.
 conversion of excess glucose into fat causes depletion in fetal
oxygen levels.
 These episodes of fetal hypoxia are accompanied by surges
in adrenal catecholamines
 hypertension,
 cardiac remodeling and hypertrophy,
 stimulation of erythropoietin, red cell hyperplasia, and
increased hematocrit.
 Polycythemia (hematocrit >65%) occurs in 5-10% High
hematocrit values in the neonate
 vascular sludging,
 poor circulation, and
 postnatal hyperbilirubinemia.

21. Maternal morbidity
 Diabetic retinopathy
 leading cause of blindness in women aged 24-64 years.
 Some form of retinopathy is present in virtually 100% of
women who have had type 1 diabetes for 25 years or more.
 half the patients with preexisting retinopathy experienced
deterioration during pregnancy,
 all the patients had partial regression following delivery and
returned to their prepregnant state by 6 months postpartum.
Consider an ophthalmologic evaluation in the first
trimester.

24.  Renal disease
 patients with underlying nephropathy can expect varying
degrees of deterioration of renal function during a pregnancy.
 As renal blood flow and glomerular filtration rate increase 3050% during pregnancy, the degree of proteinuria will also
increase.
 does not measurably alter the time course of diabetic renal
disease, nor does it increase the likelihood of progression to
end-stage renal disease.
 related to duration of diabetes and degree of glycemic control.
 Perinatal complications are greatly increased
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Preterm birth,
intrauterine growth restriction
preeclampsia

26. Elevated blood pressure
 Chronic hypertension (1 in 10 diabetic pregnancies overall)
 Women with gestational diabetes are at a significantly higher risk
of developing hypertension after the index pregnancy.
 underlying renal or retinal vascular disease are at a substantially
higher risk, with 40% having chronic hypertension.
 Patients with chronic hypertension and diabetes are at increased
risk of intrauterine growth restriction, superimposed preeclampsia,
abruptio placentae, and maternal stroke.
 Preeclampsia is more frequent among women with diabetes
(approximately 12%) versus the nondiabetic population (8%).
 Also increases with maternal age
 Increases with duration of preexisting diabetes
 The rate of preeclampsia has been found to correlate with the level
of glycemic control

27. Fetal Morbidity
 Miscarriage
 pre-existing diabetes mellitus--9-14%
 Suboptimal glycemic control has been shown to double
the miscarriage rate
 Patients with long-standing (>10 y) and poorly
controlled diabetes (glycohemoglobin exceeding 11%)
have been shown to have a miscarriage rate of up to
44%.
 Conversely, excellent glycemic control normalizes the
miscarriage rate.

28. Birth defects
 In women with overt diabetes and suboptimal glycemic control
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before conception, the likelihood of a structural anomaly is
increased 4- to8-fold.
Two-thirds of birth anomalies involve the cardiovascular and central
nervous systems.
Neural tube defects occur 13-20 times more frequently in diabetic
pregnancies,
genitourinary, gastrointestinal, and skeletal anomalies are also more
common.
the rate of anomalies was only 3.4% with glycosylated hemoglobin
values (HbA1C) of less than 8.5%, versus 22.4% with poorer
glycemic control in the periconceptional period (HbA1C >8.5%).
Clinical trials of intensive metabolic care have demonstrated that
malformation rates similar to those in the nondiabetic population
can be achieved with meticulous preconceptional glycemic control.

29. Macrosomia
Birth weight above the 90th percentile for gestational
age or greater than 4kg. Macrosomia occurs in 15-45% of
babies born to diabetic women, a 3-fold increase
The priming of β-cell mass in early gestation may account
for the persistent fetal hyperinsulinemia throughout
pregnancy and the risk of accelerated growth, even
when the mother enjoys good metabolic control in later
pregnancy
the most significant influences being gestational age at
delivery, maternal prepregnancy body mass index
(BMI), maternal height, pregnancy weight gain, the
presence of hypertension, and cigarette smoking.

30. Macrosomia
 Excess nutrient delivery to the fetus causes macrosomia
and truncal fat deposition
 Fetal birth weight correlates best with second- and thirdtrimester postprandial blood sugar levels and not with
fasting or mean glucose levels.
 When postprandial glucose values average 120 mg/dL or less,
approximately 20% of infants can be expected to be
macrosomic.
 When postprandial levels range as high as 160 mg/dL,
macrosomia rates can reach 35%.
 Role for excessive fetal insulin levels in mediating accelerated
fetal growth.

31. Macrosomia
 unique pattern of overgrowth, central deposition of
subcutaneous fat in the abdominal and interscapular areas.
Skeletal growth is largely unaffected.
 Larger shoulder and extremity circumference, a decreased
head-to-shoulder ratio, significantly higher body fat, and
thicker upper extremity skin folds compared with
nondiabetic control infants of similar weights.
 positive relationship between severity of maternal fasting
hyperglycemia and risk of shoulder dystocia, with a 1 mmol
increase in fasting glucose leading to a 2.09 relative risk for
shoulder dystocia.

33. Growth restriction
 pregnancies in women with preexisting type 1
diabetes.
 The most important predictor of fetal growth
restriction is underlying maternal vascular disease.
 pregnant patients with diabetes-associated retinal or
renal vasculopathies and/or chronic hypertension are
most at risk for growth restriction.

34. Effects of growth

35. Perinatal mortality
 current perinatal mortality rates among women who
are diabetic remain approximately twice those
observed in the nondiabetic population.
 Congenital malformations, respiratory distress
syndrome (RDS), and extreme prematurity account for
most perinatal deaths in contemporary diabetic
pregnancies

36. Birth injury
 Injuries of birth, including shoulder dystocia and
brachial plexus trauma, are more common among
infants of diabetic mothers, and macrosomic fetuses
are at the highest risk.
 With strict glycemic control, the birth injury rate has
been shown to be only slightly higher than controls
(3.2 vs 2.5%).
 Currently, clinical ability to predict shoulder dystocia
is poor. Warning signs during labor (labor protraction,
suspected fetal macrosomia, need for operative vaginal
delivery) successfully predict only 30% of these events.

38. Polycythemia
 A central venous hemoglobin
concentration greater than 20 g/dL
or a hematocrit value greater than
65% (polycythemia).
 Hyperglycemia is a powerful
stimulus to fetal erythropoietin
production, mediated by decreased
fetal oxygen tension.
 Untreated neonatal polycythemia
may promote vascular sludging,
ischemia, and infarction of vital
tissues, including the kidneys and
central nervous system.

39. Postnatal hyperbilirubinemia
 Twice that in a healthy population
 Prematurity and polycythemia are the primary
contributing factors

40.  Neonatal
Hypocalcemia
 Up to 50% of infants of
diabetic mothers have
low levels of serum
calcium (< 7 mg/100
mL).
 functional
hypoparathyroidism
 Hypoglycemia
 Approximately 15-25% of
neonates delivered from
women with diabetes during
gestation develop
hypoglycemia during the
immediate newborn period.
 Neonatal hypoglycemia is less
frequent when tight glycemic
control is maintained during
pregnancy and in labor.
 Unrecognized postnatal
hypoglycemia may lead to
neonatal seizures, coma, and
brain damage.

41. Respiratory problems
 The nondiabetic fetus achieves pulmonary maturity at
a mean gestational age of 34-35 weeks. By 37 weeks'
gestation, more than 99% of healthy newborn infants
have mature lung profiles as assessed by phospholipid
assays.
 However, in a diabetic pregnancy, the risk of
respiratory distress may not pass until after 38.5
gestational weeks.
 Until recently, neonatal respiratory distress syndrome
was the most common and serious morbidity in
infants of diabetic mothers

42. Obesity
 Excessive body fat stores, stimulated by excessive glucose
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delivery
Maternal obesity, common in type 2 diabetes, appears to
significantly accelerate the risk of infants being LGA.
Approximately 30% of fetuses of women with diabetes mellitus
in pregnancy are large for gestational age (LGA).
In preexisting diabetes mellitus, this incidence appears to be
slightly higher (38%).
growth velocity of the abdominal circumference is often well
above the growth percentiles seen in nondiabetic fetuses, and it
is higher than the fetal head and femur percentiles.
The growth of the abdominal circumference begins to rise
significantly above normal after 24 weeks.

43. Metabolic syndrome
 By age 10-16 years, offspring of diabetic pregnancy have
a 19.3% rate of impaired glucose intolerance
 The childhood metabolic syndrome
 childhood obesity,
 hypertension,
 dyslipidemia, and
 glucose intolerance.

44.  Cardiovascular risk factors
 higher levels of biomarkers for endothelial damage and
inflammation, higher leptin levels, BMI, waist
circumference, and systolic blood pressure and
decreased adiponectin levels. The association remained
significant when controlling for maternal prepregnancy
BMI.
 Neurocognitive development
 maternal GDM and low socioeconomic status were
associated with an increased risk for attentiondeficit/hyperactivity disorder (ADHD) at age 6
 children exposed to both GDM and low socioeconomic
status were at even greater risk for ADHD and also at
increased risk for compromised neurobehavioral
functioning

45. Preconceptional counselling
 Provide information, advice and support that will help to
reduce the risks of adverse pregnancy outcomes for mother
and baby.
 It is important to explain that risks can be reduced but not
eliminated.
 The importance of avoiding unplanned pregnancy should
be an essential component of diabetes education from
adolescence for women with diabetes.
 Lifestyle modification
 Diet
 Strict glycemic control
 Folic acid

46. Pre-conceptional counselling
NICE Guidelines
Women with diabetes who are planning to become pregnant
and their families should be offered information about how
diabetes affects pregnancy and how pregnancy affects
diabetes.
 The information should cover:
• the role of diet, body weight and exercise
• the risks of hypoglycaemia and hypoglycaemia
unawareness during pregnancy
• how nausea and vomiting in pregnancy can affect
glycaemic control
• the increased risk of having a baby who is large for
gestational age, which increases the likelihood of birth
trauma, induction of labour and caesarean section

47. Pre-conceptional counselling
• the need for assessment of diabetic retinopathy before
and during pregnancy
• the need for assessment of diabetic nephropathy before
pregnancy
• the importance of maternal glycaemic control during
labour and birth and early feeding of the baby in order to
reduce the risk of neonatal hypoglycaemia
• the possibility of transient morbidity in the baby during
the neonatal period, which may require admission to the
neonatal unit
• the risk of the baby developing obesity and/or diabetes in
later life.

48. Safety of medications for diabetes
before and during pregnancy
 Women with diabetes may be advised to use metformin as
an adjunct or alternative to insulin in the pre-conception
period and during pregnancy, when the likely benefits from
improved glycaemic control outweigh the potential for
harm.
 All other oral hypoglycaemic agents should be
discontinued before pregnancy and insulin substituted.
 Rapid-acting insulin analogues (aspart and lispro) are safe
to use during pregnancy.
 insufficient evidence about the use of long-acting insulin
analogues during pregnancy. Therefore isophane insulin
(NPH insulin) remains the first choice for long-acting
insulin during pregnancy.

49. First-Trimester Laboratory Testing
 more intensive use of studies that are part of normal
prenatal care (eg, ultrasonography).
 HbA1C,
 blood urea nitrogen, serum creatinine,
 thyroid-stimulating hormone, and free thyroxine levels
 spot urine protein-to-creatinine ratio
 capillary blood sugar levels 4-7 times daily.

50. Second-Trimester Laboratory
Testing
 A repeat spot urine protein-to-creatinine study in women with elevated
value in first trimester, a repeat HbA1C, and capillary blood sugar levels
4-7 times daily.
 If preeclampsia is suggested, order the following tests:
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24-hour urine collection
Blood urea nitrogen and serum creatinine
Liver function tests
Uric acid
Complete blood cell count
 Assessment of fetal well-being
 nonstress test,
 amniotic fluid index,
 fetal growth and
 Doppler ultrasonographic examination of the umbilical cord and
middle cerebral artery

51. Screening
 All pregnant women need to be screened for
gestational diabetes.
 Pregnant women with no known history of diabetes
are screened at 24-28 weeks gestation.
 Women at high risk for GDM are screened at the first
prenatal visit.
 oGTT is the test of choice in both groups.

52. Risk factors for GDM
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Increased weight (ie, BMI greater than or equal to 25)
Decreased physical activity
First degree relative with diabetes
Member of ethnic group with high prevalence of diabetes (African
American, Latino, Native American, Asian American, Pacific Islander)
Prior history of GDM or delivery of a baby greater than 4kg
Metabolic abnormalities - Hypertension, HDL less than 35
mg/dL, triglyceride level greater than 250 mg/dL
Polycystic ovarian syndrome
HbA1C 5.7% or higher
Impaired glucose tolerance or impaired fasting glucose testing in the
past
Evidence of insulin resistance (acanthosis nigricans or severe obesity)
History of cardiovascular disease

53. Effect of race
 Prevalence rates are higher in black, Hispanic, Native
American, and Asian women than in white women.
 In these high-risk populations,
 the recurrence risk with future pregnancies -68%.
 one-third will develop overt diabetes mellitus within 5
years of delivery, with higher-risk ethnicities having
risks nearing 50%.
 Race also influences many complications of diabetes
mellitus in pregnancy

54. Patient Education & Consent
 Reasons for screening
 Process of the OGTT test.
 Discussion of the ramifications of an abnormal test
 Aware that in the event of an abnormal test, treatment
needs to begin immediately, whether that entails
dietary modifications, oral hypoglycemic agents, or
insulin.

55. 100-g OGTT
 carbohydrate loading for 3 days preceding the test
(>150 g carbohydrates)
 overnight fast of 8–14 hours the night before. remain
seated during the test, and should not smoke.
 fasting plasma glucose >95mg/dL
 1-hr plasma glucose >180 mg/dL
 2-hr plasma glucose >155 mg/dL
 3-hr plasma glucose >140 mg/dL

56. Diabetes
 The standard criteria for the diagnosis of diabetes is as
follows:
 HbA1c of 6.5% or higher
 Fasting plasma glucose of 126 mg/dL or higher
 2-h plasma glucose of 200 mg/dL or higher during an 75-
g OGTT
 A symptomatic patient with random plasma glucose of
200 or higher (all plasma glucose values are recorded as
mg/dL).
 The pregnant women who meet the above criteria are
considered to have overt type 2 diabetes mellitus.

57. ACOG recommendation
 Screening for GDM at initial prenatal visit
 History
 Risk factors
 50 gram/1-hour OGTT. (> 140 mg/dl)
 The diagnosis of GDM continues to be based on the 100
gram/3-hour tolerance test
 Fasting less than 95mg/dL,
 1-hr less than 180 mg/dl,
 2-hr less than 155 mg/dL, and
 3-hr less than 140 mg/dL,
 with 2 or more abnormal values to confirm diagnosis.

58. Monitoring and Follow up
 In the event of an abnormal OGTT
 counselled on gestational diabetes mellitus
 nutritional counselling.
 Glycaemic control is less than ideal, medication should
be initiated.
 Following delivery,
 screened for persistent diabetes 6-12 weeks postpartum
 lifelong screening for prediabetes or diabetes
development every 3 years.

59. Ultrasonography
 In the first trimester,
 pregnancy dating and viability
 nuchal translucency if the fetus is at high risk for cardiac defects
(eg, because of high maternal glycohemoglobin)
 In the second trimester,
 detailed anatomy ultrasonogram at 18-20 weeks,
 fetal echocardiogram if the maternal glycohemoglobin value was
elevated in the first trimester.
 In the third trimester,
 growth ultrasonogram to assess fetal size every 4-6 weeks from 26 to
36 weeks in women with overt preexisting diabetes.
 growth ultrasonogram for fetal size at least once at 36-37 weeks for
women with gestational diabetes mellitus.
 more frequently if macrosomia is suggested.

60. White classification
 Gestational diabetes (type A)
 Class A1: gestational diabetes; diet controlled
 Class A2: gestational diabetes; medication controlled
 Pregestational diabetes
 Class B: onset at age 20 or older or with duration of less than 10
years
 Class C: onset at age 10-19 or duration of 10–19 years
 Class D: onset before age 10 or duration greater than 20 years
 Class E: overt diabetes mellitus with calcified pelvic vessels
 Class F: diabetic nephropathy
 Class R: proliferative retinopathy
 Class RF: retinopathy and nephropathy
 Class H: ischemic heart disease
 Class T: prior kidney transplant

61. Diet recommendations
 3 small meals and 2-3
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small snacks
Less carbs at breakfast
Choose foods high in
fiber
Choose foods with less
sugar and fat
Drink 8 cups of liquid
per day
Get enough vitamins and
minerals

62. Recommendations
 Calorie restriction according to BMI
 6 servings
 Not more than 50% carbohydrate
 Complex carbohydrate and cellulose
 Remaining equal portions protein and fat

63. Precautions to be taken if on insulin
 Be aware of the risk of hypoglycemia, and take a high-sugar snack
 It may be necessary to eat small snacks between meals.
 If exercise right after a meal, have a snack after the exercise.
 If exercise two hours or more after a meal, eat the snack before the
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exercise.
One serving of fruit will maintain blood sugar for most shortterm activities (about 30 minutes).
One serving of fruit plus a serving of starch will be enough for
activities that last longer (an hour or more).
Don't reduce insulin intake before exercising.
Don't inject insulin into a part of the body that will be exercised; for
example, if walking, avoid injecting into the leg.

64. SINGS AND SYMPTOMS OF GDM
Hypoglycemia (Low Blood Sugar)
CAUSES:
ONSET:
Too little food, too much insulin or diabetes medicine, or extra
exercise.
Sudden, may progress to insulin shock.
BLOOD SUGAR:
Below 70 mg/dL. Normal range: 70-115 mg/dL
WHAT TO DO?
Drink a cup of orange juice or milk or eat several hard candies
Test Blood sugar
Within 30 minutes after symptoms go away, eat a snack e.g.
sandwich, and a glass of milk
Contact doctor if symptoms don’t stop

65. Care of feet
 Check feet every day. for red spots, cuts, swelling, and blisters.
 coverage for special shoes.
 Wash feet every day. Dry them carefully, especially between the toes.
 Keep skin soft and smooth. Rub a thin coat of skin lotion over the tops
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and bottoms of feet, but not between toes.
Trim toenails straight across and file the edges with an emery board or
nail file.
Wear shoes and socks at all times. Never walk barefoot.
Protect feet from hot and cold.
Keeps the blood flowing to feet. Put feet up when sitting. Wiggle your
toes and move ankles up and down for 5 minutes, two (2) or three (3)
times a day. Don't cross legs for long periods of time. Don't smoke.

66. Indications for hospitalization
 Persistant nausea and vomiting
 Significant maternal infection
 DKA
 Poor control/compliance
 Preterm labour

67. Intra-partum management
 Absolute requirements
 Dextrose containing iv fluids
 Insulin
 Hourly glucose monitoring
 Continuous fetal heart rate monitoring
 Continuous tocodynametry
 Manage labour as normal

68. APA Insulin drip protocol
 Iv fluid mainline:d5w@125cc/hr
 Insulin drip
 Check RBS every hour
 Mix 100U regular insulin in 500cc NS(0.2U/cc)
RBS
Drip rate cc/hr
U/hour
<80
Off
0
80-100
2.5
0.5
101-140
5.0
1.0
141-180
7.5
1.5
181-220
10
2.0
>220
12.5
2.5

69. Care of the neonate
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Hypoglycemia in the newborn less than 35 mg/dL in the term infant. it is
more common in infants of women with pregestational diabetes
The newborn must be carefully monitored for at least the first 2 hours
after birth.
Early feeding and intravenous glucose are therapies commonly used,
depending on blood glucose level and symptoms.
Infant must monitored for hypocalcaemia, hypomagnesaemia,
polycythemia and hyperbilirubinemia, polycythemia, and more
common in women with pregestational diabetes, and a team approach to
monitoring and caring for these infants should be in place.
The most common newborn complication after birth is hypoglycemia
which, if uncorrected, may result in seizures.

70. Post-partum health education


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Women with pregestational diabetes should continue to be
managed by a physician goal of continued glycemic
control, determination of postpartum recovery status, and
recommendation of family planning methods.
Because of evidence that the incidence of childhood diabetes
is lower among those who were breastfed, breastfeeding
should be encouraged and supported
Breastfeeding may also promote improved glycemic and
lipid profiles in women with diabetes
Provision of an appropriate and effective contraceptive is
the first step in preconception care for a next