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 cells,resulting in an inability to produce and secrets
insulin. Type 2 diabetes: insulin resistance, a relative insulin
deficiency aswell, or it may be both. Third category: gestational
diabetes mellitus (GDM) is defined asthe onset or first recognition
of diabetes during pregnancy. Fourth category: is associated with
genetic disorders, pancreaticdiseases, drug and chemical use, and
infections
4. Other causes of diabetes Genetic defects of -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 -adrenergic
agonists Statins
5. Comparison of type 1 and 2 diabetes FeatureOnsetType 1
diabetesType 2 diabetesSuddenGradualAge at onsetMostly in
childrenMostly in adultsBody habitusThin or normalOften
obeseKetoacidosisCommonRareUsually presentAbsentLow or
absentNormal, decreased or increasedConcordance in identical
twins50%90%Prevalence~10%~90%Autoantibodies Endogenous insulin
6. 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
glomerularfiltration and impaired tubular reabsorption Glycosuria
even with blood sugar levels below 180mg/dl No treatment
required
7. Gestational diabetes mellitus (GDM) Any degree of glucose
intolerance with onset or firstrecognition 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.
8. Significance GDM offers an important opportunity for
thedevelopment, 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
9. Maternal complications 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.
10. Fetal complications 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.
11. 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
12. Glycosylated Hb
13. Risk factors The Western style diet of high fat, high
carbohydrate, 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
14. 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.
15. Physiologic changes of late pregnancy Human placental
lactogen, which is structurallysimilar 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.
16. Metabolism in Diabetes If the maternal pancreatic insulin
response is inadequate, maternaland, 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%.
17. Surging maternal and fetal glucose levels are accompaniedby
episodic fetal hyperinsulinemia. excess nutrient storage, resulting
in macrosomia. conversion of excess glucose into fat causes
depletion in fetaloxygen levels. These episodes of fetal hypoxia
are accompanied by surgesin adrenal catecholamines hypertension,
cardiac remodeling and hypertrophy, stimulation of erythropoietin,
red cell hyperplasia, andincreased hematocrit. Polycythemia
(hematocrit >65%) occurs in 5-10% Highhematocrit values in the
neonate vascular sludging, poor circulation, and postnatal
hyperbilirubinemia.
18. 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.
19. 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 Preterm birth, intrauterine growth
restriction preeclampsia
20. 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 levelof
glycemic control
21. 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.
22. Birth defects In women with overt diabetes and suboptimal
glycemic control 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.
23. 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
-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.
24. Macrosomia Excess nutrient delivery to the fetus causes
macrosomiaand 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.
25. Macrosomia unique pattern of overgrowth, central deposition
ofsubcutaneous 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.
26. Growth restriction pregnancies in women with preexisting
type 1diabetes. 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.
27. Effects of growth
28. Perinatal mortality current perinatal mortality rates among
women whoare 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
29. Birth injury Injuries of birth, including shoulder dystocia
andbrachial 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.
30. Polycythemia A central venous hemoglobinconcentration
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.
31. Postnatal hyperbilirubinemia Twice that in a healthy
population Prematurity and polycythemia are the primarycontributing
factors
32. NeonatalHypocalcemia Up to 50% of infants ofdiabetic
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.
33. Respiratory problems The nondiabetic fetus achieves
pulmonary maturity ata 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
34. Obesity Excessive body fat stores, stimulated by excessive
glucose 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.
35. Metabolic syndrome By age 10-16 years, offspring of
diabetic pregnancy havea 19.3% rate of impaired glucose intolerance
The childhood metabolic syndrome childhood obesity, hypertension,
dyslipidemia, and glucose intolerance.
36. 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
37. Preconceptional counselling Provide information, advice and
support that will help toreduce 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
38. 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
39. 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.
40. Safety of medications for diabetes before and during
pregnancy Women with diabetes may be advised to use metformin asan
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.
41. First-Trimester Laboratory Testing more intensive use of
studies that are part of normalprenatal 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.
42. Second-Trimester Laboratory Testing A repeat spot urine
protein-to-creatinine study in women with elevatedvalue in first
trimester, a repeat HbA1C, and capillary blood sugar levels 4-7
times daily. If preeclampsia is suggested, order the following
tests: 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
43. Screening All pregnant women need to be screened
forgestational 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.
44. Risk factors for GDM 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
45. Effect of race Prevalence rates are higher in black,
Hispanic, NativeAmerican, 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 5years of delivery, with higher-risk ethnicities having
risks nearing 50%. Race also influences many complications of
diabetesmellitus in pregnancy
46. 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,
treatmentneeds to begin immediately, whether that entails dietary
modifications, oral hypoglycemic agents, or insulin.
47. 100-g OGTT carbohydrate loading for 3 days preceding the
test(>150 g carbohydrates) overnight fast of 814 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
48. Diabetes The standard criteria for the diagnosis of
diabetes is asfollows: 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
areconsidered to have overt type 2 diabetes mellitus.
49. 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 100gram/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.
50. 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.
51. 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.
52. 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 1019 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
53. Diet recommendations 3 small meals and 2-3 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
54. Recommendations Calorie restriction according to BMI 6
servings Not more than 50% carbohydrate Complex carbohydrate and
cellulose Remaining equal portions protein and fat
55. 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 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.
56. 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/dLWHAT 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
dont stop
57. 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 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.
58. Indications for hospitalization Persistant nausea and
vomiting Significant maternal infection DKA Poor control/compliance
Preterm labour
59. Intra-partum management Absolute requirements Dextrose
containing iv fluids Insulin Hourly glucose monitoring Continuous
fetal heart rate monitoring Continuous tocodynametry Manage labour
as normal
60. 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) RBSDrip rate cc/hrU/hour22012.52.5
61. Care of the neonate 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.
62. Post-partum health education 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