DIABETES AND

PREGNANCY
NCM 108
FRITZIE NECITAS A. DURAN, RN
LECTURER
 The Pancreas
• The pancreas is a unique organ in that it has both endocrine
(ductless) and exocrine (with duct) types of tissue. The islets
of Langerhans form the endocrine portion, alpha islet cells
have the responsibility to secrete glucagon, and beta islet cells
secrete insulin. Insulin is essential for carbohydrate
metabolism and is also important in the metabolism of both
fats and protein. It is formed from amino acids at a rate
between 35 and 50 units per day in adults and proportionately
less in children. When serum glucose that passes through the
pancreas exceeds 100 mg/dl, beta cells immediately begin
insulin production. When serum glucose levels are low,
production decreases. Insulin production is also stimulated by
gastrin, a gastrointestinal hormone that rises when the
stomach is full as well as the levels of glucagon, cortisol, GH,
progesterone, and estrogen. Increasing levels of epinephrine
or norepinephrine inhibit the secretion of insulin in order to
preserve glucose for “flight or fight.”
• Glucose, is one of the body’s preferred sources of fuel in the form of
carbohydrates. When we eat, our body immediately starts working to process
glucose.
 Insulin
• A hormone produced by the beta cells of the islets of
Langerhans. It regulates the metabolism of
carbohydrates, fats and protein by promoting the
absorption of glucose from the blood into liver, fat and
skeletal muscle cells. in these tissues, the absorbed
glucose is converted into either glycogen via
glycogenesis or fats via lipogenesis. Beta cells are
sensitive to blood sugar levels so that they secrete
insulin into the blood in response to high level of
glucose in response to high level of glucose and inhibit
secretion of insulin when glucose levels are low. Insulin
enhances glucose uptake and metabolism in the cells,
thereby reducing blood sugar level. Their neighboring
alpha cells, by taking their cues from the beta cells,
secrete glucagon into the blood in the opposite manner:
increased secretion when blood glucose is low, and
decreased secretion when glucose concentration are
high. Glucagon increases blood glucose by stimulating
glycogenesis and gluconeogenesis in the liver. The
secretion of insulin and glucagon into the blood in
response to the blood glucose concentration is the
primary mechanism of glucose homeostasis.
Glucose Homeostasis
• The human body uses glucose as energy. It is vital for the human
body to maintain adequate levels of glucose in blood streams--but
also to ensure there is not too much glucose, which could likewise be
dangerous. When glucose levels reach high levels, the pancreas acts
by releasing insulin, a hormone, to effectively lower glucose to a
healthy level. The liver acts and converts glycogen to glucose through
the hormone glucagon (also via the pancreas) in the event of there
being too little glucose in blood. This diagram depicts this process of
Homeostasis in the manifestation of regulation of glucose levels in the
blood. This regulation ensures healthy levels of glucose in blood,
essential to the health of the human body. 
 
• The primary concern for any woman with this disorder is controlling the
balance between insulin and blood glucose levels to prevent hyperglycemia or
hypoglycemia. Both of these conditions are dangerous during pregnancy not
only because of long-term effects on the woman’s health but also because of the
threat to normal fetal growth. Infants of women with unregulated diabetes are
five times more apt to be born large for gestational age or with birth anomalies.
• If a woman’s insulin production is insufficient, glucose cannot be used by body
cells. The cells register the need for glucose, and the liver quickly converts
stored glycogen to glucose to increase the serum glucose level. Because insulin
is still not available, however, the body cells still cannot use the glucose, so the
serum glucose levels rise (i.e., hyperglycemia). When the level of blood glucose
reaches 150 mg/100 ml (normal level is 80 to 120 mg/dl), the kidneys begin to
excrete quantities of glucose in the urine (i.e., glycosuria) in an attempt to lower
the level. This causes large quantities of fluid to be excreted with urine (i.e.,
polyuria).
• As dehydration begins to occur, the blood serum becomes concentrated and
the total blood volume decreases. With the reduced blood flow, cells do not
receive adequate oxygen, and anaerobic metabolic reactions cause large stores
of lactic acid to pour out of muscles into the bloodstream. To replace needed
glucose, fat is mobilized from fat stores and metabolized for energy, pouring
large amounts of acidic ketone bodies into the bloodstream.

• As the process continues, protein stores are tapped in a final attempt to find a
source of energy. Utilizing protein for energy this way reduces the supply of
protein to body cells. As cells die, they release potassium and sodium, which
is lost from the body in the extensive polyuria. These factors combined create
an immediate severe metabolic acidosis. Long-term effects are vascular
narrowing that leads to kidney, heart, and retinal dysfunction.
 Pregestational Diabetes

• Pregestational diabetes includes patients

with Type 1 and Type 2 diabetes diagnosed
prior to pregnancy.
CLASS
Type 1
Type 2
Type 3 Gestational
diabetes
Classification of Diabetes Mellitus
Type 4 impaired
glucose
Homeostasis(diabetes
secondary to another
condition such as pancreatic
disease, hormonal
imbalance or drug
therapy(corticosteroid use)
DESCRIPTION
A state characterized by the destruction of the beta cells in the pancreas
that usually leads to absolute insulin deficiency.
a. Immune-mediated diabetes mellitus results from autoimmune
destruction of the beta cells.
b. Idiopathic type 1 refers to forms that have no known cause.
A state that usually arises because of insulin resistance combined with
a relative deficiency in the production of insulin.
A condition of abnormal glucose metabolism that arises during
pregnancy.
Possible signal of an increased risk for type 2 diabetes later in life.
A state between “normal” and “diabetes” in which the body is no
longer using and/or secreting insulin properly.
A. Impaired fasting glucose: a state when fasting plasma glucose is at
least 110 but under 126 mg/dl
B. Impaired glucose tolerance: a state when results of the oral glucose
tolerance test are at least 140 but under 200 mg/dl in the 1-hour
sample
 Type 1 Diabetes(insulin-dependent or IDDM)
• In Type 1 diabetes mellitus, there is absolute insulin deficiency related to a
cellular-mediated autoimmune destruction of the islet cells. It is a chronic
autoimmune disorder of the pancreatic islet cells that develops in
individuals who carry a genetic marker that has been identified on
chromosomes 6 and 11 and possible 10 other genes. Viral-induced, immune-
stimulated antibodies against the beta cell form. This autoimmune response
causes gradual destruction of the pancreatic beta cells.
• Juvenile onset diabetes-onset usually occur in youth(but may occur in
adulthood)
 Type 2 Diabetes(non-insulin or NIDDM)
• In Type 2 diabetes mellitus, there is insulin resistance because receptor sites at the
tissue level are not responsive to insulin. It takes more insulin to shut off the release
of glucose from the liver. People with type 2 diabetes do not carry a genetic marker,
but rather have a genetic susceptibility. Insulin resistance and pancreatic islet cell
dysfunction characterizes type 2 diabetes. When insulin resistance occurs, there is
increased insulin secretions but ineffective insulin post-receptor binding. Thus
glucose uptake by cells is decreased and hyperglycemia results.
• Maturity-onset diabetes or adult-onset diabetes. May be controlled with diet and
oral hypoglycemics or insulin; client less apt to have ketosis, except in presence of
infection. May be further classified as obese type 2 or non-obese type 2
 During Labor
• Insulin requirements: decrease related to workload
of labor and increased metabolism.
• Blood glucose alterations: hypoglycemia,
acidemia from starvation ketosis.
• Complicating factors: usually nothing by mouth
pending cesarean delivery.
 Post partum period

• Insulin requirements: decrease markedly

related to loss of placental hormones.
• Blood glucose alterations: hypoglycemia
• Complicating factors: lactation lowers insulin;
can initially complicated because supply is
established and scheduled.
 Diagnostic Testing
• Diabetes Mellitus (Type 1 and Type 2)
1. Fasting plasma glucose 126 mg/dl or greater after at
least an 8-hour fast
2. 2-hour post prandial glucose greater than 200 mg/dl
after a 75-g glucose overload
3. Symptoms of diabetes such as polyuria, polydipsia and
unexplained weight loss plus casual plasma glucose
concentration greater than 200 mg/dl
 Gestational Diabetes Mellitus

• GDM is defined as carbohydrate intolerance of variable severity

with onset or first recognition during pregnancy, particularly in
the 3rd trimester. The pancreatic beta-cell functions are impaired
in response to the increased stimulation and induced insulin
resistance. This is frequently related to chronic insulin
resistance that occurs more commonly in obese patients.
 Risk factors for developing Gestational Diabetes

• Obesity
• Age over 25 years
• History of large babies (10 lb or more)
• History of unexplained fetal or perinatal loss
• History of congenital anomalies in previous pregnancies
• History of polycystic ovary syndrome
• Family history of diabetes (one close relative or two distant ones)
• Member of a population with a high risk for diabetes (Native
American,
 Signs and symptoms

• Signs of GDM in the current pregnancy are as follows:

1. Recurrent monilial vaginitis
2. Macrosomia of the fetus on ultrasound
3. Polyhydramnios
• Signs of GDM in a previous pregnancy are as follows:
1. Prior delivery of an infant weighing more than 9 lbs
2. Previous stillbirth or an infant with congenital defects
3. History of polyhydramnios
4. History of recurrent monilial vaginitis
 Maternal Effects
1. Spontaneous abortion
2. Preeclampsia
3. Preterm labor
4. Polyhydramnios
5. Infection
6. Diabetic ketoacidosis
7. Cesarean or instrumental birth and induction
8. Retinopathy
9. hypoglycemia
1. Hypoglycemia
2.
a)
Hyperglycemia
Congenital defects
Fetal and neonatal effects
b) Macrosomia
c) Intrauterine growth restriction
d) Intrauterine fetal death
e) Ketoacidosis
f) Delayed lung maturity
g) Neonatal hypoglycemia
h) Neonatal hyperbilirubinemia
i) Neonatal polycythemia
j) Learning disabilities
k) Childhood obesity and type 2 diabetes later in life
 Diabetic Ketoacidosis
• DKA is caused by ineffective insulin combined with an elevation of counter-
regulatory hormones such as glucagon, catecholamines, cortisol and growth
hormones to move glucose into cells, leading to hyperglycemia. The liver tries to
compensate by increasing its production of glucose, only to further raise blood
glucose levels. The lack of glucose for cell use causes the body to break down fat
energy, which results in ketone release (ketosis). The respiratory system attempts to
compensate by increasing the respiratory rate and depth( Kussmaul respiration),
blowing off carbon dioxide. A decline in Ph (less than 7.4), a drop in serum
bicarbonate(less than 15 mg/dl), and an abnormal elevated anion gap( greater than
12) results.
• When the woman’s buffering system is unable to compensate, metabolic acidosis
develops. The excessive glucose and ketone bodies result in osmotic diuresis and
ketonuria with subsequent fluid and electrolyte loss, volume depletion and cellular
dehydration.
 Signs and symptoms of ketoacidosis:
• Hyperventilation or Kussmaul respirations
• Mental lethargy
• Dehydration
• Hypotension unless complicated by pregnancy-induced hypertension
• Abdominal pain; nausea and vomiting
• Fruity odor to the breath
• ketonuria
 Diagnostic Testing

• Gestational Diabetes. It is current practice to screen all patient for GDM

between 24 and 28 weeks.
1. Two-step approach: Glucose Challenge Test
The most common screening method. A glucose test is performed by initially
giving 50 g of oral glucose and 1 hour later testing the blood sugar. A blood
sugar of 139 mg/dl rules out GDM. A blood sugar level of 130-199 mg/dl should
be followed up with an oral glucose tolerance test (OGTT) to confirm GDM. If
the patient has a blood sugar level of 200 mg/dl or greater, treat as a
gestational diabetic without further testing.
2. One-step approach: Oral Glucose Tolerance Test
 An OGTT is performed without prior glucose challenge test to screen for GDM.
 Glycosylated Hemoglobin

• Hemoglobin A is normal minor hemoglobin that has a glucose link. Glucose attaches
to this hemoglobin during its normal 120-day life span. The amount depends on the
glucose in the bloodstream. Glycosylated hemoglobin ( Hb A1c) is a blood test to
determine the level of hemoglobin A that has become “sugar coated”. Therefore the
test reflects adequacy of glucose control for the previous 4 to 6 weeks. Hb A1c
levels above 6% indicates elevated glucose during the 4 to 6 weeks and are
associated with an increased incidence of congenital anomalies. Therefore tis test is
used to screen women with diabetes before conception or at the initial prenatal visit
and every 2 to 3 months throughout the pregnancy.
 Antepartum Management

• The goal of management of the pregnant woman with diabetes are as follows:
1. Maintain fasting, premeal, and bedtime glucose levels between 60 and 99 mg/dl
2. Keep postprandial glucose levels between 100 and 129 mg/dl
3. Keep the 2 am and 4 am glucose between 60 and 99 mg/dl
4. Achieve a treatment Hb A1c concentration 6%or below
5. Prevent episodes of hypoglycemia
6. Prevent DKA
 Monitoring and control of Diabetes includes:

• Blood glucose monitoring

• Urine testing
• Insulin management
• Diet management
• Exercise recommendation
• Antepartum fetal surveillance
 Blood Glucose Monitoring

• It is accomplished by daily self-monitoring of blood glucose by the patient

and Hb A1c tests every 4 to 6 weeks to confirm glycemic control.
• Self-monitoring of glucose should be done 3 to 10 times a day, depending
on the difficulty of glycemic control. The capillary blood glucose (CBG)
samples are taken before meals and snacks, 60 to 90 minutes after meal, at
bed time, and occasionally between 2 and 4 am.
 Urine testing

• Ketones-ketonuria may be caused by dietary insufficiencies such as low

carbohydrate intake, low calorie intake or skipped meals. It can also occur if
ketoacidosis is present.
• Glucosuria- is not used as a means of determining management because of
lowered renal threshold for glucose
 Therapeutic Management( Insulin Management)
DESCRIPTION METHODS
Insulin Needed by Short-acting insulin may
therapy pregestational and be used alone or with
gestational diabetics an intermediate type.
who are uncontrolled with Two thirds of daily insulin
diet or oral therapy. needs are given
Necessary for the before breakfast and
cells to take glucose one third before
from the dinner. Insulin should
Bloodstream be given
subcutaneously and at
a 90-degree angle to
the skin. The injection
site should generally
be the same each
injection (arms OR
legs OR abdomen).
PRECAUTIONS
Early in pregnancy,
insulin needs may
be less. Later in
pregnancy, increased insulin
may be needed.
Women should eat
immediately after
injecting insulin to
avoid
hypoglycemia.
Different body
areas take up
insulin at different
rates. Rotate within
the same type of
injection site.
 Therapeutic Management
DESCRIPTION METHOD CAUTION

Insulin pump An insulin pump is an continuous rate (basal) The patient should
therapy automatic pump of insulin is given to clean the site daily
with thin tubing, the patient through the and cover it with a
which is placed pump, and the patient dressing to keep it
subcutaneously, can program the pump clean. The site also
most often on the to give extra doses as needs to be
woman’s abdomen. boluses prior to meals changed every 24–
Insulin is given or correctional doses 48 hr to ensure
through this tube related to her blood optimal absorption
and injection of glucose values after and decrease
insulin is therefore meals. infection.
eliminated.
 Types of Insulin

• The usual type of insulin used for the pregnant woman with diabetes is a
biosynthetic human insulin( Humulin), made by genetically programming
Escherichia coli bacteria to produce insulin.
 Insulin Classifications

Type Appearance Onset Peak(hr) Duration(hr)

Rapid-acting Clear solution 10-15 minutes 1 1/2 3-5

Short-acting Clear solution 0.5 hr 3-4 6-8

Intermediate-acting Cloudy suspension 2-4 hr 4-12 12-24

 Calculation Guidelines for Insulin During
Pregnancy
Trimester Insulin dosage(unit/kg body weight)

prepregnant 0.6

1st trimester 0.7

2nd trimester 0.8

3rd trimester until 36 weeks 0.9

3rd trimester from 36 to 40 weeks 1.0

Postpartum 0.6
 Oral glucose lowering agents
• Oral glucose lowering agents have not been recommended during
pregnancy because of the risk for fetal anomalies and reactive
hypoglycemia.
• Metformin is an effective treatment of anovulation in women with
polycystic ovary syndrome. Its continued use in during pregnancy has been
shown in preliminary trails to reduce the risk of spontaneous abortion and
lower fasting insulin levels in these patients. Metformin, has not been FDA-
approved for use during pregnancy, therefore, its use is restricted to
investigational research.
 Diet Management

• Consideration must be given to pre-

pregnancy weight, general health status,
dietary habits, activity level and insulin
therapy.
 Exercise recommendations

•Exercise is contraindicated in the

presence of complications.
Maternal surveillance with preexisting diabetes

• Hb A1c test every 4 to 6 weeks

• Blood glucose fingerstick each prenatal visit
• Urine for protein, sugar, nitrate and leukocyte esterase at each prenatal visit
• Kidney function with a 24-hour creatinine clearance and total protein to be done
each trimester
• Retinal examination in the 1st trimester and then as indicated
• Thyroid panel
 Antepartum fetal surveillance

• Ultrasound
• Alpha-fetoprotein
• Fetal biophysical tests
• Amniocentesis
 Preterm labor management

• A single course of corticosteroids is recommended

for all pregnant women at risk for preterm delivery
between 24 to 34 weeks gestation.
• Nifedipine is the preferred tocolytic drug.
 Intrapartum management

• The woman with well controlled diabetes who has no

complications does not need to deliver before term if the fetus is
not macrosomic and the biophysical profile is reassuring.
• Early delivery will be necessary if the woman has not had good
glucose control.
• In any case, an induction or cesarian birth may be scheduled.
 Nursing Interventions for Diabetes During
• Nutrition-
a reasonable body weight should be achieved
Pregnancy
promote eating a wholesome, balanced diet
saturated fats and sugary foods must be limited
emphasize importance of 28 g/day of fiber
Eat foods from all food groups
Use portion control
• Elimination-
Drink 8-10 glasses of water a day and emptying of bladder every 2 hours to prevent infection
• Sleep and exercise-Exercise is an important component in establishing and maintaining glucose control; improved
insulin sensitivity is evident after 4 weeks of exercise. However in the presence of complications such as uncontrolled
hypertension, advance retinopathy and severe autonomic or peripheral neuropathy, a regular exercise program maybe
contraindicated.
• Coping
• Self monitoring of glucose
• Hypoglycemia management
Intrapartum nursing interventions for diabetes

• Preterm labor-magnesium sulfate or indomethacin

• Corticosteroids- 2 doses of 12 mg betamethasone administered IM 24 hours apart
• Insulin management
• Continuous fetal monitoring
• Labor progress-assess for complications
• Cesarean delivery
 Postpartum nursing interventions for Types 1
and 2 Diabetes

• Insulin
• Education
• Breastfeeding
 Postpartum interventions for GDM

• Monitoring
• Education
• Lifestyle modifications
• Family planning
 A Woman with Hypothyroidism
• Hypothyroidism, or underproduction of the thyroid hormone, is a rare condition in late adolescents and
especially rare in pregnancy because women with symptoms of untreated hypothyroidism are often
anovulatory and unable to conceive. A woman who does conceive can then face another obstacle in that she
can have difficulty increasing thyroid functioning to a necessary pregnancy level, which can then lead to
early spontaneous miscarriage. Women with hypothyroidism fatigue easily, tend to be obese, their skin is dry
(myxedema), and they have little tolerance for cold. It may be associated with an increased incidence of
extreme nausea and vomiting (i.e., hyperemesis gravidarum).
• Most women with hypothyroidism take levothyroxine (Synthroid) to supplement their lack of thyroid
hormone. A woman who is taking levothyroxine needs to consult with her primary care provider when she is
planning on becoming pregnant to be certain her dose of this will be high enough to sustain a pregnancy. She
needs to come for an early diagnosis and close follow-up as soon as she suspects she is pregnant (1 week past
her missed menstrual period). As a rule, her dose of levothyroxine will need to be increased as much as 20%
to 30% for the duration of the pregnancy to simulate the increase that would normally occur in pregnancy Be
certain a woman realizes the importance of taking this increased dose. Also, caution women that they should
take levothyroxine at a different time from any medication containing iron, calcium, or any soy product by
about 4 hours to be certain there is no problem with the absorption of the drug .After the pregnancy, the dose
of levothyroxine prescribed for pregnancy must be gradually tapered back to the prepregnancy level for both
her health and so she can breastfeed safely. Be certain a woman does not continue to take her pregnancy dose
(e.g., in trying to be economical and use up her higher dose pills), or she could pass beyond normal thyroid
function and develop hyperthyroidism.
 A Woman with Hyperthyroidism
• Hyperthyroidism, or overproduction of thyroid hormone, causes symptoms such as a rapid heart rate,
exophthalmos (i.e., protruding eyeballs), heat intolerance, heart palpitations, and weight loss.
Sometimes called Graves disease, it is more apt to be seen in pregnancy than is hypothyroidism. If
undiagnosed, a woman may develop heart failure because her heart, already stressed, cannot manage
the increasing blood volume that occurs with pregnancy. She is also more prone than the average
woman to symptoms of gestational hypertension, fetal growth restriction, and preterm labor.
• If hyperthyroidism is not regulated during pregnancy, an infant may be born with symptoms of
hyperthyroidism because of the excess stimulation he or she receives in utero. The newborn may
appear jittery with tachypnea and tachycardia. An assay of fetal cord blood will reveal the level of
thyroxine (T4) and thyroid-stimulating hormone and the need for therapy in the infant. Women
receiving smaller or minimal doses of antithyroid drugs may breastfeed, although women receiving
large doses of these drugs may be advised not to breastfeed because they are excreted in breast milk.
• Surgical treatment to reduce the functioning of the maternal thyroid gland can be accomplished, but this is
generally not the treatment of choice during pregnancy because of the need for general anesthesia. After a
pregnancy, if a woman desires other children, the procedure might be suggested as an interpregnancy procedure
so she does not enter a second pregnancy with hyperthyroidism.
That in all things God maybe glorified