Gestational Diabetes Mellitus Third trimester—there is rapid decrease in
glucose level and return to its pre-pregnant
Is defined as any degree of glucose intolerance
with onset or first recognition during
pregnancy.
Anatomy and Physiology:
A normal body uses insulin as a channel for
glucose to enter the cells for utilization. This
process is also applicable with the fetus (during
pregnancy) for growth and development. As the
fetus grows, the maternal body executes
automatic response by doubling the level of
glucose level through lowering insulin secretion
and with the aid of some gestational hormones
that antagonizes the effects of insulin, a process
known as protective mechanism. Along with
this, this mechanism causes the rise of placental
lactogen, estrogen, and progesterone to cause
the following effects:
1. Antagonizes the effects of insulin,
2. Prolong the elevation of stress hormones
(cortisol, epinephrine, and glucagon)
3. Degradation of insulin by the placenta. The
total effect of these mechanisms raises the
maternal glucose level for fetal usage.
Hyperglycemia normally occurs with protective
mechanism that predisposes a pregnant mother
in the triggering of her pre-diabetic state or
heighten an existing diabetes mellitus.
The effects of pregnancy on diabetes mellitus
are summarized as:
First trimester—glucose level is relatively stable
or may decrease
Second trimester—there is rapid increase in
glucose level
state.
Etiology:
During normal pregnancy, resistance to insulin
action increases. In most pregnancies,
pancreatic beta cells are able to compensate for
increased insulin demands, and normoglycemia
is maintained. In contrast, women who develop
GDM have deficits in beta-cell response leading
to insufficient insulin secretion to compensate
for the increased insulin demands. Risk is
increased by:
 Age: due to age-related decreased
pancreatic beta-cell reserve
 Obesity: leads to increased insulin
resistance, which is further
compounded by pregnancy
 Smoking: increases insulin resistance
and decreases insulin secretion
 Polycystic ovarian syndrome:
associated with insulin resistance and
obesity
 Nonwhite ancestry
 Family history of type 2 diabetes
 Low-fiber and high-glycemic index diet
 Weight gain as a young adult:
correlates with risk
 Lack of physical activity: exercise
increases insulin sensitivity and may
impact body weight
 Prior GDM: GDM recurs in as many as
80% of subsequent pregnancies.
Pathophysiology:
Products of the placenta, including tumor
necrosis factor-alpha (TNF-alpha) and human
placental lactogen (also known as human
chorionic somatomammotropin), are thought to
play key roles in inducing maternal insulin
resistance. Insulin resistance is most marked in
the third trimester - the reason that screening
has traditionally been performed at this point.
Women who develop GDM have deficits in
beta-cell function rendering them unable to
adapt to pregnancy. In GDM, as in type 2
diabetes, the deficit in beta-cell function is
usually multifactorial and polygenetic. However,
unmasked by the increased insulin needs of
pregnancy, autoimmune diabetes and maturity-
onset diabetes of youth (MODY) may
occasionally be first recognized as GDM.
Hyperglycemia in late pregnancy is associated
with macrosomia and neonatal hypoglycemia,
hyperbilirubinemia, and hypocalcemia, [17] [18]
as well as adverse maternal outcomes, including
gestational hypertension, preeclampsia, and
cesarean delivery. The Hyperglycemia and
Adverse Pregnancy Outcomes (HAPO) study
showed that even mild increases in maternal
glycemia raise pregnancy risk of macrosomia
and related outcomes, and showed no glucose
threshold values for such risks.
Clinical Manifestation:
 Polyuria or increased
urination. Polyuria occurs because
the kidneys remove excess sugar
from the blood, resulting in a
higher urine production.
 Polydipsia or increased
thirst. Polydipsia is present because
the body loses more water as
polyuria happens, triggering an
increase in the patient’s thirst.
 Polyphagia or increased
appetite. Although the patient may
consume a lot of food but glucose
could not enter the cells because of
insulin resistance or lack of insulin
production.
 Fatigue and weakness. The body
does not receive enough energy
from the food that the patient is
ingesting.
 Sudden vision changes The body
pulls away fluid from the eye in an
attempt to compensate the loss of
fluid in the blood, resulting in
trouble in focusing the vision.
Symptoms of Diabetes Mellitus:
 Tingling or numbness in hands or
feet. Tingling and numbness occur
due to a decrease in glucose in the
cells.
 Dry skin. Because of polyuria, the
skin becomes dehydrated.
 Skin lesions or wounds that are
slow to heal. Instead of entering the
cells, glucose crowds inside blood
vessels, hindering the passage
of white blood cells which are
needed for wound healing.
 Recurrent infections. Due to the
high concentration of glucose,
bacteria thrives easily.
Complications:
 Hypoglycemia. Hypoglycemia occurs
when the blood glucose falls to less
than 50 to 60 mg/dL because of too
much insulin or oral hypoglycemic
agents, too little food, or excessive
physical activity.
 Diabetic Ketoacidosis. DKA is
caused by an absence or markedly
inadequate amounts of insulin and
has three major features of
hyperglycemia, dehydration and
electrolyte loss, and acidosis.
 Hyperglycemic Hyperosmolar
Nonketotic Syndrome. HHNS is a
serious condition in which
hyperosmolarity and hyperglycemia
predominate with alteration in the
sense of awareness.

Diagnostic:
Hypoglycemia may occur suddenly in a patient
considered hyperglycemic because their blood
glucose levels may fall rapidly to 120 mg/dL or
even less.
 Serum glucose: Increased 200–1000
mg/dL or more.
 Serum acetone (ketones): Strongly
positive.
 Fatty acids: Lipids, triglycerides, and
cholesterol level elevated.
 Serum osmolality: Elevated but
usually less than 330 mOsm/L.
 Glucagon: Elevated level is
associated with conditions that
Nursing Assessment
produce (1) actual hypoglycemia, (2)
relative lack of glucose (e.g.,
trauma, infection), or (3) lack of
insulin. Therefore, glucagon may be
elevated with severe DKA despite
hyperglycemia.
 Urine: Positive for glucose and
ketones; specific gravity and
osmolality may be elevated.
Medication:
 Insulin
 Glyburide
 Metformin
Medical Management
 Normalize insulin activity. This is the
main goal of diabetes treatment —
normalization of blood glucose levels to
reduce the development of vascular
and neuropathic complications.
 Intensive treatment. Intensive
treatment is three to four insulin
injections per day or continuous
subcutaneous insulin infusion, insulin
pump therapy plus frequent blood
glucose monitoring and weekly contacts
with diabetes educators.
 Exercise caution with intensive
treatment. Intensive therapy must
be done with caution and must be
accompanied by thorough
education of the patient and family
and by responsible behavior of
patient.
 Diabetes management has five
components and involves constant
assessment and modification of the
treatment plan by healthcare
professionals and daily adjustments
in therapy by the patient.Nursing
Management
 Assess the patient’s history. To
determine if there is presence of
diabetes, assessment of history of
symptoms related to the diagnosis
of diabetes, results of blood glucose
monitoring, adherence to
prescribed dietary, pharmacologic,
and exercise regimen, the patient’s
lifestyle, cultural, psychosocial, and
economic factors, and effects of
diabetes on functional status should
be performed.
 Assess physical condition. Assess
the patient’s blood pressure while
sitting and standing to detect
orthostatic changes.
 Assess the body mass index and
visual acuity of the patient.
 Perform examination of foot,
skin, nervous system and mouth.
  Laboratory examinations. HgbA1C,
fasting blood glucose, lipid profile,
microalbuminuria test, serum
creatinine level, urinalysis, and ECG
must be requested and performed.
Diagnoses:
 Risk for unstable blood glucose
level related to insulin resistance,
impaired insulin secretion, and
destruction of beta cells.
 Risk for infection related to delayed
healing of open wounds.
 Deficient knowledge related to
unfamiliarity with information, lack
of recall, or misinterpretation.
 Risk for disturbed sensory
perception related to endogenous
chemical alterations.
 Impaired skin integrity related to
delayed wound healing.
 Ineffective peripheral tissue
perfusion related to too much
glucose in the bloodstream
Nursing Interventions
The healthcare team must establish
cooperation in implementing the following
interventions.
 Educate about home glucose
monitoring. Discuss glucose
monitoring at home with the patient
according to individual parameters
to identify and manage glucose
variations.
 Review factors in glucose
instability. Review client’s common
situations that contribute to glucose
instability because there are
multiple factors that can play a role
at any time like missing meals,
infection, or other illnesses.
 Encourage client to read labels. The
client must choose foods described
as having a low glycemic index,
higher fiber, and low-fat content.
 Discuss how client’s antidiabetic
medications work. Educate client on
the functions of his or her
medications because there are
combinations of drugs that work in
different ways with different blood
glucose control and side effects.
 Check viability of insulin. Emphasize
the importance of
checking expiration dates of
medications, inspecting insulin for
cloudiness if it is normally clear, and
monitoring proper storage and
preparation because these affect
insulin absorbability.
 Review type of insulin used. Note
the type of insulin to be
administered together with the
method of delivery and time of
administration. This affects timing of
effects and provides clues to
potential timing of glucose
instability.
 Check injection sites
periodically. Insulin absorption can
vary day to day in healthy sites and
is less absorbable in
lipohypertrophic tissues.