GESTATIONAL DIABETES MELLITUS
Prolong the elevation of stress hormones
Gestational Diabetes Mellitus (GDM) is one of the
most common types of diabetes mellitus and
considered the most complication of pregnancy. This
health problem is like pregnancy-induced
hypertension (PIH) that develops during pregnancy
and disappears after delivery of fetus, or as maternal
body returns to its pre-pregnant state.
Gestational Diabetes Mellitus may or may not with
co-existing maternal diabetes. It heightens the level
of diabetes (if with previous diabetes) by a notch in
response to the rise in fetal carbohydrate demand.
40% of pregnant mothers who develops GDM will
eventually develop non-insulin dependent diabetes
mellitus (NIDDM or Type II DM) within 5 years.
TYPES OF GDM
 Gestational Diabetes Mellitus (GDM) Type
A1: abnormal oral glucose tolerance test
(OGTT) but normal blood glucose levels during
fasting and 1-2 hours after meals; diet
modification is sufficient to control glucose
levels
 Type A2: abnormal OGTT compounded by
abnormal glucose levels during fasting and/or
after meals; additional therapy with insulin or
other medications is required
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 autonomic 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.
(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 the protective
mechanism that predisposes a pregnant mother in the
triggering of her pre-diabetic state, or heightens an
existing diabetes mellitus.
The effects of pregnancy on diabetes mellitus are
summarized as:
1. First Trimester – glucose level is relatively
stable or may decrease
2. Second Trimester – there is rapid increase in
glucose level
3. Third Trimester – there is rapid decrease
glucose level and return to its pre-pregnant state
FACTS ABOUT INSULIN
1. The insulin is a normal body hormone that is
produced by the beta cells of the Islets of
Langerhans in the pancreas.
2. The release of insulin is regulated by a negative
feedback in response to high glucose level. The
high glucose level may come from excessive
glucagon action or through high carbohydrate
intake.
3. The insulin secretion of the pancreas and its
action on the liver makes it maintain a normal
value of 80-120 mg/dL.
4. Insulin is essential in the following actions:
a. Carbohydrates – utilization of glucose by the
cells
b. Proteins – conversion of amino acids to replace
muscle tissues
c. Fats – conversion of excess glucose to fatty acids
and store them to adipose tissues
d. Endothelial and nerve cells are the only
cells/tissues that can use glucose even without
insulin.
e. Low insulin level causes the rise in plasma
glucose concentration and glycosuria.
f. Diabetes mellitus develops as the body secretes
low amount or as body cells rejects its utilization.
Etiology
Gestational diabetes is a disorder of late
pregnancy (typically), caused by the increased
pancreatic stimulation associated with pregnancy.
RISK FACTORS
1. Obesity
2. Family history of DM
3. Age of >45 years old (when got pregnant)
4. Previous delivery of baby weighing 9 lbs or more
5. History of any autoimmune disease
6. Belonging to/with ethnic background from
African American, Latino, and native Americans
7. History of previous GDM
8. With any level of hypertension
9. With elevated high-density lipoprotein
CLINICAL MANIFESTATIONS
The clinical manifestations of GDM coincide with
the signs and symptoms of other types of diabetes
mellitus. These are popularly known as the “3Ps” or
polydipsia, polyuria, and polyphagia. Aside from
these manifestations, there are also other sign and
symptoms that are general manifestations and
pregnancy-specific manifestations.
GDM:
 Higher glucose level (20-30 mg/dL) than the
pre-pregnant level
 Very rapid weight gain
 Polyhydramnios
 Recurrent monilial infections
 Glycosuria
 Nocturia
 Large for gestational age (LGA) or small for
gestational age (SGA) fetus
 More severe state of edema
DM:
 Blurred vision
 Vulvar pruritus
 Paresthasia
 Peripheral neuropathy
 Weakness
 Normal/elevated pulse rate and temperature
 Normal/decreased blood pressure
 Kussmaul’s respiration
 Dehydration
 Recurrent infections
 Non-healing wounds
ASSESSMENT FINDINGS
1. Associated findings include a poor obstetric
history, including spontaneous abortions,
unexplained stillbirth, unexplained
hydramnios, premature birth, low birth weight
or birth weight exceeding 4,000 g (8lb, 13 oz),
and birth of a newborn with congenital
anomalies.
2. Common clinical manifestations include:
 Glycosuria on two successive office visits
 Recurrent monilial vaginitis
 Macrosomia of the fetus on ultrasound
 Polyhydramnios
3. Laboratory and diagnostic study findings.
 Fasting blood sugar test will reveal
elevated blood glucose levels.
 A 50-g glucose screen (blood glucose
level is measured 1 hour after client
ingests a 50-g glucose drink) reveals
elevated blood glucose levels. The normal
plasma threshold is 135 to 140 mg/dL.
 A 3- hour oral glucose tolerance test
(performed if 50-g glucose screen results
are abnormal) reveals elevated blood
glucose levels. (Table 1)
 The glycosylated hemoglobin (HbA 1c)
test (measures glycemic control in the 4 to
8 weeks before the test is performed;
performed on women with pre-existing
diabetes) results reflect enzymatic bonding
of glucose to hemoglobin A amino acids.
This is a useful indicator of overall blood
glucose control. The upper normal level of
HbA1c is 6% of total hemoglobin.
  Screens for fetal (and later, neonatal)
complications, including:
 Maternal serum alpha-fetoprotein level
to assess risk for neural tube defects in
newborn.
 Ultrasonography to detect fetal
structural anomalies, macrosomia, and
hydramnios.
 Nonstress test (as early as 30 weeks),
contraction stress test, and biophysical
profile because of risk of unexplained
intrauterine fetal demise in the
antepartum period.
 Lung maturity studies (by
amniocentesis) to determine
lecithinsphingomyelin (L/S) ratio and to
detect phosphatidylglycerol (PG); the
adequacy of L/S and PG, predictor of
the newborn’s ability to avoid
respiratory distress
PATHOPHYSIOLOGY
1. The remainder of this review will discuss
molecular processes underlying the
pathophysiology of GDM. GDM is usually
the result of β-cell dysfunction on a
background of chronic insulin resistance
during pregnancy and thus both β-cell
impairment and tissue insulin resistance
represent critical components of the
pathophysiology of GDM. In most cases,
these impairments exist prior to pregnancy
and can be progressive—representing an
increased risk of T2DM post-pregnancy. A
number of additional organs and systems
contribute to, or are affected by, GDM.
These include the brain, adipose tissue,
liver, muscle, and placenta. The pancreatic
beta cell functions are impaired in response
to the increased pancreatic stimulation and
induced insulin resistance.
 Beta Cell Dysfunction
The primary function of β-cells is to store and
secrete insulin in response to glucose load.
When β-cells lose the ability to adequately sense
blood glucose concentration, or to release
sufficient insulin in response, this is classified as
β-cell dysfunction. β-cell dysfunction is thought
to be the result of prolonged, excessive insulin
production in response to chronic fuel excess.
However, the exact mechanisms underlying β-
cell dysfunction can be varied and complex.
Defects can occur at any stage of the process:
pro-insulin synthesis, post-translational
modifications, granule storage, sensing of blood
glucose concentrations, or the complex
machinery underlying exocytosis of granules. β-
cell dysfunction is exacerbated by insulin
resistance. Reduced insulin-stimulated glucose
uptake further contributes to hyperglycemia,
overburdening the β-cells, which have to
produce additional insulin in response. The
direct contribution of glucose to β-cell failure is
described as glucotoxicity.
 Chronic Insulin Resistance
Insulin resistance occurs when cells no longer
adequately respond to insulin. At the molecular
level, insulin resistance is usually a failure of
insulin signaling, resulting in inadequate plasma
membrane translocation of glucose
transporter—the primary transporter that is
responsible for bringing glucose into the cell to
use as energy. The rate of insulin-stimulated
glucose uptake is reduced by 54% in GDM
when compared with normal pregnancy. While
insulin receptor abundance is usually
unaffected, reduced tyrosine or increased
serine/threonine phosphorylation of the insulin
receptor dampens insulin signaling. In addition,
altered expression and/or phosphorylation of
downstream regulators of insulin signaling,
including insulin receptor substrate (IRS)-1,
phosphatidylinositol 3-kinase and GLUT4, has
been described in GDM. Many of these
molecular changes persist beyond pregnancy.
 Neurohormonal Networks
Neurohormonal dysfunction has been implicated
in the pathogenesis of diseases of insulin
resistance, such as that present in GDM. This
network regulates appetite, active energy
expenditure, and basal metabolic rate, and it is
made up of a complex network of central and
peripheral. These contribute to GDM by
 influencing adiposity and glucose utilization.
This network is highly regulated by the
circadian clock, which may explain why
pathological sleep disorders or those individuals
undertaking shift work are correlated with GDM
rates. Neural networks controlling body weight
are most likely set in early life, as demonstrated
in animal studies. For example, rats that are both
under- and over-fed in early life experience
epigenetic alteration of the regulatory set-point
of hypothalamic neurons. This adds to the
previously mentioned suggestion that
predisposition to GDM may be set in the womb.
 Leptin
Leptin is a satiety hormone secreted primarily
by adipocytes in response to adequate fuel
stores. It primarily acts on neurons within the
arcuate nucleus of the hypothalamus to decrease
appetite and increase energy expenditure.
Specifically, leptin inhibits appetite-stimulators
neuropeptide Y and agouti-related peptide, and
it activates the anorexigenic polypeptide pro-
opiomelanocortin. When leptin was first
discovered, it was lauded as a potential
treatment for obesity. Like insulin resistance, a
degree of leptin resistance occurs in normal
pregnancy, presumably to bolster fat stores
beyond what would usually be required in the
non-pregnant state. Leptin resistance is further
increased in GDM, resulting in hyperleptinemia.
However, pre-pregnancy BMI is a stronger
predictor of circulating leptin than GDM.
The placenta also secretes leptin during human
pregnancy. In fact, the placenta is responsible
for the majority of plasma leptin during
pregnancy. Placental leptin production is
increased in GDM, probably as a result of
placental insulin resistance, and this further
contributes to hyperleptinemia. This is also
thought to facilitate amino acid transport across
the placenta, contributing to fetal macrosomia.
 Adiponectin
Similar to leptin, adiponectin is a hormone that
is primarily secreted by adipocytes. However,
plasma adiponectin concentrations are inversely
proportional to adipose tissue mass, with low
concentrations in obese individuals. GDM is
similarly associated with decreased adiponectin.
In contrast to leptin, there is a stronger
association of adiponectin with insulin
resistance than with adiposity. Adiponectin
enhances insulin signaling and fatty acid
oxidation, and it inhibits gluconeogenesis.
Furthermore, adiponectin stimulates insulin
secretion, by upregulating insulin gene
expression and exocytosis of insulin granules
from β-cells.
 Adipose Tissue
Adipose tissue both ensures that energy is
partitioned safely and it actively secretes
circulatory factors, including adipokines (the
aforementioned leptin and adiponectin) and
cytokines.
 Liver
GDM is associated with upregulated hepatic
glucose production (gluconeogenesis).
Gluconeogenesis is increased in the fasted state,
and not adequately suppressed in the fed state.
This is not believed to be entirely the result of
inaccurate glucose sensing due to insulin
resistance, as the majority of glucose uptake by
the liver (~70%) is not insulin dependent.
Common factors between the insulin signaling
pathway and the pathways controlling
gluconeogenesis, such as PI3K, might
contribute to these effects. Increased protein
intake and muscle breakdown may also
stimulate the process by providing excess
gluconeogenesis substrate.
 Placental Transport
The placenta contributes to insulin resistance
during pregnancy via its secretion of hormones
and cytokines. As the barrier between the
maternal and fetal environments, the placenta
itself is also exposed to hyperglycemia and its
consequences during GDM. This can impact
transport of glucose, amino acids, and lipids
across the placenta:
Glucose—Glucose is the primary energy source
for the fetus and the placenta, and therefore
must be readily available at all times. For this
reason, insulin is not required for the placental
transport of glucose. However, the placenta still
 expresses the insulin receptor, and insulin
signaling can influence placental metabolism of
glucose. The receptiveness of the placenta to
glucose uptake means that it is particularly
sensitive to maternal hyperglycemia, and this
directly contributes to increased fetal growth
and macrosomia.
Protein—Amino acid transport across the
placenta is also an important determinant of
fetal growth. These can also be modulated by
pro-inflammatory cytokines. Altered amino acid
transport may also be one mechanism by which
excess protein intake contributes to GDM.
Lipids—Finally, while GDM has traditionally
been described as a disease of hyperglycemia,
the rise in obesity-associated GDM has
prompted a greater focus on the role of
hyperlipidemia in GDM. The majority of
placental gene expression alterations in GDM
occur in lipid pathways (67%), as compared
with glucose pathways. Preferential activation
of placental lipid genes is also associated with
GDM compared with T1DM. These data
correlate with the results of the HAPO Study,
which revealed independent effects of maternal
obesity and glucose on excessive fetal growth.
Therefore, it appears that GDM influences the
placental transport of glucose, amino acids, and
fatty acids, and that all three must be considered
when discussing the impact of GDM on
placental function and fetal growth.
COMPLICATIONS
The chronic effects or the uncontrolled glucose level
during pregnancy would lead to the development of
the following complications:
 Preterm labor and delivery
 Urinary tract infection (UTI)
 Infertility
 Stillbirth
 PIH – pre-eclampsia – eclampsia
 Congenital anomalies
 Spontaneous abortion
Also, a woman who developed or experienced GDM
is expected to have type 2 diabetes mellitus within 5
years for the rest of her life.
DIAGNOSIS
 Blood glucose monitoring—this can either
be done through fasting blood sugar (FBS)
or randomly. This reveals the glucose level
and indicates the plan of care needed.
 Glucose tolerance test (GTT)—to evaluate
the response of insulin to loading glucose.
 Glycated haemoglobin
(Glycohemoglobin)—measures glycemic
control by evaluating the attachment of
glucose to freely permeable erythrocytes
during their whole life cycle.
 C-peptide Assay (connecting peptide
assay)—useful when the presence of insulin
antibodies interferes with direct insulin
assay.
 Fructosamine assay—is much more useful
than glycosylated hemoglobin tests in cases
of hemoglobin variants.
 Urine glucose and ketone monitoring—may
be performed in cases where blood glucose
monitoring is not available, but, is not as
accurate as the former.
 Amniocentesis
 Non-stress test
 Sonography
NURSING DIAGNOSES
1. Altered nutrition: more or less than body
requirements related to weight gain
2. High risk pregnancy: high risk for infection,
ketosis, fetal demise, cephalopelvic
disproportion, polyhydramnios, congenital
anomalies, preterm labor.
3. Knowledge deficit related to disease and
insulin use and interaction.
MANAGEMENT
Information is crucial to help women understand the
importance of good glucose control for her health
and the health of her baby. Good glucose control
throughout pregnancy will reduce the risk of fetal
macrosomia, trauma during birth, induction of
labour and/or caesarean section, neonatal
hypoglycaemia and perinatal death (14).
Alongside strict monitoring of blood glucose with
input from an endocrinologist, women will also be
offered an increased antenatal care package
including more frequent ultrasound scans to assess
the size and well-being of the baby and liquor
volume.
Blood glucose monitoring kits should be given to
women and self-monitoring should be taught with
repeat prescriptions for necessary equipment and
medications e.g. needles, sharps bins.
Treatment
The main form of treatment is blood glucose control
and the initial treatment offered is dependent on the
results of the OGTT (see Table 2).
Lifestyle changes
Simple lifestyle changes are enough in many
women to control their glucose level and all women
should be referred to a dietician to review their diet
and provide information on low glycaemic index
foods. In addition to this, exercise has been shown
to stabilise post prandial blood glucose and reduce
the need for insulin.
Metformin
Metformin is a well-established drug that reduces
the amount of glucose created in the liver and
makes the body more sensitive to insulin. In detail,
metformin is a biguanide oral antidiabetic
medication and it works by suppressing hepatic
gluconeogenesis, increasing insulin sensitivity and
decreasing the absorption of glucose from the
gastrointestinal tract. This glucose-lowering therapy
should be offered first to women who have
uncontrolled hyperglycaemia unless
contraindicated.
When metformin was compared to insulin it was
found to have no significant differences between
outcomes such as shoulder dystocia and infants
born large for gestational age. Additionally the
administration is considered much easier and
preferred compared to insulin.
Glibenclamide
Glibenclamide is also a well-established medicine
that drives the pancreas to produce more insulin. In
more detail, glibenclamide is a sulphonylurea and
acts by stimulating insulin release from the beta-
cells in the pancreas. There are no significant
differences between the use of insulin and
metformin compared to glibenclamide for the
prevention of shoulder dystocia or large for
gestational age, however there is no long-term data
for the effects of glibenclamide in pregnancy and
therefore metformin and insulin are used
preferentially.
Insulin
When oral medications don't control gestational
diabetes, insulin is needed. Exogenous insulin is
used in conjunction with diet, exercise and
metformin if required for glucose control. Insulins
that are used preferentially are isophane/detemir
insulin and lispro/aspart insulin as long-acting and
short-acting insulin respectively. It is important to
warn women of the effects and prevention of
hypoglycaemic events. Users must also be made
aware of DVLA guidelines with insulin use.
Blood glucose aims
Women should record their blood sugar monitoring
daily. If they have repeatedly high blood glucose
they should seek medical advice in order to change
or increase their current management. Those on
glibenclamide and insulin should maintain a blood
glucose above 4mmol/l in order to prevent
problematic hypoglycaemias.
NURSING MANAGEMENTS
Assessment
History taking on:  Teach/present the list of things/foods
that need to be available at all times
a. First presentation of the manifestations of
(in case of hypoglycemic attacks)
diabetes (3 P’s)
 Have identification band indicating
b. First diagnosis of DM
the health condition (DM) for fainting
c. Family members with DM
instances
Review of systems: 4. Activity tolerance
 Plan for regular exercise
1. Weight gain, increasing  Increase carbohydrate intake before
fatigue/weakness/tiredness exercise
2. Skin lesions, infections, hydration, signs of  Instruct to avoid exercise of blood
poor wound healing
glucose level exceeds 250 mg/dL and
3. Changes in vision – floaters, halos, blurred
urine ketones are present
vision, dry/burning eyes, cataract, glaucoma
 Advise to use abdomen for insulin
4. Gingivitis, periodontal disease
injection if arms and legs are used for
5. Orthostatic hypotension, cold extremities,
exercise
weal pedal pulses
5. Skin integrity
6. Diarrhea, constipation, early satiety,
 Avoid alcohol use, instead, lotion
bloating, flatulence, hunger and thirst
 Teach on proper foot care
7. Frequent urination, nocturia, vaginal
 Advise to stop smoking and alcohol
discharge
use
8. Numbness and tingling of the extremities,
6. Fetal well-being
decrease pain and temperature sensation
 Continuous monitoring of fetal
INTERVENTIONS activities and fetal heart tone
 Monitor fetal activities during
1. Nutrition
maternal activities
 Assess timing and content of meals
 Monitor early signs of labor
 Instruct on importance of a well-
 Advise to report of any discharge
balanced diet
coming from the vagina
 Explain the importance of exercise
 Monitor daily weight and advice to
 Plan for a weight reduction course
report on rapid weight gain
2. Insulin use
7. Educative
 Encourage verbalization of feelings
 Teach on lifestyle modifications
 Demonstrate and explain insulin
 Advice to see psychologists with
therapy
other family members for therapies
 Allow client to do self-administration on the possibilities of fetal
 Review mastery of the whole process abnormalities
3. Injury from hypoglycemia  Advice to call emergency response
 Monitor maternal blood glucose level team in case of emergency
 Instruct on insulin-activity-diet  Advise to religiously follow the
interaction health instructions
 Teach on the signs and symptoms of
hypoglycemia
Nursing Interventions Rationale

Assess and record dietary pattern and caloric To help in evaluating client’s understanding
intake using a 24-hour recall. and/or compliance to a strict dietary regimen.

Assess understanding of the effect of stress on It is proven that stress can increase serum blood
diabetes. Teach patient about stress glucose levels, creating variations in insulin
management and relaxation measures. requirements.

Weigh the client every prenatal visit. Encourage

Weight gain serves as an indicator for determining
the client to periodically monitor weight at
caloric adjustments.
home between visits.

Nausea and vomiting may be brought about by

Observe for the presence of nausea and
a deficiency in carbohydrates, which may result
vomiting, especially during the first trimester.
in the metabolism of fats and development of ketosis.

Teach the importance of regularity of meals and

Eating very frequent small meals improves insulin
snacks (e.g., three meals or 4 snacks) when
function.
taking insulin.

Insulin needs for the day can be adjusted based on

Teach and demonstrate client to monitor sugar periodic serum glucose readings. Note: Values
using a finger-stick method. obtained by reflectance meters may be 10-15%
lower/higher than plasma levels.

Metabolism and maternal/fetal needs fluctuates during

the gestation period, requiring close monitoring and
Provide information regarding any required
adaptation. Research suggest antibodies against insulin
changes in diabetic management; e.g., use of
may cross the placenta, causing inappropriate fetal
human insulin only, changing from oral diabetic
weight gain. The use of human insulin decreased the
drugs to insulin, self-monitoring of serum blood
development of these antibodies. Reducing
glucose levels at least twice a day (e.g., before
carbohydrates to less than 40% of the calories ingested
breakfast and before dinner) and
reduces the degree of a postprandial peak
reducing/changing time for ingesting
of hyperglycemia. Because pregnancy provides severe
carbohydrates.
morning glucose intolerance, the first meal of the day
should be small, with minimal carbohydrates.

Hypoglycemia may be more sudden or severe during

Provide information regarding the signs and the first trimester, owing to increased usage of glucose
symptoms and difference of hyperglycemia or and glycogen by a client and developing fetus, as well
hypoglycemia. as low levels of the insulin antagonist human placental
lactogen (HPL).

Recommend monitoring urine ketones on
awakening and when a planned meal or snack is
delayed
Instruct client to treat symptomatic
hypoglycemia, if it occurs, with an 8-oz glass of
milk and to repeat in 15 minutes if serum
glucose levels remain below 70 mg/dl.
Discuss the type of insulin, dosage and schedule
(e.g., usually 4 times/day: 7:30am-NPH; 10am-
regular; 4pm-NPH; 6pm-regular).
Ketoacidosis occurs more frequently during the
second and third trimester because of the resistance to
insulin and elevated HPL levels.
Sustained or intermittent pulse of hyperglycemia re
mutagenic and teratogenic for the fetus in the first
trimester; may also cause fetal
hyperinsulinemia, macrosomia, inhibition of lung
maturity, cardiac dysrhythmia, neonatal hypoglycemia,
and risk of permanent neurologic damage.
Maternal effects of hyperglycemia can
include hydramnios, vaginal and urinary tract
infections, hypertension and spontaneous termination
of pregnancy.
Insufficient caloric intake is reflected by ketonuria,
indicating a need for an increased intake of
carbohydrates or additional snack in the dietary plan
(e.g., recurrent presence of ketonuria on awakening
may be eliminated by 3 am a glass of milk).
The presence of ketones during the second trimester
may reflect “accelerated starvation” as the diminished
effectiveness of insulin results in a catabolic state
during fasting periods (e.g., skipping meals), causing
maternal metabolism of fat. Adjustment of insulin
type, dosage, and/or frequency must be required.
Using plenty of simple carbohydrates to treat
hypoglycemia causes serum glucose values to elevate.
A combination of complex carbohydrates and protein
maintains normoglycemia longer and helps maintain
the stability of serum glucose throughout the day.
Division of insulin dosage considers basal maternal
needs and mealtime insulin-to-food ratio and allows
more freedom in meal-scheduling. The total daily
dosage is based on gestational, current maternal body
weight, and serum glucose levels. A mix of NPH and
regular human insulin helps mimic the normal insulin
release pattern of the pancreas, minimizing

Adjust diet or insulin regimen to meet
individual needs.
Monitor serum blood glucose levels (Fasting
blood sugar, preprandial 1 and two hr
postprandial) on the first visit, then as indicated
by client’s condition.
Ascertain results of HbA1c every 2-4weeks.
Coordinate multispecialty care conference as
appropriate.
Refer to a registered dietician to individualize
diet and counsel regarding dietary questions.
Prepare for hospitalization if diabetes is not
controlled.
“peak/valley” effect of serum glucose level. Note:
Although some providers may choose to manage
clients with GDM with oral hypoglycemic agents,
insulin is still the drug of choice.
Prenatal metabolic needs change throughout the
trimesters, and adjustment is determined by weight
gain and laboratory test results. Insulin needs in the
first trimester are 0.7 unit/kg of body weight. Between
18-24 weeks of gestation, it increases to 0.8 unit/kg; at
34 weeks’ gestation, 0.9 unit/kg, and 1.0 unit/kg by 36
weeks gestation.
Incidence of fetal and newborn abnormalities is
decreased when fasting blood sugar levels range
between 60 and 100 mg/dl, preprandial levels between
60 and 105 mg/dl, 1-hr postprandial remains below
140 mg/dl, and 2-hr postprandial is less than 120
mg/dl.
Provide an accurate picture of average serum glucose
control during the preceding 60 days. Serum glucose
control takes six weeks to normalize.
Provides an opportunity to review the management of
both pregnancy and diabetic condition, and to plan for
special needs during intrapartum
and postpartum periods.
Diet-specific to the individual is necessary to maintain
normoglycemia and to obtained desired weight gain.
In-depth teaching promotes understanding of own
needs and clarifies misconceptions, especially for a
client with gestational diabetes.
Infant morbidity is linked to maternal hyperglycemia-
induced fetal hyperinsulinemia.

EVALUATION

1. Body weight is within the normal range for the age of gestation.
2. Demonstrates proper technique in self-administration of insulin
3. No episodes of hypoglycemia as claimed by the client
4. No skin problems/lesions.
5. Verbalized readiness on the possible fetal defects.
6. Stable feta heart rate.

References:

https://www.google.com/amp/s/www.rnspeak.com/gestational-diabetes-mellitus-case-study/amp/
https://www.nursinginpractice.com/gestational-diabetes-primary-care
https://www.rnpedia.com/nursing-notes/maternal-and-child-nursing-notes/gestational-diabetes/
https://nurseslabs.com/gestational-diabetes-mellitus-nursing-care-plans/