DE GUZMAN, CAMERON JOSH B.

APRIL 26, 2021

2BSN-B RLENCM109

Gestational Diabetes Mellitus

A Jessa Tolentino, 34-year-old woman G2 T1 P0 A0 L1 M0 who is in her second pregnancy she is seen for prenatal care at 24 weeks
gestation. Her weight is 220 lb/ 99kg, and her blood pressure is 130/80 mmHg. Uterine size is appropriate for gestational age which is just
above the umbilicus of the mother. The patient's past obstetric history includes the vaginal delivery of a 9 lb, 8 oz. male infant at 40 weeks
gestation, 8 years ago in Cabuyao Hospital. The patient reports that the child is doing well. Her family history reveals that her mother has type
2 diabetes mellitus. She is given a dipstick to check her glucose level and the result shows 3+ glycosuria and negative ketones.

The findings of glycosuria makes the nurse to check a glucose determination before the patient leaves the clinic. The usual approach to
screening would be a 50-g oral glucose load administered to the patient between 24 and 28 weeks gestation when the "diabetigenic stress" of
pregnancy is present. The patient's capillary glucose reading, performed in the clinic, was 193 mg/dl. She was instructed to return the next
morning for a fasting venous plasma glucose, which was 143 mg/dl. Given this finding, the diagnosis of GDM was established.
ASSESSMENT DIAGNOSIS INFERENCE PLANNING INTERVENTIONS RATIONALE EVALUATIONS
Independent
Subjective: Risk for Risk for Short Term: 1.Monitor for signs and 1.When insulin is unavailable, blood Short Term:
mother has complications of complications of After 3 hours symptoms of diabetic glucose levels rise and the body After 3 hours of NI,
type 2 hyperglycemia hyperglycemia in of NI, patient ketoacidosis: metabolizes fat for energy- patient verbalized
diabetes in relation to relation to Diabetes shall have • Anion gap producing ketone bodies. Excessive the understanding
mellitus Diabetes mellitus verbalized • Blood glucose level >300 ketone bodies cause headaches, of causative
mellitus -Describes a person understanding mg per dL nausea, vomiting, and abdominal factors and
Objective: experiencing or at of causative • Positive plasma ketone, pain. Respiratory rate and depth purpose of
T: 37 high risk to factors and acetone breath increase to help increase CO2 individual
experience a blood purpose of • Headache excretion and reduce acidosis. therapeutic
P: 90 glucose level that is individual • Kussmaul’s respirations Glucose inhibits water reabsorption interventions and
too low or too high therapeutic • Anorexia, nausea, in the renal glomerulus, leading to medications.
R: 17 for metabolic interventions vomiting osmotic diuresis with severe loss of
function and • Tachycardia water, sodium, potassium, and The mother will be
BP: 130/80 medications. • Decreased blood phosphates. Diabetic ketoacidosis well informed
pressure occurs in type I diabetes about the risk of
FHT: 120bpm The nurse will • Polyuria, polydipsia hypoglycemia or
manage and • Decreased serum 2.continous external fetal hyperglycemia
Fundal Height: minimize sodium, potassium, and monitoring is an indirect,
23cm episodes of phosphate levels noninvasive procedure to ensure Long Term:
hypoglycemia and have clear tracings that define After 2 days of NI,
Dipstick test: or 2.Perform EFM to monitor fetal status. the patient have
3+ glycosuria hyperglycemia. the fetal heart rate of the maintained her
and negative baby 3. Accurate assessments are glucose level and
ketones Long Term: needed during the acute stage (first stable vital signs.
After 2 days of 3. Continue to monitor 10 to 12 hours) to prevent
Capillary NI, the patient hydration status every 30 overhydration or underhydration.
glucose test: shall have minutes; assess skin
193 mg/dl maintained moisture and turgor, urine 4. Careful monitoring enables early
her glucose output and specific detection of medication-induced
venous plasma level and gravity, and fluid intake. hypoglycemia or continued
glucose test: stable vital hyperglycemia.
143 mg/dl signs. 4.Continue to monitor
blood glucose levels 5. Acidosis causes hyperkalemia
according to protocol and hyponatremia. Insulin therapy
promotes potassium and
5.Monitor serum phosphate return to the cells,
potassium, sodium, and causing serum hypokalemia and
phosphate levels. hypophosphatemia
6. Monitor neurologic
status every hour.
7.Carefully protect client’s
skin from microorganism
invasion, injury, and
shearing force; reposition
every 1 to 2 hours.
8.Do not allow a
recovering client to drink
large quantities of water.
Give a conscious client ice
chips to quench thirst.
9. Monitor cardiac
function and circulatory
status; evaluate:
•Rate, rhythm (cardiac,
respiratory)
• Skin color
• Capillary refill time,
central venous pressure
• Peripheral pulses
• Serum potassium
6.Fluctuating glucose levels,
acidosis, and fluid shifts can affect
neurologic functioning.
7. Dehydration and tissue hypoxia
increase the skin’s vulnerability to
injury.
8. Excessive fluid intake can cause
abdominal distention and
vomiting.)
9. Severe dehydration can cause
reduced cardiac output and
compensatory vasoconstriction.
Cardiac dysrhythmias can result
from potassium imbalances.
10. Effective management is a
team effort.
11. The goal is a consistent, well-
balanced diet to ensure normal
growth and development of the
baby.

10. Teach about condition,

insulin therapy, self-
monitoring of glucose,
nutrition, exercise, and
prevention of
complications.

Dependent
11. Consult with dietitian
for nutritional
management.