A G1P0A0, 23 years old, gestational age 31+ 6 weeks came to Dr.

General Hospital Moewardi after

coming to the midwife with information on high blood pressure and diagnosed with severe pre-
eclampsia in primigravida preterm pregnancy has not been delivered.

Preeclampsia is a condition that usually occurs in over 20 weeks of pregnancy which is characterized by a
sudden increase in blood pressure and the discovery of proteinuria or an increase in serum creatinine or
pulmonary edema or an increase in liver function or thrombocytopenia or headache, epigastrium, visual
impairment. Preeclampsia is always associated with placental dysfunction. The placenta in patients with
preeclampsia usually occurs in infarction and sclerosis in the arterioles. Criteria for severe preeclampsia
(PEB): systolic / diastolic blood pressure> 160/110 mmHg at the time of the 15 minute examination using
the same arm; proteinuria> 5 grams / 24 hours or> 3 + dipstick in urine samples when collected at least
four hours.

Risk factors for preeclampsia are nullipara, obesity, history of preeclampsia in previous pregnancies, old
age pregnancy, history of chronic hypertension, and history of diabetes. Patients in this case have two
risk factors that have been mentioned that may be the cause of preeclampsia, namely nullipara and
obesity. First pregnancy is one of the risk factors of preeclampsia which is based on several factors,
namely: in primipara usually there is immune maladaptation, greater insulin resistance, and an
imbalance of angiogenic factors. In the first pregnancy there is usually an increase in the secretion of
anti-angiogenic proteins in the circulation which inhibits vascular endothelial growth factor (VEGF) and
placental growth factor (PGF). This can affect the condition and interfere with the function of the
placenta.

Obesity is also a risk factor for these patients. In pregnant women who are obese there is a metabolic
disorder that affects the state of pregnancy. The mechanism of preeclampsia that may occur in obese
pregnant women is the presence of insulin resistance which disrupts NO function and causes oxidative
stress, an increase in the work of the sympathetic nerve, and an increase in the expression of
angiotensinogen by adipose tissue. The high level of free fatty acids in obese women induces oxidative
stress and can cause vascular damage. In addition, adipose tissue also produces several inflammatory
mediators that can alter endothelial function.

Preterm and not yet in labor are established from the history that the patient has not felt the regular
tightness of the stomach and blood mucus has not been felt out. Apart from the history, examination
needs to be done to support the diagnosis. From the results of the leopold examination in this patient,
the baby's impression is elongated, the lower presentation is the head, the back on the right. On this
examination the fetus has a head that has not entered the pelvis. It has not been found that his, DJJ is
145x / minute, and TFU is 24 cm. On examination the VU is quiet, the vaginal wall is in normal range, lio
portio, closed, blood (-), discharge (-). From the results of the genital examination it can be concluded
that the patient has not yet been delivered.

Laboratory results showed blood hemoglobin (11.1 g / dl), hematocrit (33%), elevated erythrocytes (3.74
x106 / uL), leukocytes (13 thousand / uL) and creatinine (0.4 mg / dl). Examination of urine protein is +1.
Ultrasound examination was obtained by a single fetus, intrauterurine, head presentation, DJJ (+), FB:
BPD: 8.43, AC: 26.63, FL: 5.95, EFW: 1754 grams, amniotic fluid was sufficient, and not clear congenital
major disorder, the impression of the fetus is in good condition.

This patient is given PEB protap therapy to prevent patients from falling into eclampsia or impending
eclampsia. The PEB procedure is oxygenation with nasal cannula 3 liters per minute, ringer lactate
infusion 20 drops per minute, injection of MgSO4 20% 4 grams in 15 minutes (initial dose) and injection
of MgSO4 20% 1 gr / hour for 24 hours (maintenance dose) and administration of nifedipine if the
patient's blood pressure is ≥ 160/110 mmHg. Requirements for administering MgSO4 are patella (+)
reflexes, respiration rate 16-20x per minute, amount of urine at least 30 cc in 4 hours. During
administration of MgSO4 urine the patient's output must be controlled by inserting a catheter and
calculating the fluid balance. This is so that in this patient electrolyte balance is maintained and there is
no hypermagnesia. MgSO4 given functions as seizure prophylaxis, tocolytic, antihypertensive and
diuretic. If the patient has MgSO4 poisoning, a calcium gluconate antidote can be given. Patients are also
given conservative therapy to maintain pregnancy.