Pre-eclampsia and Hypertensive Disorders in Pregnancy

The development of pre-eclampsia occurs in two stages. The first stage starts early in pregnancy as the decidua gets invaded by the syncytiotrophoblast for implantation. The erosion of the muscular wall & endothelium of the spinal arteries is abnormal. Thurs the placenta is not appropriately supplied by oxygen though no features are detected clinically. The second stage occurs between the 16th-20th week. The oxidatively stressed [inadequately oxygen supplied placenta] placenta releases factors leading to damage of endothelial cells, which form endothelium in the maternal circulation (Amaral et al., 2017). Eventually, the endothelial cells’ dysfunction and maternal systemic inflammatory response lead to clinical features of pre-eclampsia.

Predisposing factors

• Pre-pregnancy hypertension is also referred to as existing or chronic hypertension before conception because of damage to the various endothelium.
• Previous history of pre-eclampsia because of the probability of re-occurrence.
• Pre-
• pregnancy hypertension is also referred to as existing or chronic hypertension before conception because of the various endothelium damage.
• Being a primigravida because of the maternal immune response to a fetal antigen from the father. (Amaral et al., 2017)
• Change of male partner: The fetal antigen from the sperm sensitizes antibodies’ production by the maternal body, hence endothelial cells dysfunction, leading to high sensitivity to angiotensin II= HTN.

General Clinical Features

The blood pressure reading is 140/90 mmHg & above, taken on two consecutive occasions, at least 2- 4 hours apart, excessive weight gain; due to fluid retention, edema, initially of ankles, later fingers, face & legs, and finally becomes generalized edema to include the abdomen, sacral region & vulva, results from severe fluid retention. There is fatigue due to inadequate blood supply to body tissues, abdominal discomforts; reported as indigestion, stomachache & constipation because of insufficient blood supply, palpitations; because of increased peripheral resistance, visual disturbances; blurred vision, flashlight, double vision, and sometimes temporary blindness (Raynor & Marshall, 2014).   The patient will also present with headache, either frontal or occipital because of raised/ increased intracranial pressure, proteinuria, signifying renal damage, severe epigastric pain, and sometimes a tinge of jaundice, due to liver involvement.

Diagnostic Factors

• BP readings are of 140/90 mmHg or greater, measured on two consecutive occasions, 2-4 hrs apart. Specifically, diagnosis is based on a rise of the systolic pressure with 30mmhg & diastolic pressure with 15mmhg above the typical values, for that client, at least two occasions, 4 hours or more apart.
• There is presence of detectable protein of 1 (one) plus(+) or more on a reagent/ strip testing, in clean catch urine specimens [m.s.s.u] taken at least 4 hours apart.
• There is a high rate of fluid retention in the legs, face, hands, abdomen, sacral, and vulva.

Specific Management

In mild pre-eclampsia, closely monitor noted signs through weekly antenatal clinic and advice the mother on; bed rests in a left lateral position to improve renal and placental blood supply. Administer sedatives like phenobarbitone 30mg every eight hours to ensure rest and sleep and monitor the fetal kicks and report to the hospital if they are noted to be decreasing or absent.

In moderate pre-eclampsia; immediately admit the mother to the hospital, Inform the doctor, nurse her in a quiet area, preferably dim lit to facilitate rest & sleep, control visitors & administer sedatives as well, give a balanced diet with extra proteins, fiber, low in salt and carbohydrates, monitor the fetal kicks and report to hospital if they are noted to be decreasing or are absent. Administer antihypertensive; Aldomet 250-500mg TDS or nifedipine 20mg BD (Cox et al., 2019). Offer psychological support to control anxiety. Maintain a fluid balance chart and weigh on alternate days to monitor edema. Regularly evaluate the progress through interviewing and physical examination findings.

In severe pre-eclampsia, admit the mother at first contact because she is on the verge of developing eclampsia. Inform the doctor immediately for medical management. Nurse them in a quiet dimmed lit area and on complete bed rest. Encourage her to sleep in the left lateral position to improve blood supply to kidneys & placental beds. Maintain records of observations and consult practioner nurse. Take vital signs every 2 hours. Do urinalysis on every specimen. Fill the fluid chart & for gross edema, restrict fluid intake to 2litres in 24hours. Enquire for symptoms of headache and epigastric pain. Check for fetal kick/movement every 3 hours. Do Doppler ultrasound to measure the efficiency of blood flow to the placenta. (Raynor & Marshall, 2014).   Offer psychological support to the mother and family

Administer parental antihypertensive, i.e., hydralazine 10mg I .v slowly stat.  Alternatively, magnesium sulfate 20% solution 4gm IV for 10-15 minutes. (Cox et al.,2019)  Then follow promptly with 10 gm of 50% solution MgSo4, 5gm on each buttock, deep IM with 2% lignocaine in the same syringe.

Observe the usual precautions before giving mgso4. Closely monitors blood pressure every 15 to 30 minutes to diagnose sudden hypotension signs, which is dangerous to both the mother & fetus. As soon as the diastolic pressure stabilizes to a range of 90-100mhg, then change to oral antihypertensive, e.g., Aldomet 500mg TDS or nifedipine 20mg BD either sublingually or orally (Raynor & Marshall, 2014). For preterm delivery anticipation, administer steroid=dexamethasone 4mg BD 1.m for 4/7 to prevent respiratory distress syndrome.

As the condition gets controlled, re-introduce to limited daily activity and allow pregnancy to continue to term. However, if she is admitted at term or condition does not improve irrespective of the gestation age, emergency cesarean section is highly recommended. The development of eclampsia can happen if the condition is not controlled. Eclampsia can lead to intrauterine fetal death or stillbirth because of severe placental dysfunction.