Hypertensive diseases in pregnancy #1

• with Preexisting vascular disease
• with a genetic predisposition

source(https://en.wikipedia.org/wiki/public_domain)

Abnormal trophoblastic invasion of uterine vessels:
Terminal uterine vessels are known as spiral arteries.
In the normal process of implantation and development of the placenta, these arteries undergo extensive remodeling as they are invaded by endovascular trophoblasts. The spiral arteries dilates so that enough blood can get to the foetus. At the end of this remodeling, the spiral artery is made of thin adventitial layer lined by trophoblasts. It is considerably dilated in diameter and is known as the uteroplacental vessel. This invasion occurs in two phases involving two thirds of the decidua. The vessels are remodeled up to the terminal resistance portion of the vessel into the myometrial layer leading to marked decrease in the resistance to blood flow into the uteroplacental vessels and into the intervillous space.As placentation progresses, trophoblastic invasion incorporates more vessels and more decidual arteries are tapped for intervillous circulation.
The invasion depth in the second-phase trophoblastic invasion might however be deficient in patients who eventually develop pre-eclampsia.The insufficient depth allows more decidual spiral arteries to retain the resistance portion of the vessel, which prevents adequate dilation of these vessels.The contractile portion of these vessels also remains intact, which has profound implication for the effect of vasomotor regulators of circulation.
This also leads to release of endothelium-damaging mediators from ischemic placenta
The result is hypertension, proteinuria and edema, plus intrauterine growth restriction (due to poor oxygen and nutrient transfer to foetus)

Immunologic theory:
There is inadequate maternal antibody response to the fetal allograft resulting in fetal allograft rejection resulting in vascular damage from circulating immune complexes in some pregnant women. It means that the woman's body recognizes the foetus as foreign.
Examples of support for this theory are nulliparous women or women who have changed their partners in subsequent pregnancies. These women have limited fetal and hence paternal antigen exposure resulting in PET.

Disseminated intravascular coagulation (DIC) theory:
There is damage to the placenta which can cause release of thromboplastin. Thromboplastin then cause disseminated intra vascular coagulopathyand fibrin deposition in the kidney and placenta resulting in development of hypertension and placental insufficiency.This is evidenced by decrease in number of circulating platelets, increase in fibrin degradation products, reduction in fibrinolytic activity observed in some cases of pre-eclampsia.

What could be a risk factor for developing Pre-ecclampsia?
Nulliparity

Multiparous with preeclampsia in previous pregnancy and/or >10 years subfertility
Multiple pregnancy
Hydatidiform mole
Diabetes mellitus
Hydropic pregnancy
Oocyte donation or donor insemination

Extremes of age (<20years and >35years)
Obesity - BMI > 35kg/m2
Family history of pre-eclampsia
New partner increases risk of re-occurence
Previously fathered a pre-eclamptic pregnancy in another woman

Prolonged exposure to paternal antigens can reoccur with the same partner at a later gestation
Pre-existing hypertension, renal disease
Pre-existing vascular disease like Collagen vascular disease

What are the signs and symptoms of pre-ecclampsia?
The manifestation of signs and symptoms would depend on the severity and progression of the disease.
There may be no symptoms especially in mild cases.
The clinical features includes;

• increased blood pressure This is a constant feature seen in this condition
• Proteinuria due to damage to the kidneys a result of deposition of fibrin and damage to the glomerulus as a result of vasoconstriction resulting in reduced blood supply to the kidneys
  -Oedema (non dependent) due to reduction in oncotic pressure from loss of protein in urine.

-Brisk reflexes

-fundal height may be less than gestational age due to inadequate supply of nutrients and oxygen. This implies that the foetus has intrauterine growth restriction.

Cerebral manifestation in severe cases could manifest as headaches, dizziness, tinnitus, drowsiness,hypereflexia. This manifestation could be due to reduced oncotic pressure as a result of loss of protein in urine leading to accumulation of fluid in the brain. This fluid in the brain will then manifest with features of raised intracranial pressure.

Visual changes: blurred vision, diplopia, flashes of light, blindness. These visual changes are due to vasoconstriction in the vessels of the eye.

Gastrointestinal symptoms: epigastric pains, nausea and vomiting: due to congestion of gastric mucosa and/ or cerebral oedema

Renal symptoms: oliguria, anuria, haematuria and haemoglobinuria.

Signs of HELLP syndrome
H- haemolysis
E- Elevated
L- liver enzymes
L- Low
P- platelet count

Management

The management principles for pre-ecclampsia is aimed at:

• Control of hypertension
• Prevention of fits(convulsion)
• Safe mother followed by delivery of a live matured baby.The safety of the mother is considered first. In severe cases the fetus is sacrificed in the interest of the mother.

Since the main cause of pre-ecclampsia is in the abnormalities of the placenta, the main cure would be to remove the placenta which would imply delivery of the baby whether at term or not. The decision as when to deliver should depend on disease progression, maternal condition and gestational age. However if delivery is immediate, mode of delivery should be dependent on fetal condition and favourability of the cervix.

Most women with mild preecclamptic cases will benefit from bed rest as it is good therapy for fetal survival because it reduces blood pressure, improves utero placental flow(due to less stressful and less secretions of stress hormones) and aids fetal growth such that the fetus is matured enough to decrease prolonged neonatal intensive care admission( the closer to term delivery, the shorter the stay)
In cases of Severe preeclampsia, a wide variety of antihypertensives are used and also sedatives. Selection of the drug to use is of great importance and should be done by an expert.
The ideal antihypertensive used should be able to :-

• Lower blood pressure effectively,predictably and permanently
• Ensure fetal growth and well being by increasing utero placental blood flow
• Reverse renal vascular spasm and prevent pathological changes
• Be safe and free from side effects to mothers and babies
• Be convenient to use with reasonable margin of safety

The drugs that can be used include;

• Labetalol
• Magnesium sulfate
• Hydralazine
• Methyldopa
• Nifedipine
• Diazepam

Clinical assessment of fetal well being such as symphysiofundal height daily or twice weekly, cardotocogragh (CTG),daily fetal kick chart,serial ultra sound scan should be done and if there is fetal compromise or worsening of disease, the baby should be delivered.

What are the complications of pre-ecclampsia?
Complications of pre-ecclampsia can be divided into maternal complication and foetal complications.
Maternal complications

• Convulsions and coma (Eclampsia)
• Cerebral haemorrhage
• Stroke
• DIC
• Acute renal failure
• Hepatic Failure
• Liver rupture
• HELLP
• Encephalopathy
• Abruptio placentae
• Residual chronic hypertension in about 1/3 of cases
• Recurrent pre-eclampsia in next pregnancies
• Maternal mortality

Foetal complications

• Intra uterine growth restriction (IUGR)
• Oligohydramnios

Placenta infarcts

• Uteroplacental insufficiency
• Prematurity and its complications
• Still births
• Neonatal deaths.

What are the ways of preventing pre-ecclampsia?
The aetiology is diverse, therefore prevention is difficult. However, here are some preventive measures below
-Low dose aspirin is known to help if given to women at high risk of pre-eclampsia after 12weeks of gestation.

• Calcium supplementation
• Anti-oxidants like Vitamins C and E

What is the outcome of pre-ecclamptic women after delivery?
Studies have shown that complications tend to correlate with the age of the patient and severity of the disease. It has also been observed to recur in women with chronic hypertension.

References

1. Obstetrics by ten teachers nineteenth edition
2. Textbook of obstetrics and gynecology
3. wikipedia
4. All pictures are free source pictures from wikipedia and free to use .

Thank you for reading.

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