University of San Agustin

General Luna St., 5000 Iloilo City, Philippines

www.usa.edu.ph
COLLEGE OF NURSING, NUTRITION & DIETETICS
NURSING DEPARTMENT

JANAGAP, AXEL JUNE G. BSN 2-A

PREECLAMPSIA

Definition:

- Preeclampsia is a quick or sudden onset of high blood pressure after the 20th week of pregnancy. This
condition causes high blood pressure, swelling of the hands and face, abdominal pain, blurred vision,
dizziness, and headaches. In some cases, seizures can occur—this is called eclampsia (pronounced ih-
KLAMP-see-uh). The only definite cure for preeclampsia and eclampsia is to deliver the baby. If this would
result in a preterm birth, then the maternal and fetal risks and benefits of delivery need to be balanced
with the risks associated with the infant being born prematurely.

Pathophysio:
- Pre-eclampsia has a complex pathophysiology, the primary cause being abnormal placentation.
Defective invasion of the spiral arteries by cytotrophoblast cells is observed during pre-eclampsia. Recent
studies have shown that cytotrophoblast invasion of the uterus is actually a unique differentiation
pathway in which the fetal cells adopt certain attributes of the maternal endothelium they normally
replace. In pre-eclampsia, this differentiation process goes awry. The abnormalities may be related to the
nitric oxide pathway, which contributes substantially to the control of vascular tone. Moreover, inhibition
of maternal synthesis of nitric oxide prevents embryo implantation.14 Increased uterine arterial
resistance induces higher sensitivity to vasoconstriction and thus chronic placental ischemia and oxidative
stress. This chronic placental ischemia causes fetal complications, including intrauterine growth
retardation and intrauterine death. In parallel, oxidative stress induces release into the maternal
circulation of substances such as free radicals, oxidized lipids, cytokines, and serum soluble vascular
endothelial growth factor 1. These abnormalities are responsible for endothelial dysfunction15 with
vascular hyperpermeability, thrombophilia, and hypertension, so as to compensate for the decreased
flow in the uterine arteries due to peripheral vasoconstriction.
Endothelial dysfunction is responsible for the clinical signs observed in the mother, ie, impairment of the
hepatic endothelium contributing to onset of the HELLP (Hemolysis, Elevated Liver enzymes and Low
Platelet count) syndrome, impairment of the cerebral endothelium inducing refractory neurological
disorders, or even eclampsia. Depletion of vascular endothelial growth factor in the podocytes makes the
endotheliosis more able to block the slit diaphragms in the basement membrane, adding to decreased
glomerular filtration and causing proteinuria. Finally, endothelial dysfunction promotes microangiopathic
hemolytic anemia, and vascular hyperpermeability associated with low serum albumin causes edema,
particularly in the lower limbs or lungs.
The crucial issue to understand is that the prime mover of pre-eclampsia is abnormal placentation. Two
common theories appear to be interlinked, ie, a genetic theory1,16 and an immunological
theory.17,18 Several susceptibility genes may exist for pre-eclampsia.16,19 These genes probably interact
in the hemostatic and cardiovascular systems, as well as in the inflammatory response. Some have been
identified, and in candidate gene studies they have provided evidence of linkage to several genes,

Email: cn@usa.edu.ph | Tel. No.: 0999-997-1485 | Fax No.: (033) 337-4403

 University of San Agustin
General Luna St., 5000 Iloilo City, Philippines
www.usa.edu.ph
COLLEGE OF NURSING, NUTRITION & DIETETICS
NURSING DEPARTMENT

including angiotensinogen on 1-q42–43 and eNOS on 7q36; other main important loci are 2p12, 2p25,
9p13, and 10q22.1.16
Pre-eclampsia can be perceived as an impairment of the maternal immune system that prevents it from
recognizing the fetoplacental unit. Excessive production of immune cells causes secretion of tumor
necrosis factor alpha which induces apoptosis of the extravillous cytotrophoblast.17 The human
leukocyte antigen (HLA) system also appears to play a role in the defective invasion of the spiral arteries,
in that women with pre-eclampsia show reduced levels of HLA-G and HLA-E.18 During normal
pregnancies, the interaction between these cells and the trophoblast is due to secretion of vascular
endothelial growth factor and placental growth factor by natural killer cells. High levels of soluble fms-like
tyrosine kinase 1 (sFlt-1), an antagonist of vascular endothelial growth factor and placental growth factor,
have been found in women with pre-eclampsia.17,18 Accordingly, assays of sFlt-1, placental growth
factor, endoglin, and vascular endothelial growth factor, all of which increase 4–8 weeks before onset of
the disease, may be useful predictors of pre-eclampsia. Recent data show the protective role of heme
oxygenase 1 and its metabolite, carbon monoxide, in pregnancy, and identify this as a potential target in
the treatment of pre-eclampsia.

Signs and Symptoms:

 Excess protein in urine (proteinuria) or other signs of kidney problems
 Decreased levels of platelets in blood (thrombocytopenia)
 Increased liver enzymes that indicate liver problems
 Severe headaches
 Changes in vision, including temporary loss of vision, blurred vision or light sensitivity
 Shortness of breath, caused by fluid in the lungs
 Pain in the upper belly, usually under the ribs on the right side
 Nausea or vomiting

Diagnostics :

Mild preeclampsia is diagnosed when a pregnant woman has

 Systolic blood pressure (top number) of 140 mmHg or higher or diastolic blood pressure (bottom
number) of 90 mmHg or higher and either
 Urine with 0.3 or more grams of protein in a 24-hour specimen (a collection of every drop of urine
within 24 hours) or a protein-to-creatinine ratio greater than 0.3
or
 Blood tests that show kidney or liver dysfunction
 Fluid in the lungs and difficulty breathing
 Visual impairments

Severe preeclampsia occurs when a pregnant woman has any of the following:

 Systolic blood pressure of 160 mmHg or higher or diastolic blood pressure of 110 mmHg or higher on
two occasions at least 4 hours apart while the patient is on bed rest
 Urine with 5 or more grams of protein in a 24-hour specimen or 3 or more grams of protein on 2
random urine samples collected at least 4 hours apart

Email: cn@usa.edu.ph | Tel. No.: 0999-997-1485 | Fax No.: (033) 337-4403

 University of San Agustin
General Luna St., 5000 Iloilo City, Philippines
www.usa.edu.ph
COLLEGE OF NURSING, NUTRITION & DIETETICS
NURSING DEPARTMENT

 Test results suggesting kidney or liver damage—for example, blood tests that reveal low numbers of
platelets or high liver enzymes
 Severe, unexplained stomach pain that does not respond to medication
 Symptoms that include visual disturbances, difficulty breathing, or fluid build UP.

Eclampsia occurs when women with preeclampsia develop seizures. The seizures can happen before or
during labor or after the baby is delivered.

Medical and Nursing Management:

- The overall management of preeclampsia includes supportive treatment with antihypertensives and
anti-epileptics until definitive treatment - delivery. In preeclampsia without severe features, patients are
often induced after 37 weeks gestation after with or without corticosteroids to accelerate lung maturity.
These patients are monitored more closely with antenatal testing twice a week. If severe features are
present, induction is considered as early as 34 weeks, although the benefits must outweigh the risks of
preterm delivery. Patients with severe features are admitted and monitored on bed rest until
delivery.First-line antihypertensives for preeclampsia/eclampsia include hydralazine, labetalol, and
nicardipine.

 Hydralazine: The recommended dose of hydralazine hydrochloride is 5-10 mg (IV/IM) given every 15
minutes up to a dose of 20 mg IV (or 30 mg IM). If no change in pressure after 20 minutes, should
think about another agent.

 Labetalol: Recommended initial dose of labetalol hydrochloride is 20 mg, slow injection. May be
preferred because of a lack of reflex tachycardia and hypotension (if pushed slow), or increased
intracranial pressure. Be cautious if a patient has a history of a previous myocardial disease or
preexisting congestive heart failure or asthma.

 Nicardipine: Nicardipine can cause less reflex tachycardia than nifedipine. Recommended initial rate
is 5mg/hour and can be adjusted by 2.5 mg/hour every 5 minutes until the reduction of MAP of 15%
has been achieved, or a maximum dose of 15 mg/hour has been reached.

Medications are titrated to an average BP of 140/90. Seizures are treated with IV magnesium as a loading
dose of 4 g over 5 to 10 minutes, followed by an infusion of 1g/hr maintained for 24 hours after the last
seizure. Lorazepam and phenytoin may be used as second-line agents but are avoided due to fetal effects.
Other supportive measures include sparing use of diuretics and fluid restriction to avoid pulmonary and
cerebral edema.

Email: cn@usa.edu.ph | Tel. No.: 0999-997-1485 | Fax No.: (033) 337-4403

 University of San Agustin
General Luna St., 5000 Iloilo City, Philippines
www.usa.edu.ph
COLLEGE OF NURSING, NUTRITION & DIETETICS
NURSING DEPARTMENT

REFERENCES:
Pre-eclampsia: Pathophysiology, diagnosis, and management. (n.d.). PubMed Central
(PMC). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148420/
What health problems can develop during pregnancy? (n.d.).
https://www.nichd.nih.gov/. https://www.nichd.nih.gov/health/topics/preconceptioncare/conditioni
nfo/health-problems?fbclid=IwAR0H2Uj0XxmLNAB3qp2sp1H5rVBYsJMCqv8CcrVaqF4h-
4uGKHImHv8I8t0
Preeclampsia - Symptoms and causes. (2022, April 15). Mayo
Clinic. https://www.mayoclinic.org/diseases-conditions/preeclampsia/symptoms-causes/syc-20355745
How do health care providers diagnose preeclampsia, eclampsia, and HELLP syndrome? (n.d.).
https://www.nichd.nih.gov/. https://www.nichd.nih.gov/health/topics/preeclampsia/conditioninfo/di
agnosed

Email: cn@usa.edu.ph | Tel. No.: 0999-997-1485 | Fax No.: (033) 337-4403