Pregnancy Induced Hypertension: Definition of Terms
Pregnancy Induced Hypertension: Definition of Terms
Pregnancy Induced Hypertension: Definition of Terms
• Pregnancy-Induced Hypertension
• Eclampsia CONDITIONS THAT ARE PRONE TO DEVELOP PIH
• Pre-eclampsia
• HELLP Syndrome • black race
• multiple pregnancy
PREGNANCY INDUCED HYPERTENSION • young primigravid ( 20 yo )
• old primigravid ( older than 40 yo )
th
• poor socioeconomic condition that may lead to
• Hypertension that develops after the 20 week of
history of malnutrition
gestation to a previously normotensive woman.
• experiencing polyhydramnious
• It includes preeclampsia, eclampsia and gestational
• cardio , renal and dm complications
hypertension
PATHOPHYSIOLOGIC CHANGES
Definition of Terms
HYPERTENSION
• rapid rise in BP • exist once the patient has experienced a grand mal
• rapid weight gain seizure
• generalized edema
• Increased proteinuria EFFECTS OF PREECLAMPSIA AND ECLAMPSIA
• epigastric pain
• severe headache • Cardiovascular changes:
• visual disturbances • Decreased cardiac output,
• oliguria (<120 ml in 4 hrs) Hemoconcentration, Thrombocytopenia,
• severe nausea and vomiting Prolonged thrombin time, Abnormal
formation of red blood cells
Clinical manifestations of severe Preeclampsia • Endocrine and Metabolic changes:
• Increased levels of the hormones such as
• BP exceeding 160/110 mmHg on two readings Renin, Angiotension II, Aldosterone, ADH
taken 6 hours apart with the client on bed • Increased extracellular fluid volume
• Proteinuria exceeding 5g/24 hrs. • Renal Changes
• Oliguria <than 400ml in 24 hours • Reduced renal perfusion and glomerular
• headache filtration rate
• blurred vision, spots before the eyes • Elevated creatinine, uric acid, and urea
• pitting edema of the sacrum, face, upper extremities • Decreased excretion of calcium in the urine
• dyspnea, nausea and vomiting • Decreased urine output
• epigastric pain • Proteinuria
COMPLICATIONS
Signs & Symptoms
• Abruptio Placenta
• Cerebral Hemorrhage
• Hepatic Failure
• Acute Renal Failure
• Prematurity
• Perinatal death
• Maternal death
MANAGEMENT CRITERIA
` HOME MANAGEMENT
• BP is 140/90 below
• There is low proteinuria
• There is no fetal growth retardation
• Fetal well being is assured; good fetal movement
PREECLAMPSIA
• All signs and symptoms of eclampsia • Evaluate laboratory status such as BUN, creatinine,
• Convulsion followed by coma liver enzymes and 24-hour uric acid levels
• Oliguria • Monitor daily weight
• Pulmonary edema • Monitor fetal well-being
• Deep tendon reflexes
• After evaluation:
ECLAMPSIA • Severe preeclampsia remain for
hospitalization.
• is an extension of preeclampsia and is characterized
by the client experiencing seizures
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• Mild preeclampsia discharged for home • Monitor for impending signs of convulsions
treatment. • Monitor urinary output accurately
Ambulatory Management • Weigh daily
• Check laboratory tests
• Bed rest should be emphasized • Initiate safety precautions
• Position? • Raise side rails
• Diet modification • Put bed at lowest position
• Low? High? • Have emergency equipment's
• Teach on how to self monitor available
• BP, weight, S&S, count fetal movements, • Manage during convulsions
urine specimen • Always monitor for impending
• Report any worsening of condition such as signs of convulsions
increasing BP. • Maintain patent airway and protect patient
from self injury
• Turn patient to side
• Place pillow under patients head
• Do not restrict movements
• Oliguria Note:
• Antidote for Mg S04 toxicity – Calcium Gluconate
- fat cell is resistant to insulin..
HELLP SYNDROME - Elevated maternal glucose results in elevated fetal
glucose., this stimulates fetal pancreatic production
• Hemolysis, Elevated Liver Enzyme and Low Platelet of insulin which increase fetal hyperinsulemia
• A variation of PIH resulting into increase growth and fat deposition
• A serious condition that cause 24 % maternal - Hyperglycemia is considered teratogenic that
mortality rate and infant mortality rate of 35 % directly affect the yolk sac development.
- Usually occur at the midpoint of pregnancy when The values are conformed Diabetes are shown below
insulin resistance is noticeable.
RISK FACTORS
• Obesity
• History of large babies Monitoring woman with GDM
• History of unexplained fetal loss
• History of congenital anomalies in previous - glygocylated hgb- is used to detect the degree of
pregnancy hyperglycemia present.
- This is a measure of the amount of glucose attached
• Family history of diabetes
to hgb
• Population group
• (Native American, Hispanic and Asian)
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( as glucose circulates in the bloodstreams, it binds to a — Intermediate insulin - given before breakfast- peak
portion of the total hgb in the blood. The amount of glucose action is after lunch or late in the afternoon just
that attaches to hgb will be high if the hgb has been exposed before dinner.
to a greater level of glucose than normally present. — Regular insulin- given before breakfast - peak action
is just after breakfast.
- measuring glygocylated hgb is advantageous
because it reflects the average blood glucose level Note:
over the past 4to 6 weeks ( the time the red blood
cells were picking up the glucose). Not just the level — to prevent hypoglycemia
on the day of testing. The upper normal level of - Bcoz, they cross the placenta and are potentially
HbA1c is 6% of the total hgb. teratogenic to a fetus.
- Knowing when insulin reachers its peak level makes
2. Ophthalmic- done once during pregnancy for a woman serum glucose monitoring meaningful and alerts
with GDM and at each trimester for women with known woman to the time of the day when they are most
diabetes.( background retinal changes such as increased apt to be hypoglycemic.
exudate, dot hemorrhage, and macular edema can progress
during pregnancy. If proliferation retinopathy was present If hypoglycemia is present
before pregnancy, this also progresses and can lead to
blindness. — Common time for hypoglycemia
— 2nd and 3rd months before insulin resistance peak
- laser- to halt these changes can be done during
pregnancy with risk to the fetus. Note:
Pathophysiology of PIH