1. Situation of Risk: Hypertensive Disorders of Pregnancy
Pam Jordan, PhD, RNC

2. Hypertensive Disorders of Pregnancy
Leading cause of maternal mortality worldwide
Occur in 12-22% of all pregnancies
Encompasses a spectrum of diagnoses
Chronic hypertension
Preeclampsia
Mild
Severe
Preeclampsia superimposed on chronic HTN
Gestational hypertension
How do we define hypertension?
Systolic BP ≥ 140
Diastolic BP ≥ 90

3. Hypertensive Disorders of Pregnancy
Chronic hypertension
Hypertension diagnosed prior to pregnancy or prior to 20 weeks gestation
If one of the other hypertensive disorders of pregnancy is diagnosed during pregnancy but persists after 12 weeks postbirth, a retroactive diagnosis of chronic hypertension may be made

4. Hypertensive Disorders of Pregnancy
Preeclampsia-eclampsia
Affects 10% of all first pregnancies
A systemic disease with hypertension developing after the 20th week of pregnancy and accompanied by proteinuria
Eclampsia is the convulsive stage of the disease
Used to be called pregnancy induced hypertension [PIH]

5. Hypertensive Disorders of Pregnancy
Preeclampsia superimposed on chronic HTN
Up to 25% of women with chronic hypertension develop preeclampsia
Women with hypertension who develop new onset proteinuria, proteinuria before the 20th week gestation, or sudden uncontrolled hypertension
Has the highest rates of both maternal and fetal morbidity and mortality

6. Hypertensive Disorders of Pregnancy
Gestational hypertension
Develops in 5-6% of all pregnancies in the US
Hypertension detected for the first time after 20 weeks gestation without proteinuria
Relatively benign without underlying physiological changes
May be treated with medication
Definitive diagnosis made postpartum.

7. Preeclampsia Disease of pregnancy that ranges from mild to severe
Hypertension accompanied by underlying systemic pathology that can have severe maternal and fetal impact
10% of all pregnancies
Most common complication of pregnancy
No consensus as to cause
Only cure is delivery of the placenta

8. Preeclampsia Diagnosed after the 20th week of pregnancy
Documented normal blood pressures prior to 20 weeks gestation
Mild preeclampsia
Systolic BP >140 and <160 and diastolic BP > 90 and <110 on at least two occasions at least 6 hours apart
At least 300 mg/DL of protein in a 24 hour urine
Severe preeclampsia
Systolic BP≥160 and diastolic BP≥110 on at least two occasions at least 6 hours apart
At least 5 grams of protein in a 24 hour urine

9. Preeclampsia
NOTE: urine protein assessed by dip sticks are not considered accurate
NOTE: urine collections for protein of less than a full 24 hours are not considered accurate
NOTE: increases of blood pressure over baseline [pre- pregnancy or pregnancy values] are not of value in the diagnosis of pre-eclampsia

10. Preeclampsia
In the past, a woman was considered to have pre-eclampsia if she demonstrated the triad of
Hypertension
Proteinuria
Edema
These are no longer the diagnostic criteria because edema is common during pregnancy

11. Criteria for Severe Preeclampsia
Systolic BP ≥160 and diastolic BP ≥90**
Proteinuria > 5 grams /24 hours**
Oliguria <500 cc/24 hours
Headache and/or visual disturbances
Pulmonary edema
**most common criteria

12. Criteria for Severe Preeclampsia [continued]
Epigastric pain
Impaired liver function of unknown etiology
Thrombocytopenia [low platelets]
IUGR or oligohydramnios
Elevated serum creatinine
Eclampsia [grand mal seizures]

13. Preeclampsia Definitions
Idiopathic multisystem, pregnancy-specific syndrome of reduced organ perfusion [NIH]
Deterioration of renal function
Hepatic involvement
Pulmonary edema
Hematologic involvement
Neurological involvement
IUGR
Syndrome defined by hypertension and proteinuria that also may be associated with a myriad of other signs and symptoms [ACOG]
Preeclampsia is unique to human pregnancy

14. Pathophysiology
Something starts at the time of implantation of the placenta that sets up a cascade of events leading to pre-eclampsia.
Inadequate maternal vascular response to implantation
Endothelial dysfunction
Abnormal development of the arterial system within the uteroplacental network
Exaggerated inflammatory response with resultant generalized vasospasm, activation of platelets, ongoing coagulopathy, and abnormal hemostasis
Proposed two stage model
Stage 1: poorly perfused placenta
Stage 2: interactions of placental derived factors with maternal constitutional factors
Role of oxidative stress, inflammatory response, and increased coagulation complement activation

15. Pathophysiology
In normotensive pregnancies the spiral arteries of the uterus widen to accommodate the 10 fold increase in blood flow
In women with preeclampsia, the spiral arteries remain thick walled resulting in suboptimal placental perfusion
Vasospasm and activation of a cascade of coagulation events which form occlusive microthrombae
Uteroplacental perfusion can be decreased by 50% before the onset of symptoms
The resulting ischemia leads to endothelial cell dysfunction resulting in multiorgan endothelial cell damage and dysfunction
This triggers generalized vasospasm with reduced tissue perfusion to all organs and increased peripheral vascular resistance which manifests in elevated blood pressure

17. Pathophysiology: Liver
Increased microvascular fat deposits in the liver, which may be the cause of epigastric pain
There may be hemorrhagic necrosis in the liver, which can cause subcapsular hematoma and result in right upper quadrant pain or epigastric pa
Liver damage may be mild or may progress to HELLP syndrome [Hemolysis, Elevated Liver enzymes, and Low Platelets] which occurs in about 1 in 5 women with severe preeclampsia-life threatening condition

18. Pathophysiology: Kidney
In 70% of women with preeclampsia, glomerular endothelial damage, fibrin deposits, and resulting ischemia reduce renal plasma blood flow and glomerular filtration rate
Protein is excreted in the urine
Uric acid, creatinine, and calcium clearance are reduced and oliguria develops as the condition worsens
Oliguria is a sign of severe preeclampsia and kidney damage
Oliguria = less than 500 cc/24 hours

19. Pathophysiology: Vascular
The coagulation system is activated and thrombocytopenia occurs, possibly due to increased platelet aggregation and deposition at site of endothelial damage, activating the clotting cascade
A platelet count below 100,000 cells/mm3 is an indication of severe preeclampsia [normal 150, ,000 cells/mm3]
The leakage of serum protein into interstitial spaces and into urine, by way of damaged capillary walls, results in decreased serum albumin and tissue edema
Pulmonary edema is most commonly caused by volume overload related to left ventricular failure as a result of extremely high vascular resistance

20. Pathophysiology: Brain
Endothelial damage to the brain results in fibrin deposits, edema, and cerebral hemorrhage, which may lead to hyperreflexia and severe headaches and can progress to eclampsia
Retinal arterial spasms may cause blurring or double vision, photophobia, or scotoma [islands of loss of vision or visual acuity surrounded by areas of normal vision]

21. Effect of Preeclampsia: Summary

22. Risk Factors Nulliparity Age <19 and >35 Obesity
Multiple gestation
Family history of preeclampsia [more common in daughters of women who had pre-eclampsia and in pregnancies fathered by sons of women who had pre-eclampsia]
Preexisting hypertension or renal disease
Preeclampsia or eclampsia with prior pregnancies
Diabetes mellitus

23. Maternal Risks: Life-threatening
Cerebral edema/hemorrhage/stroke
Disseminated intravascular coagulation
HELLP syndrome
Pulmonary edema
Congestive heart failure
Hepatic failure
Renal failure
Placental abruption; maternal hemorrhage

24. Fetal and Neonatal Risks
Prematurity-preterm delivery may be indicated related to deterioration of maternal status
Intrauterine growth restriction (IUGR) related to reduced uteroplacental perfusion
Low birth weight
Fetal intolerance of labor because of reduced placental perfusion
Stillbirth

25. Symptoms General malaise
“Not feeling well. I’m just not myself.” “Something is wrong.” “I think I have the flu.”
Nausea and vomiting in late pregnancy should be considered abnormal.
Severe headaches not relieved with acetaminophen.
Right upper quadrant pain [just below the ribs on the right side: liver] May be confused with heartburn.
Sudden weight gain; Sudden swelling of hands, face, feet
Problems with vision [blurred vision, flashing lights or spots before the eyes]

26. Assessment Criteria Edema Reflexes 1+ = slight pitting; normal
2+ = somewhat deeper pit than in l+; may be normal
3+ = the pit is noticeably deep and the extremity is swollen and full; abnormal
4+ = the pit is deeper yet and remains when the finger is removed/the extremity is shiny with extremely taut skin; abnormal
Pitting can also be documented as the depth of the pitting in mm
0 = No response; abnormal
1+ = Diminished response; low normal
2+ = Average response; normal
3+ = Brisker than average; may not be abnormal
4+ = Hyperactive,; very brisk, jerky, or clonic response; abnormal
Clonus is measured in number of beats
What is the woman’s normal?

27. Laboratory Analyses Complete blood count Platelet count
Liver function tests [ALT, AST]
Renal function tests [creatinine, BUN, Uric acid]
Urinalysis and microscopy
24 hour urine collection for protein and creatinine clearance
Blood type and antibody screen [in anticipation of possible hemorrhage]

28. Laboratory Analyses Platelet count Renal function
<150,000 = thrombocytopenia
<100,000 extreme high risk for coagulopathy [epidural risk]
Liver function
ALT increases
AST increases
Watch for hypoglycemia
Watch for hyperbilirubinemia and jaundice
Renal function
Serum creatinine increases
Creatinine clearance decreases
BUN increases as creatinine increases
Uric acid increase may be an early finding
Urinalysis and microscopy to rule out an inflammatory process in the kidneys

30. OUTPATIENT TREATMENT: Mild Preeclampsia
Bedrest: therapeutic boredom
Environmental control
Limit visitors
Calming activities
Decrease maternal stress
Increased fluids
Monitoring of symptoms and BP
Upper arm cuff
Correct size
Warm tub soaks
Fetal surveillance at home
Very unclear if bedrest helps; probably not strict, but 2 hrs tid may help

31. Indications for Inpatient Management
Systolic BP ≥160 or diastolic BP ≥100
Proteinuria
Headache or epigastric pain, neurologic or visual symptoms
Hypertension or proteinuria in the presence of other risk factors
Indications of fetal compromise [IUGR, oligohydramnios]

32. Goals of Inpatient Management
Use pharmacologic management to prevent mortality/morbidity
Use pharmacologic management to extend pregnancy
Fetal considerations
Fetal lung maturity: Betamethasone
Magnesium sulfate neuroprotection
Get the baby born: definitive treatment
Cervical ripening and induction labor
Cesarean birth

33. Inpatient Management Initiation of an intravenous line
These women are usually initially volume depleted
Remember that this disease involves endothelial dysfunction
Beware of fluid overload which could lead to pulmonary edema
Insertion of a foley catheter
Strict intake and output
Fetal monitoring
Pay particular attention to baseline fetal heart rate and variability

34. Inpatient Management: Magnesium Sulfate
Magnesium sulfate therapy: A high alert medication
Always administer using an infusion pump
Have calcium gluconate available at the bedside to reverse magnesium toxicity
Assess for signs of magnesium toxicity
Reduced or absent deep tendon reflexes [as long as DTRs are present there is not Mg toxicity]
Confusion, reduced responsiveness [assess LOC, orientation X 3]
Respiratory depression [assess respiratory rate, depth, auscultate lungs]
Serum Mg levels

35. Inpatient Management: Antihypertensives
To achieve BP control to prevent cerebrovascular accident while trying to maintain pregnancy or achieve delivery
May be included as part of expectant management of severe pre-eclampsia related solely to BP criteria
Used to prevent cerebrovascular hemorrhage/stroke

36. Inpatient Management: Anihypertensives: Hydralazine HCl [Apresoline]
Causes direct peripheral vasodilatation
Increases cardiac output and heart rate
Dosages: 5 mg IV or 10 mg IM
5-10 mg every 20 to 30 minutes
Maximum dosage is 20 mg IV or 30 mg IM
If there is no response up to maximum dosage, change medications
Can cause rebound tachycardia
More likely to get rebound hypotension

37. Inpatient Management: Anihypertensives: Labetalol
Selective alpha and non-beta antagonist
Reduces vascular resistance without increasing cardiac output or heart rate
Dosage: initial 20 mg IV
If the effect is suboptimal, then administer 40 mg IV 10 minutes later
If the effects is still suboptimal, administer 80 mg IV 10 minutes later for two additional doses
Maximum dosage of 300 mg
May see bradycardia and hypoglycemia in the fetus/newborn

38. Important Notes
A respiratory rate > 24/min indicates respiratory dysfunction.
If a woman cannot say more than one word at a time, she is in respiratory failure.
A heart rate > 120 in a pregnant woman needs attention.
A heart rate > 140 in a pregnant woman is a pre-cardiac arrest heart rate.
Pregnant women can remain coherent right up until they code.
Magnesium sulfate may prevent seizures but does not effect disease progression

39. Nursing Care Diligent assessment of Blood pressure and heart rate
Respiratory rate [breath sounds]/dyspnea
Deep tendon reflexes/clonus
Level of consciousness/orientation X 3/slurred speech
Edema [presence and extent]
Intake and output
Signs of bleeding
Visual alterations
Epigastric pain/nausea/vomiting
Headache

40. Nursing Care Monitor Create a calm, minimally stimulating environment
Lab values
Uterine contractions
Fetal heart rate patterns
Effects of pharmacologic therapies [desired and untoward]
Create a calm, minimally stimulating environment
Provide emotional support and information to client/family
The woman may look completely normal, yet be critically ill
Treatment makes the woman feel worse

41. Postpartum: Maternal Care
Magnesium sulfate infusion 24 hours postpartum if required antenatally
New onset preeclampsia-eclampsia can develop in first 48 hours postpartum
HELLP syndrome may develop postpartum
Persistent elevated BP > 150/100 requires antihypertensive therapy
BP may be labile requiring antihypertensive therapy
Discharge planning: careful follow up, continue BP monitoring if on antihypertensives, pregnancy planning and contraception, when to call provider

42. Postpartum: Newborn Care
Observe for signs of magnesium toxicity for hours if maternal magnesium administered close to birth
Increased risk associated with maternal magnesium sulfate:
May observe hypotonia and lethargy for up to 48 hours
Higher risk hypoglycemia and hypocalemia

43. Resources The key resource was the AWHONN educational webinar:
Enhancing the Management of Pre-eclampsia
Presented by Judith Poole, PhD, MBA/MHA, RNC-OB
[One of the best benefits of belonging to your nursing specialty professional organization is access to evidence based practice via many different modalities.]
Both the National Institutes of Health [NIH] and the American College of Obstetricians and Gynecologists [ACOG] have working groups and resources on hypertension in pregnancy.