Gestational Hypertension Gestational Hypertension

Peggy Foster, RN, MSNPeggy Foster, RN, MSN

Sandy Warner, RNC- OB, MSNSandy Warner, RNC- OB, MSN

INCIDENCE and IMPACTINCIDENCE and IMPACT

Complicates 6-10% of all Pregnancies in U.S.Complicates 6-10% of all Pregnancies in U.S. 3-8 % of Healthy Primiparas3-8 % of Healthy Primiparas 18% of Multiparas with prior Hx 18% of Multiparas with prior Hx

1: 2,000-2,500 Pregnancies1: 2,000-2,500 Pregnancies Mortality estimated 3-5% of those with Mortality estimated 3-5% of those with

seizuresseizures The Preeclampsia Foundation (2007) The Preeclampsia Foundation (2007)

estimates the annual cost of Preeclampsia in estimates the annual cost of Preeclampsia in the United States is $7 Billion the United States is $7 Billion

SYMPTOMS—3 ClassicSYMPTOMS—3 Classic

High Blood PressureHigh Blood Pressure ProteinuriaProteinuria EdemaEdema

OTHER ASSOCIATED OTHER ASSOCIATED SYMPTOMSSYMPTOMS

Neurological symptoms (Cerebral or Visual Neurological symptoms (Cerebral or Visual Disturbances):Disturbances):

• Hyper-reflexia—Brisk reflexes (+/- Clonus)Hyper-reflexia—Brisk reflexes (+/- Clonus)• HeadachesHeadaches• Blurring of vision—Double VisionBlurring of vision—Double Vision• ScotomaScotoma

Epigastric or RUQ painEpigastric or RUQ pain Pulmonary edema or cyanosisPulmonary edema or cyanosis Impaired liver function of unclear etiologyImpaired liver function of unclear etiology ThrombocytopeniaThrombocytopenia

Classification of Hypertensive Classification of Hypertensive States of PregnancyStates of Pregnancy

Gestational hypertensionGestational hypertension development of mild HTN during pregnancydevelopment of mild HTN during pregnancy

• Previous normal B/P, no proteinuria and labs WNLPrevious normal B/P, no proteinuria and labs WNL

PreeclampsiaPreeclampsia Development of HTN and proteinuria after 20 Development of HTN and proteinuria after 20

wks pregnancywks pregnancy• Previous normal B/PPrevious normal B/P• With molar pg, can develop before 20 wksWith molar pg, can develop before 20 wks

EclampsiaEclampsia• Seizures in preeclamptic ptSeizures in preeclamptic pt

Classification continuedClassification continued

Chronic HTNChronic HTN HTN occurring before pregnancy or B/P > 140/90 or HTN occurring before pregnancy or B/P > 140/90 or

greater before 20 wks on 2 occasions, 6 hrs apartgreater before 20 wks on 2 occasions, 6 hrs apart

Preeclampsia superimposed on chronic HTNPreeclampsia superimposed on chronic HTN Development of preeclampsia or eclampsiaDevelopment of preeclampsia or eclampsia

In pt with chronic HTNIn pt with chronic HTN

National High Blood Pressure Education Program Working Group (2000)National High Blood Pressure Education Program Working Group (2000)

DescriptionDescription

Preeclampsia—Pts with ↑ BP with Proteinuria, edema, or bothPreeclampsia—Pts with ↑ BP with Proteinuria, edema, or both Further classified as Mild or Severe to reflect the extent of end-organ damageFurther classified as Mild or Severe to reflect the extent of end-organ damage Severe Preeclampsia Criteria with 1 or more of:Severe Preeclampsia Criteria with 1 or more of:

BP BP ≥≥160 mm Hg systolic of 160 mm Hg systolic of ≥≥ 110 diastolic on 2 occasions 6 hours apart 110 diastolic on 2 occasions 6 hours apart with the patient at bedrest with the patient at bedrest

Proteinuria > 5 gms in 24 hours or 3+ to 4+ on qualitative assessmentProteinuria > 5 gms in 24 hours or 3+ to 4+ on qualitative assessment Oliguria Oliguria ≤≤ 400 ml in 24 hours400 ml in 24 hours Cerebral or visual disturbancesCerebral or visual disturbances Epigastric or RUQ pain, N&VEpigastric or RUQ pain, N&V Pulmonary edema or cyanosisPulmonary edema or cyanosis Impaired liver function of unclear etiologyImpaired liver function of unclear etiology ThrombocytopeniaThrombocytopenia

Eclampsia—those with ↑ BP, seizures, +/- ComaEclampsia—those with ↑ BP, seizures, +/- Coma NOTE: Eclampsia is a consequence of severe pre-eclampsia—however it is not NOTE: Eclampsia is a consequence of severe pre-eclampsia—however it is not

always preceded by always preceded by ↑ ↑ BP, significant proteinuria or edemaBP, significant proteinuria or edema

Other considerations—TimewiseOther considerations—Timewise

Gestational Hypertension usually occurs in Gestational Hypertension usually occurs in the 3the 3rdrd Trimester Trimester

Preeclampsia occurs ≥ 20 weeks gestationPreeclampsia occurs ≥ 20 weeks gestation Chronic Hypertension when Chronic Hypertension when ↑↑ BP is BP is

present <20 weeks &/or persists > 42 present <20 weeks &/or persists > 42 weeks PPweeks PP

HYPERTENSIVE DISORDERS OF HYPERTENSIVE DISORDERS OF PREGNANCY—PREGNANCY—Sibai, 2002Sibai, 2002

CLINICAL FINDINGS CHRONIC HYPERTENSION

GESTATIONAL HYPERTENSION

PREECLAMPSIA

Time of Onset of Hypertension

< 20 weeks Usually in 3rd Trimester

≥ 20 weeks

Degree of Hypertension

Mild or severe Mild Mild or severe

Proteinuria Absent Absent Usually present

Hemoconcentration Absent Absent Severe Disease

Thrombocytopenia Absent Absent Severe Disease

Hepatic Dysfunction Absent Absent Severe Disease

RISK FACTORSRISK FACTORS Pre-existing hypertension (high blood pressure)Pre-existing hypertension (high blood pressure) Kidney diseaseKidney disease DiabetesDiabetes Mother's age < 20 or >40Mother's age < 20 or >40 Multiple Gestation (twins, triplets)Multiple Gestation (twins, triplets) Molar PregnancyMolar Pregnancy 11stst Pregnancy (or 1 Pregnancy (or 1stst pregnancy with a given pregnancy with a given

Partner) (Note: Lower risk if had Ab with that Partner) (Note: Lower risk if had Ab with that partner)partner)

Genetic History (Daughters of Preeclamptic Genetic History (Daughters of Preeclamptic Mothers, and also Men born to Preeclamptic Mothers, and also Men born to Preeclamptic mothers who then father children) mothers who then father children) (Lachmeijer, 2002 (Lachmeijer, 2002 and Esplin, 2001 and Skjaerven, 2005)and Esplin, 2001 and Skjaerven, 2005) Over 70 different genes associated Over 70 different genes associated (Entrez, 2007)(Entrez, 2007)

Other Risk FactorsOther Risk Factors

ObesityObesity Preeclampsia in Previous PregnancyPreeclampsia in Previous Pregnancy Poor Outcome in Previous PregnancyPoor Outcome in Previous Pregnancy Pre-existing Medical or Genetic ConditionsPre-existing Medical or Genetic Conditions IDDMIDDM Thrombophilias (Anti-phospholipid/Clotting Thrombophilias (Anti-phospholipid/Clotting

DisordersDisorders Factor 5 LeidenFactor 5 Leiden

CAUSE AND POSSIBLE CAUSESCAUSE AND POSSIBLE CAUSES The Etiology is unknown (Sibai, 2005)The Etiology is unknown (Sibai, 2005) Originally called Toxemia, because thought that there was Originally called Toxemia, because thought that there was

a “Toxin” which caused Preeclampsiaa “Toxin” which caused Preeclampsia Emerging consensus suggests that inadequate trophoblast Emerging consensus suggests that inadequate trophoblast

invasion fails to remodel the uterine spiral arteries. This invasion fails to remodel the uterine spiral arteries. This shallow implantation compromises placental blood flow--shallow implantation compromises placental blood flow--leading to placental ischemia and necrosis—Microscopic leading to placental ischemia and necrosis—Microscopic debris from the necrotized placenta may circulate in debris from the necrotized placenta may circulate in mother’s blood stream—leading to endothelial dysfunction, mother’s blood stream—leading to endothelial dysfunction, ↓↓ ing perfusion to maternal organs—resulting in ing perfusion to maternal organs—resulting in vasoconstriction and micro-thrombi evidenced by severe vasoconstriction and micro-thrombi evidenced by severe end-organ pathology end-organ pathology (Khong,1986; Smarason,1993; Roberts,1989, (Khong,1986; Smarason,1993; Roberts,1989, Levine & Karumanchi, 2005)Levine & Karumanchi, 2005)

CAUSE AND POSSIBLE CAUSESCAUSE AND POSSIBLE CAUSES

The recent completion of Human Genome The recent completion of Human Genome project may lead to Dx by Microarray project may lead to Dx by Microarray analysis (Founds, et al. JOGNN, Mar/April, analysis (Founds, et al. JOGNN, Mar/April, 2008)2008)

PATHOPHYSIOLOGYPATHOPHYSIOLOGY

Vasospasm and endothelial damage first Vasospasm and endothelial damage first described in 1918described in 1918

Vasospasm causes Vasospasm causes ↑ ↑ BP—restriction of BP—restriction of blood flow associated with endothelial cell blood flow associated with endothelial cell damage which stimulates platelet and damage which stimulates platelet and fibrinogen utilizationfibrinogen utilization

Researchers unsure if vasospasm causes Researchers unsure if vasospasm causes vessel damage or vise versavessel damage or vise versa

Pathophysiology con’tPathophysiology con’t

Also a change in sensitivity to vasopressors Also a change in sensitivity to vasopressors (angiotension and norepinephrine)(angiotension and norepinephrine) Linked to 2 prostaglandins (prostacylin > Linked to 2 prostaglandins (prostacylin >

thromboxane)thromboxane)• Both produced by placentaBoth produced by placenta• Placenta has ineffective trophoblastic invasion, resulting in Placenta has ineffective trophoblastic invasion, resulting in

decrease placental blood supply to fetus. This decreased decrease placental blood supply to fetus. This decreased blood supply then produces chemical factors which enter the blood supply then produces chemical factors which enter the maternal circulation and affect the entire vasculature of the maternal circulation and affect the entire vasculature of the mom.mom.

COMPLICATIONSCOMPLICATIONS Cardio-VascularCardio-Vascular

Stroke or Cerebral hemorrhageStroke or Cerebral hemorrhage Renal insufficiency or failure Renal insufficiency or failure

↓ ↓ GFR, ↓ Uric acid clearance, and Na retentionGFR, ↓ Uric acid clearance, and Na retention Glomerular damage results in ↑ ProteinuriaGlomerular damage results in ↑ Proteinuria

Hepatic damage caused by vasospasm and Hepatic damage caused by vasospasm and ischemia may lead to Liver rupture, ischemia may lead to Liver rupture, hemorrhage, and necrosis hemorrhage, and necrosis ALT—formerly known as SGPT—released when liver ALT—formerly known as SGPT—released when liver

is damagedis damaged AST—formerly known as SGOT—released when liver AST—formerly known as SGOT—released when liver

and heart muscle and kidneys are damagedand heart muscle and kidneys are damaged Symptoms RUQ pain, Nausea/VomitingSymptoms RUQ pain, Nausea/Vomiting

COMPLICATIONS cont’dCOMPLICATIONS cont’d

NeurologicNeurologic Visual disturbances—blurring of vision, spots in visual Visual disturbances—blurring of vision, spots in visual

fields, temporary blindness—probably caused by fields, temporary blindness—probably caused by vaso-spasm of retinal artery, can also have retinal vaso-spasm of retinal artery, can also have retinal detachmentdetachment

Seizures—which may result in coma or deathSeizures—which may result in coma or death

Hematologic—HELLPHematologic—HELLP Respiratory Failure—related to Pulmonary Respiratory Failure—related to Pulmonary

EdemaEdema Maternal and/or fetal deathMaternal and/or fetal death

Uteroplacental complicationsUteroplacental complications

IUGRIUGR OligohydramniosOligohydramnios Fetal HypoxiaFetal Hypoxia Category II or III tracingCategory II or III tracing Placental AbruptionPlacental Abruption Increased, absent or reverse doppler flow Increased, absent or reverse doppler flow

studiesstudies Low BPP score < 6Low BPP score < 6 Fetal deathFetal death

HELLP SYNDROMEHELLP SYNDROME H—HemolysisH—Hemolysis EL—Elevated liver enzymesEL—Elevated liver enzymes LP—Low PlateletsLP—Low Platelets

Occurs 15-20% patients with Severe Pre-eclampsia Occurs 15-20% patients with Severe Pre-eclampsia (Sibai, 1993)(Sibai, 1993)

Pathophysiology—Vasospasms cause endothelial Pathophysiology—Vasospasms cause endothelial damage to liver—leads to platelet aggregation, damage to liver—leads to platelet aggregation, adherence and fibrin deposits—results in hemorrhage, adherence and fibrin deposits—results in hemorrhage, rupture of hepatic vessels and necrosis—may lead to rupture of hepatic vessels and necrosis—may lead to hepatic infarction and rupturehepatic infarction and rupture

Sx’s liver rupture—sudden RUQ and upper abdominal Sx’s liver rupture—sudden RUQ and upper abdominal pain, shoulder pain, nausea and vomitingpain, shoulder pain, nausea and vomiting

A ruptured liver requires immediate surgical intervention, A ruptured liver requires immediate surgical intervention, but may still result in ~but may still result in ~ 3030% % mortalitymortality

EXAMS AND TESTSEXAMS AND TESTS 24 Hour urine for Protein and Creatinine Clearance24 Hour urine for Protein and Creatinine Clearance Alkaline Phosphatase --Normal U/L (30 to 120)Alkaline Phosphatase --Normal U/L (30 to 120) LDH Lactate Dehydrogenase U/L (100-225) LDH Lactate Dehydrogenase U/L (100-225) AST (Aspartate aminotransferase) (SGOT) U/L (5 to 45)AST (Aspartate aminotransferase) (SGOT) U/L (5 to 45) ALT (Alanine aminotransferase) (SGPT) U/L (5 to 45)ALT (Alanine aminotransferase) (SGPT) U/L (5 to 45) Albumin g/L (38-55)Albumin g/L (38-55) Uric Acid (less than 5)Uric Acid (less than 5) CBCCBC Clotting StudiesClotting Studies

Platelets (> 150,000)Platelets (> 150,000) Prothrombin Time Seconds (11 to 13.5)Prothrombin Time Seconds (11 to 13.5) Partial Thromboplastin time (25-39 secs)Partial Thromboplastin time (25-39 secs) Fibrinogen (150-300 mg/dL)Fibrinogen (150-300 mg/dL)

Blood Component TherapyBlood Component Therapy

ComponentComponent ContentContent VolumeVolume GoalGoalPackedPacked

RBC’sRBC’s

RBC RBC

1 unit 1 unit ↑ ↑ Hct 3Hct 3%%

200-275 mL200-275 mL Hct 30%Hct 30%

FFPFFP Clotting factorsClotting factors

1 unit 1 unit ↑ ↑ Fibrinogen 10 Fibrinogen 10 mg/dLmg/dL

180-200 mL180-200 mL Replace clotting Replace clotting factors factors Fibrinogen > Fibrinogen > 100mg/dL100mg/dL

CryoprecipitateCryoprecipitate Clotting factorsClotting factors

1 unit 1 unit ↑ ↑ Fibrinogen 10 Fibrinogen 10 mg/dLmg/dL

15-20 mL15-20 mL Replace clotting Replace clotting factors factors Fibrinogen > Fibrinogen > 100mg/dL100mg/dL

Platelet Platelet concentrationconcentration

Platelets 1 unit Platelets 1 unit ↑ count ↑ count 50,00050,000

50 mL50 mL Platelet count Platelet count 50,000 or >50,000 or >

Lab Values in DICLab Values in DIC

Platelets Platelets ↓↓ (150,000) (150,000) Fibrinogen Fibrinogen ↓↓ Protime ProlongedProtime Prolonged PTT ProlongedPTT Prolonged Anti-thrombin III Anti-thrombin III ↓↓ FDP (Fibrin Degradation Products or (FSP’s—FDP (Fibrin Degradation Products or (FSP’s—

Fibrin Split Products) Greater than 40Fibrin Split Products) Greater than 40 D-DimerD-Dimer ↑ ↑

TREATMENTTREATMENT CURE: DELIVERYCURE: DELIVERY Mode of delivery is patient-specific and Mode of delivery is patient-specific and

depends on maternal condition and fetal depends on maternal condition and fetal statusstatus

Steroids to ↑ fetal lung maturitySteroids to ↑ fetal lung maturity Seizure Prophylaxis:Seizure Prophylaxis:

Magnesium Sulfate 4-6 gm loading dose Magnesium Sulfate 4-6 gm loading dose (over 15-30 minutes)(over 15-30 minutes)

Maintenance—continuous infusion 1-3 Maintenance—continuous infusion 1-3 gm/hourgm/hour

MAGNESIUM SULFATE MAGNESIUM SULFATE CONSIDERATIONSCONSIDERATIONS

Let patient know treatment effects and possible Let patient know treatment effects and possible sensations: flushing, sluggish thoughts, etcsensations: flushing, sluggish thoughts, etc

Irritating to Vein—use large veinIrritating to Vein—use large vein Metabolized in Kidney, so must verify adequate Urinary Metabolized in Kidney, so must verify adequate Urinary

output (≥ 30 ml/hour) Patient may need Foley Catheteroutput (≥ 30 ml/hour) Patient may need Foley Catheter Therapeutic range 4-8 mg/dLTherapeutic range 4-8 mg/dL

Loss of DTR’s 9-12 mg/dLLoss of DTR’s 9-12 mg/dL Respiratory arrest > 15 mg/dLRespiratory arrest > 15 mg/dL Cardiac arrest >25-30 mg/dLCardiac arrest >25-30 mg/dL

Calcium Gluconate is AntidoteCalcium Gluconate is Antidote 10 mL of 10% solution given IV slowly over 1-3 minutes until 10 mL of 10% solution given IV slowly over 1-3 minutes until

signs of overdose are reversedsigns of overdose are reversed

Magnesium Sulfate considerationsMagnesium Sulfate considerations Anticipate Cesarean Delivery—Make sure Anticipate Cesarean Delivery—Make sure

consents signed/All personnel informedconsents signed/All personnel informed Relaxes smooth muscleRelaxes smooth muscle Verify Respirations are > 12Verify Respirations are > 12 Relaxes uterus and patients often need Relaxes uterus and patients often need

Oxytocin supplementation for laborOxytocin supplementation for labor Relaxes smooth muscle in Vessels and may Relaxes smooth muscle in Vessels and may

↓ ↓ BP—but is given to BP—but is given to ↓ CNS Irritability↓ CNS Irritability Relaxes digestive system—after delivery may Relaxes digestive system—after delivery may

see constipation see constipation Babies may be lethargic with decreased suck Babies may be lethargic with decreased suck

and slowed GI motilityand slowed GI motility

TREATMENTTREATMENT Treat BP—challengingTreat BP—challenging

Pt may be Volume depleted, volume adequate, or volume Pt may be Volume depleted, volume adequate, or volume overloaded. . .Usually not give Diureticsoverloaded. . .Usually not give Diuretics

Consider too the Placenta is used to working with Consider too the Placenta is used to working with ↑ ↑ pressures—pressures—if decrease BP too much may see Late decelerationsif decrease BP too much may see Late decelerations

Antihypertensive AgentsAntihypertensive Agents Apresoline (Hydralazine)Apresoline (Hydralazine) LabetololLabetolol Calcium channel blocker (Nifedipine)Calcium channel blocker (Nifedipine) Not ACE inhibitors—associated with fetal anomalies and Not ACE inhibitors—associated with fetal anomalies and

immune system dysfunction immune system dysfunction Correct Blood DiscrepanciesCorrect Blood Discrepancies

PlateletsPlatelets FFPFFP Whole BloodWhole Blood

OTHER CONSIDERATIONSOTHER CONSIDERATIONS Watch for changes in Fetal Status—since is a Watch for changes in Fetal Status—since is a

chronic condition affecting placenta—often chronic condition affecting placenta—often associated with Late decelerations and associated with Late decelerations and Metabolic acidosisMetabolic acidosis

Watch patient for Pulmonary EdemaWatch patient for Pulmonary Edema Oxygenation Oxygenation ACCURATE Intake and Output ACCURATE Intake and Output NPO—may need C/SNPO—may need C/S Minimize stimulation to patient and sensoriumMinimize stimulation to patient and sensorium

Limited visitorsLimited visitors Dimmed lights/sounds/ odorsDimmed lights/sounds/ odors Seizure observations and precautionsSeizure observations and precautions

Home care for preeclampsiaHome care for preeclampsia

Fetal Movement assessment 2 x/dayFetal Movement assessment 2 x/day Bi weekly NSTBi weekly NST Modified bedrestModified bedrest Daily monitoring of blood pressure, weight, Daily monitoring of blood pressure, weight,

urine proteinurine protein Consider anti-hypertensive med (Aldomet, Consider anti-hypertensive med (Aldomet,

Labetalol)Labetalol) Anticipatory guidance/pt educationAnticipatory guidance/pt education

Nursing care for PreeclampsiaNursing care for Preeclampsia

Lateral bedrestLateral bedrest Daily lab workDaily lab work Daily weightDaily weight I and OI and O Assess for headache, visual changes, epigastric Assess for headache, visual changes, epigastric

pain, reflexes, edema, lung auscultationpain, reflexes, edema, lung auscultation Vitals q 4 hoursVitals q 4 hours Psychosocial needsPsychosocial needs

PREVENTION—PREVENTION—Research--no benefit to dateResearch--no benefit to date

↑ ↑ Protein DietProtein Diet ↑ ↑ CalciumCalcium ↑ ↑ MagnesiumMagnesium Fish and evening Primrose oilFish and evening Primrose oil Antihypertensive drugs ( with Diuretics)Antihypertensive drugs ( with Diuretics) Aspirin Therapy—had Aspirin Therapy—had ↑ ↑ rates of Abruptio rates of Abruptio

PlacentaPlacenta ↓ ↓ Sodium DietSodium Diet ↑ ↑ HeparinHeparin ↑ ↑ Vitamins E and CVitamins E and C Folic acid—still being researchedFolic acid—still being researched

OTHER POSSIBLE TREATMENTOTHER POSSIBLE TREATMENT

Outside U.S. -- instead of Magnesium Outside U.S. -- instead of Magnesium Sulfate, other centers use:Sulfate, other centers use: Benzodiazepines (i.e. Librium, Xanax, Valium, Benzodiazepines (i.e. Librium, Xanax, Valium,

Halcion, Restoril, Ativan)Halcion, Restoril, Ativan) Phenytoin (Dilantin)Phenytoin (Dilantin)