Hypertensive Disorders With Pregnancy

Hypertensive Disorders With Pregnancy

Amr Nadim, MD Professor of Obstetrics & Gynecology

Ain Shams Maternity and Women’s Hospital

[[email protected]]

• C.G. is a 39 year old married white female gravida 2, para 0, with one spontaneous abortion who presented for prenatal care at 14 weeks gestation. Blood pressure at that time was 130/80. The patient had no significant medical history and her gynecologic history was significant only for oral contraceptive use several years ago. The patient noted that her physician stopped the birth control pills after only two cycles, but the patient was not told why.

• The pregnancy had been unremarkable until approximately one month ago when the patient noted increased swelling of her hands and feet. A 6 Kg. weight gain in two weeks time was noted. Blood pressure at that time was 124/78. There was no urinary protein. On the day prior to admission, at 28 weeks, the patient presented with a blood pressure of 160/98 and had been sent home to bedrest with instructions to take a single baby aspirin daily. On the day following, the patient was noted at home to have a persistent blood pressure of 180/100.

Avant propos…

• Complicates 7-10% of pregnancies

– 70% Preeclampsia-eclampsia

– 30% Chronic hypertension

– Eclampsia 0.05% incidence

• 20% of Maternal Deaths

• Cause of 10% of Preterm birth

• Etiology unknown

• Young female 3 fold increased risk

• African American 2 fold increased risk

• Multifetal pregnancies

– Twins

– Triplets

• Hypertension

• Diabetes Mellitus

• Renal Disease

• Collagen Vascular Disease

Hypertension during Pregnancy: Classification

• Pregnancy-induced hypertension– Hypertension without proteinuria/edema– Preeclampsia

• mild• severe

– Eclampsia• Coincidental HTN: preexisting or

persistent• Pregnancy-aggravated HTN

– superimposed preeclampsia– superimposed eclampsia

• Transient HTN: occurs in 3rd trimester, mild

Preeclampsia: Definition

• Hypertension– > 140/90– relative no longer considered diagnostic

• Proteinuria– > 300 mg/24 hours or 1or 2+ on urine

dipstick– may occur late

• Edema (non-dependent)– so common & difficult to quantify it is rarely

evoked to make or refute the diagnosis

Criteria for Severe Preeclampsia

• SBP > 160 mm Hg• DBP > 110 mm Hg• Proteinuria > 5 g/24

hr. or 3-4+ on dipstick

• Oliguria < 500 cc/24 hr.

serum creatinine• Pulmonary edema or

cyanosis

• CNS symptoms (HA, vision changes)

• Abdominal (RUQ) pain• Any feature of HELLP

– hemolysis liver enzymes– thrombocytopenia

• IUGR or oligohydramnios

Preeclampsia: Risk Factors• Nulliparity (or, more correctly, primipaternity)• Chronic renal disease• Angiotensinogen gene T235• Chronic hypertension• Antiphospholipid antibody syndrome• Multiple gestation• Family or personal history of preeclampsia• Age > 40 years• African-American race• Diabetes mellitus

Etiology and Prevention

• Etiology is unknown.• Many theories:

– genetic– immunologic– dietary deficiency (calcium, magnesium,

zinc)• supplementation has not proven effective

– placental source (ischemia)

Etiology and Prevention• A major underlying defect is a relative

deficiency of prostacyclin vs. thromboxane• Normally (non-preeclamptic) there is an 8-10

fold in prostacyclin with a smaller in thromboxane– prostacyclin salutatory effects dominate

• vasodilation, platelet aggregation, uterine tone

• In preeclampsia, thromboxane’s effects dominate thromboxane (from platelets, placenta) prostacyclin (from endothelium, placenta)

Preeclampsia Prophylaxis: Aspirin

• Aspirin has been extensively studied as a targeted therapy to thromboxane production

• CLASP study, A multicenter RCT[CLASP Collaborative Group, Lancet 1994;343:619-29]

– 9364 women, risk factors for PIH or IUGR or who had PIH or IUGR

– 60 mg ASA daily vs. placebo– Small reduction (12%) in occurrence of PIH– Small reduction in preterm deliveries: 20 vs

22%– No difference in neonatal outcome

Preeclampsia Prophylaxis: Aspirin

• NIH study of high-risk patients, RCT, 60 mg aspirin daily vs. placebo [Caritis, et al., N Engl J Med 1998;338:701-5]

– pre-gestational DM (471 patients)– chronic hypertension (774 patients)– multifetal gestations (688 patients)– prior history of preeclampsia (606 patients)

• No reduction in development of preeclampsia in any subgroup or groups in aggregate

• No difference in perinatal death, preterm delivery, IUGR, maternal or fetal hemorrhagic complications

Preeclampsia: Mechanism

• At this time the most widely accepted proposed mechanism for preeclampsia is:

Global Endothelial Cell Dysfunction

• Endothelial cell dysfunction is just one manifestation of a broader intravascular inflammatory response – present in normal pregnancy– excessive in preeclampsia– Proposed source of inflammatory stimulus:

placenta

Pathophysiology

Of importance, and distinguishing preeclampsia

from chronic or gestational hypertension, is

that preeclampsia is more than hypertension; it

is a systemic syndrome, and several of its

“non-hypertensive” complications can be life-

threatening when blood pressure elevations

are quite mild.

Pathophysiology: Cardiovascular

• In severe preeclampsia, typically hyperdynamic with normal-high CO, normal-mod. high SVR, and normal PCWP and CVP.

• Despite normal filling pressures, intravascular fluid volume is reduced (30-40% in severe PIH)

• Variations in presentation depending on prior treatment and severity and duration of disease

• Total body water is increased (generalized edema)

Pathophysiology: Cardiovascular

• Preeclamptic patients are prone to develop pulmonary edema due to reduced colloid oncotic pressure (COP), which falls further postpartum:

Colloid oncotic pressure:Antepartum Postpartum

Normal pregnancy: 22 mm Hg 17 mm HgPreeclampsia: 18 mm Hg 14 mm Hg

Pathophysiology

• Respiratory:– Airway is edematous; use smaller ET tube (6.5) risk of pulmonary edema; 70% postpartum

• Renal:– Renal blood flow & GFR are decreased– Renal failure due to plasma volume or renal

artery vasospasm– Proteinuria due to glomerulopathy

• glomerular capillary endothelial swelling w/subendothelial protein deposits

– Renal function recovers quickly postpartum

Pathophysiology: Hepatic

• RUQ pain is a serious complaint– warrants imaging, especially when

accompanied by liver enzymes– caused by liver swelling, periportal

hemorrhage, subcapsular hematoma, hepatic rupture (30% mortality)

• HELLP syndrome occurs in ~ 20% of severe preeclamptics.

Pathophysiology• Coagulation:

– Generally hypercoagulable with evidence of platelet activation and increased fibrinolysis

– Thrombocytopenia is common, but fewer than 10% have platelet count < 100,000

– DIC may occur, • Acutely esp. with placental abruption

• Neurologic:– Symptoms: headache, visual changes,

seizures– Hyperreflexia is usually present– Eclamptic seizures may occur even w/out BP

• Possible causes: hypertensive encephalopathy, cerebral edema, thrombosis, hemorrhage, vasospasm

Hypertension during Pregnancy: Classification

• Pregnancy-induced hypertension– Hypertension without proteinuria/edema– Preeclampsia

• mild• severe

– Eclampsia• Coincidental HTN: preexisting or

persistent• Pregnancy-aggravated HTN

– superimposed preeclampsia– superimposed eclampsia

• Transient HTN: occurs in 3rd trimester, mild

Classification

• Chronic hypertension

• Preeclampsia-eclampsia

• Preeclampsia Superimposed upon chronic hypertension or Renal Disease

• Gestational hypertension (only during pregnancy)

• Transient hypertension (only after pregnancy)

Chronic Hypertension

Defined as hypertension diagnosed

• Before pregnancy• Before the 20th week of

gestation• During pregnancy and not

resolved postpartum

Gestational Hypertension

• Gestational Hypertension:–Systolic >140–Diastolic>90–No Proteinurea–25% Develop Pre-eclampsia

Gestational HypertensionDiagnosis of gestational hypertension:• Detected for first time after midpregnancy• No proteinuria• Only until a more specific diagnosis can be

assigned postpartum

If:If:• BP returns to normal by 12 weeks postpartum,

diagnosis is transient hypertension. • BP remains high postpartum, diagnosis is

chronic hypertension.• Proteinurea develops Superimposed

Preeclampsia is diagnosed (25% incidence)

Preeclampsia-Eclampsia

• Occurs after 20th week (earlier with

trophoblastic disease)

• Increased BP (gestational BP elevation)

with proteinuria

• ‘LL’ Edema is NOT part of this definition

Diagnosis of Preeclampsia-Eclampsia

• Gestational Hypertension:–Systolic >140–Diastolic>90

• Proteinuria is defined as urinary excretion– 0.3 g protein or greater in a 24-hour– +2 or greater on urine dip specimen

Blood Pressure Measurement

How would you measure the Blood Pressure for a pregnant lady?


• Blood pressure • Measure blood pressure

– in the sitting position, – with the cuff at the level of the heart. – Inferior vena caval compression by the gravid

uterus while the patient is supine can alter readings substantially, leading to an underestimation of the blood pressure.

– Blood pressures measured in the left lateral position similarly may yield falsely low values if the blood pressure is measured in the higher arm and the cuff is not maintained at heart level.

• Allow women to sit quietly for 5-10 minutes before measuring the blood pressure.

Blood Pressure Assessment:Patient preparation and posture

Standardized technique:

Patient1. No caffeine in the preceding hour.2. No smoking or nicotine in the preceding 15-30 minutes.3. No use of substances containing adrenergic stimulants

such as phenylephrine or pseudoephedrine (may be present in nasal decongestants or ophthalmic drops).

4. Bladder and bowel comfortable.5. Quiet environment. Comfortable room temperature.6. No tight clothing on arm or forearm.7. No acute anxiety, stress or pain.8. Patient should stay silent prior and during the

procedure.



Posture

• The patient should be calmly seated for at least 5 minutes, with his or her back well supported and arm supported at the level of the heart. His or her feet should touch the floor and legs should not be crossed.

• The patient should be instructed not to talk prior and during the procedure.

Recommended Technique for Measuring Blood

Pressure• Standardized

technique:

– Use a mercury manometer or a recently calibrated aneroid or a validated electronic device.

– Aneroid devices should only be used if there is an established calibration check every 6-12 months.

Recommended Technique for Measuring Blood Pressure

AAMI=Association for the Advancement of Medical Instrumentation;BHS=British Hypertension Society; IP: International Protocol.

Office

Home / Self

• Electronic oscillometric devices:– Use a validated electronic

device according to BHS, AAMI or IP standards.

– For self blood pressure measurement devices, a logo on the packaging ensures that this type of device and model meets the international standards for accurate blood pressure measurement.


(cont.)–Select a–cuff with the appropriate size

Cuff size

Arm circumference (cm) Size of Cuff (cm)

From 18 to 26 9 x 18 (child)

From 26 to 3312 x 23 (standard adult model)

From 33 to 41 15 x 33 (large, obese)

More than 4118 x 36 (extra large, obese)

Recommended Technique for Measuring Blood Pressure (cont.)

– Locate brachial and radial pulse

– Position cuff at the heart level

– Arm should be supported


– To exclude possibility of auscultatory gap, increase cuff pressure rapidly to 20-30 mmHg above level of disappearance of radial pulse

– Place stethoscope over the brachial artery


– Drop pressure by 2 mmHg / sec• Appearance of sound (phase I

Korotkoff) = systolic pressure

– Record measurement

– Drop pressure by 2 mmHg / beat

• Disappearance of sound (phase V Korotkoff) = diastolic pressure

– Record measurement

– Take 2 blood pressure measurements, 1 minute apart


(cont.)Systolic BP

Diastolic BP

Possible readings:184 / 100136 / 100184 / 86 = correct136 / 86

200

180

160

140

120

100

80

60

40

20

0

No sound

Clear sound

Muffled sound

Muffled sound

No sound

Phase 1

Phase 3

Phase 4

Phase 5

Muffling Phase 2Auscultato

ry gapNo sound

mm Hg

Korotkoff sounds


• Blood pressure– Record Korotkoff sounds I (the first sound) and V

(the disappearance of sound) to denote the systolic blood pressure (SPB) and DPB, respectively.

– In about 5% of women, an exaggerated gap exists between the fourth (muffling) and fifth (disappearance) Korotkoff sounds, with the fifth sound approaching zero. In this setting, record both the fourth and fifth sounds (eg, 120/80/40 with sound I = 120, sound IV = 80, sound V = 40).



• For initial readings, take the blood pressure in both arms and subsequently measure it in the arm with the highest reading.

• Thereafter, take two measurements on the side where BP is highest.


Record the blood pressure to the closest 2 mmHg on the manometer

as well as the arm used

and whether the patient was supine, sitting or standing.


• Avoid digit preference for five (5) or zeros (0) by not rounding up or down.

• Record the heart rate.


• The seated blood pressure is used to determine and monitor treatment decisions.

• The standing blood pressure is used to test for postural hypotension, if present, which may modify the treatment.


Standing position

For patients over age 65, diabetics and patients being treated with antihypertensives, check if there are postural changes while taking blood pressure reading, i.e. after one to five minutes in the standing position and under circumstances when the patients complains of symptoms suggestive of hypotension.

Classification of Preeclampsia-Eclampsia

•Mild Pre-eclampsia•Severe Pre-eclampsia


• Criteria for Severe Preeclampsia (one or more)– Blood Pressure: >160 systolic, >110

diastolic– Proteinurea: >5gm in 24 hours, over 3+

urine dip– Oligurea: less than 400ml in 24 hours– CNS: Visual changes, headache,

scotomata, mental status change– Pulmonary Edema– Epigastric or RUQ Pain: Usually indicates

liver involvement


• Criteria for Severe Preeclampsia (one or more)– Impaired Liver Function tests

– Thrombocytopenia: <100,000

– Intrauterine Growth Restriction: With or without abnormal doppler assessment

– Oligohydramnios

Classification of Preeclampsia Superimposed Upon Chronic Hypertension

• Hypertension and no proteinuria < 20 weeks:

New-onset proteinuria after 20 weeks

• Hypertension and proteinuria < 20 weeks:

– Sudden increase in proteinuria

– Sudden increase in BP in women whose hypertension was well controlled

– Thrombocytopenia (platelet count <100,000 cells/mm3)

– Increase in ALT or AST to abnormal levels

Clinical Implications of Preeclampsia

• Preeclampsia ranges from mild to severe.• Progression may be slow or rapid – hours to

days to weeks.

For clinical management, preeclampsia should be over diagnosed to prevent maternal and perinatal morbidity and mortality – primarily through timing of

delivery.

Symptoms of Preeclampsia

• Visual disturbances typical of preeclampsia are scintillations and scotomata. These disturbances are presumed to be due to cerebral vasospasm.

• Headache is of new onset and may be described as frontal, throbbing, or similar to a migraine headache. However, no classic headache of preeclampsia exists.

• Epigastric pain is due to hepatic swelling and inflammation, with stretch of the liver capsule. Pain may be of sudden onset, it may be constant, and it may be moderate-to-severe in intensity.

Symptoms of preeclampsia

• While mild lower extremity edema is common in normal pregnancy, rapidly increasing or nondependent edema may be a signal of developing preeclampsia. However, this signal theory remains controversial and recently has been removed from most criteria for the diagnosis of preeclampsia.

• Rapid weight gain is a result of edema due to capillary leak as well as renal sodium and fluid retention.

Physical Findings in Preeclampsia

• Blood Pressure • Proteinurea• Retinal vasospasm or Retinal

edema • Right upper quadrant (RUQ)

abdominal tenderness stems from liver swelling and capsular stretch

Physical findings in Preeclampsia

– Brisk, or hyperactive, reflexes are common during pregnancy, but clonus is a sign of neuromuscular irritability that raises concern.

– Among pregnant women, 30% have some lower extremity edema as part of their normal pregnancy. However, a sudden change in dependent edema, edema in nondependent areas such as the face and hands, or rapid weight gain suggests a pathologic process and warrants further evaluation

Differential Diagnosis

• Documentation of HBP before conception or before gestational week 20 favors a diagnosis of chronic hypertension (essential or secondary).

• HBP presenting at midpregnancy (weeks 20 to 28) may be due to early preeclampsia, transient hypertension, or unrecognized chronic hypertension.

Laboratory Tests

High-risk patients presenting with normal BP:

• Hematocrit • Hemoglobin• Serum uric acid• If 1+ protein by routine urinalysis (clean catch)

present obtain a timed collection for protein and creatinine

• Accurate dating and assessment of fetal growth• Baseline sonogram at 25 to 28 weeks

Laboratory Tests

Patients presenting with hypertension before gestation week 20:

• Same tests as described for high-risk patients presenting with normal BP

• Early baseline sonography for dating and fetal size

Laboratory Tests

Patients presenting with hypertension after midpregnancy:

• Quantification of protein excretion

• Hemoglobin and hematocrit and platelet count

• Serum creatinine, uric acid, and transaminase level

• Serum albumin, LDH, blood smear, and coagulation profile

Preeclampsia: Treatment

• Goal is to prevent eclampsia and other severe complications.

• Attempts to treat preeclampsia by natriuresis or by lowering BP may exacerbate pathologic changes.

• Palliate maternal condition to allow fetal maturation and cervical ripening.


Maternal Evaluation

• Goals:– Early recognition of preeclampsia

– Observe progression, both to prevent maternal complications and protect well-being of fetus.

• Early signs:– BP rises in late second and early third

trimesters.

– Initial appearance of proteinuria is important.

Fetal Monitoring


• Maternal Evaluation…When To Hospitalize?– Often, hospitalization recommended with new-

onset preeclampsia to assess maternal and fetal conditions.

– Hospitalization for duration of pregnancy indicated for preterm onset of severe gestational hypertension or preeclampsia.

– Ambulatory management at home or at day-care unit may be considered with mild gestational hypertension or preeclampsia remote from term

Preeclampsia

Indication of Delivery

Preeclampsia

• Antepartum Management of

Preeclampsia

– Little to suggest therapy alters the

underlying pathophysiology of preeclampsia.

– Restricted activity may be reasonable.

– Sodium restriction and diuretic therapy

appear to have no positive effect.

Obstetric Management

• Classically “stabilize and deliver”


• Medical management while

awaiting delivery:– use of steroids X 48 hours if fetus < 34 wks

– antihypertensives to maintain DBP < 105-

110

– magnesium sulfate for seizure prophylaxis

– monitor fluid balance, I/O, daily weights,

symptoms, reflexes, HCT, plts, LFT’s,

proteinuria


• Indications for expedited delivery:– fetal distress

BP despite aggressive Rx

– worsening end-organ function

– development or worsening of HELLP

syndrome

– development of eclampsia

Antihypertensive Therapy• Most commonly, for acute control: hydralazine,

labetolol• Nifedipine may be used, but unexpected

hypotension may occur when given with MgSO4

• For refractory hypertension: nitroglycerin or nitroprusside may be used– Nitroprusside dose and duration should be limited to

avoid fetal cyanide toxicity– Usually require invasive arterial pressure mon

• Angiotensin-converting enzyme (ACE) inhibitors contraindicated due to severe adverse fetal effects

Seizure Prophylaxis & Treatment

• Magnesium sulfate vs. phenytoin for seizure prophylaxis in preeclampsia Lucas, et al., N Engl J Med 1995;333:201-5.– 2138 patients (75% had mild PIH)– Maternal & fetal outcomes similar except 10

seizures in the phenytoin group (0 in MgSO4)

• Mg vs. diazepam & Mg vs. phenytoin for preventing recurrent seizures in eclampticsEclampsia Trial Collaborative Group, Lancet

1995;345:1455– Mg pts were 52% or 67% less likely to have a

recurrent seizure than diazepam or phenytoin pts

Seizure Prophylaxis

• Evidence is strong that magnesium sulfate is indicated for – seizure treatment in eclamptics– seizure prophylaxis in severe

preeclamptics

• Role of magnesium prophylaxis in mild preeclamptics is less clear– awaits large, prospective, randomized,

placebo-controlled trial

Magnesium Sulfate• Magnesium sulfate has many effects; its

mechanism in seizure control is not clear.– NMDA (N-methyl-D-aspartate) antagonist– vasodilator

• Brain parenchymal vasodilation demonstrated in preeclamptics by Doppler ultrasonography

– increases release of prostacyclin• Potential adverse effects:

– toxicity from overdose (respiratory, cardiac) bleeding hypotension with hemorrhage uterine contractility

Magnesium Sulfate• Renally excreted• Preeclamptics prone to renal failure• Magnesium levels must be monitored

frequently either clinically (patellar reflexes, urinary output) or by checking serum levels q 6-8 hours

• Therapeutic level: 4-7 meq/L• Patellar reflexes lost: 8-10 meq/L• Respiratory depression: 10-15 meq/L• Respiratory paralysis: 12-15 meq/L• Cardiac arrest: 25-30 meq/L

• Treatment of magnesium toxicity:– stop MgSO4, IV calcium, manage airway

Treatment of Eclampsia• Seizures are usually short-lived.• If necessary, small doses of barbiturate or

benzodiazepine (STP, 50 mg, or midazolam, 1-2 mg) and supplemental oxygen by mask.

• If seizure persists or patient is not breathing, rapid sequence induction with cricoid pressure and intubation should be performed.

• Patient may be extubated once she is completely awake, recovered from neuromuscular blockade, and magnesium sulfate has been administered.

Anesthetic Goals of Labor Analgesia in Preeclampsia

• To establish & maintain hemodynamic stability (control hypertension & avoid hypotension)

• To provide excellent labor analgesia• To prevent complications of preeclampsia

– intracerebral hemorrhage– renal failure– pulmonary edema– eclampsia

• To be able to rapidly provide anesthesia for C/S

Regional vs. General Anesthesia in Preeclampsia

• Epidural anesthesia would probably be preferred by many anesthesiologists in a severely preeclamptic pt in a non-urgent setting

• For urgent cases it is reassuring to know that spinal is also safe

• This allows us to avoid general anesthesia with the potential for encountering a swollen, difficult airway and/or labile hypertension

Regional vs. General Anesthesia in Preeclampsia

• General anesthesia is a well-known hazard in obstetric anesthesia: – 16X more likely to result in

anesthetic-related maternal mortality – Mostly due to airway/respiratory

complications, which would only be exaggerated in preeclampsiaHawkins, Anesthesiology 1997;86:273

Platelets & Regional Anesthesia in Preeclampsia

• Prior to placing regional block in a preeclamptic

it is recommended to check the platelet count.

• No concrete evidence at to the lowest safe

platelet count for regional anesthesia in

preeclampsia

• Any clinical evidence of DIC would

contraindicate regional anesthesia.

Hazards of General Anesthesia

in Preeclampsia• Airway edema is common

– Mandatory to reexamine the airway soon before induction

– Edema may appear or worsen at any time during the course of disease

• tongue & facial, as well as laryngeal

• Laryngoscopy and intubation may severe BP– Labetolol & NTG are commonly used acutely

– Fentanyl (2.5 mcg/kg), alfentanil (10 mcg/kg), lidocaine may be given to blunt response

Hazards of General Anesthesia

in Preeclampsia• Magnesium sulfate potentiates

depolarizing & non-depolarizing muscle relaxants– Pre-curarization is not indicated.– Initial dose of succinylcholine is not

reduced.– Neuromuscular blockade should be

monitored & reversal confirmed.

Invasive Central Hemodynamic Monitoring in

Preeclampsia• Usually reserved for patients with

complications– oliguria unresponsive to modest fluid

challenge (500 cc LR X 2)– pulmonary edema– refractory hypertension

• may have increased CO or increased SVR

• Poor correlation between CVP and PCWP in PIH – However, at most centers anesthesiologists

would begin with CVP & follow trend• not arbitrarily hydrate to a certain number

– If poor response, change to PA catheter

Conclusions

• Preeclampsia is a serious multi-organ system disorder of pregnancy that continues to defy our complete understanding.

• It is characterized by global endothelial cell dysfunction.

• The cause remains unknown.

• There is no effective prophylaxis.

Conclusions• Delivery is the only effective cure.

• Magnesium sulfate is now proven as the best medication to prevent and treat eclampsia.

• Epidural analgesia for labor pain management & regional anesthesia for C/S have many beneficial effects & are preferred.

Antihypertensive Therapy

• Patients with chronic hypertension should continue on their pre-pregnancy medication if NOT contraindicated with pregnancy.

• The usual cut off to prescribe Antihypertensives with pregnancy is 150/100.

• Care should be taken NOT to compromise the fetal circulation by bringing the blood pression down to normal.

Alpha-methyl Dopa

• The most commonly used and presumably the safest with pregnancy.

• The usual dose starts with 250mg tds to be increased up to 2 grams per day.

• It blocks the adrenaline release at post synaptic sites.

Hydralazine

• Dose: 5-10 mg every 20 minutes• Onset: 10-20 minutes• Duration: 3-8 hours• Side effects: headache, flushing,

tachycardia, lupus like symptoms• Mechanism: peripheral

vasodilator

Labetalol

• Dose: – IV:20mg, then 40, then 80 every 20 minutes,

for a total of 220mg – Oral 100 mg bid to be increased up to 200 mg

qid. ( maximum 2400mg daily)

• Onset: 1-2 minutes• Duration: 6-16 hours• Side effects: hypotension• Mechanism: Alpha and Beta block

Nifedipine

• Dose: 10 mg po, not sublingual• Onset: 5-10 minutes• Duration: 4-8 hours• Side effects: chest pain,

headache, tachycardia• Mechanism: CA channel block

Clonidine

• Dose: 1 mg po• Onset: 10-20 minutes• Duration: 4-6 hours• Side effects: unpredictable, avoid

rapid withdrawal• Mechanism: Alpha agonist, works

centrally

Nitroprusside

• Dose: 0.2 – 0.8 mg/min IV• Onset: 1-2 minutes• Duration: 3-5 minutes• Side effects: cyanide

accumulation, hypotension• Mechanism: direct vasodilator

Preeclampsia

• Indications for Delivery in Preeclampsia

• Maternal– Gestational age 38 weeks

– Platelet count < 100,000 cells/mm3

– Progressive deterioration in liver and renal function

– Suspected abruptio placentae

– Persistent severe headaches, visual changes, nausea, epigastric pain, or vomiting

Delivery should be based on maternal and fetal conditions as well as gestational age.

Preeclampsia

• Indications for Delivery in

Preeclampsia

• Fetal

– Severe fetal growth restriction

– Nonreassuring fetal testing results

– Oligohydramnios

Preeclampsia

• The “cure” for preeclampsia is delivery– The “cure” is always beneficial for

the mother, although c-section might be needed

– The “cure” may be deleterious for the fetus

Preeclampsia

• Route of Delivery

– Vaginal delivery is preferable.

– Aggressive labor induction (within 24 hours).

– Neuraxial (epidural, spinal, and combined

spinal-epidural) techniques offer advantages.

– Hydralazine, nitroglycerin, or labetalol may

be used as pretreatment to reduce

significant hypertension during delivery.

Preeclampsia

• Anticonvulsive Therapy– Indicated to prevent recurrent

convulsions in women with eclampsia or to prevent convulsions in women with preeclampsia.

– Parenteral magnesium sulfate reduces the frequency of eclampsia and maternal death. (Caution in renal failure.)

Treatment of Acute Severe Hypertension in Pregnancy

• SBP > 160 mm Hg and/or DBP > 105 mm Hg– Parenteral hydralazine is most

commonly used.– Parenteral labetalol is second-line drug

(avoid in women with asthma and CHF.)– Oral nifedipine used with caution.

(Short-acting nifedipine is not approved by FDA for managing hypertension.)

– Sodium nitroprusside may be used in rare cases.

Postpartum Counseling and Followup

• Counseling for Future Pregnancies• Risk of recurrent preeclampsia

increases with– Preeclampsia before 30 weeks (40%)– Multiparas as compared with nulliparas

or new father– Risk of recurrent preeclampsia may be

substantially greater in African Americans.

Remote Prognosis

• Preeclampsia-Eclampsia– The more certain the diagnosis of

preeclampsia, the lower the prevalence of remote cardiovascular disorders.

– Preeclampsia-eclampsia in subsequent pregnancies helps define future risk.

– Gestational hypertension in any pregnancy increases remote cardiovascular risk.

Eclampsia• Women older than 40 years with

preeclampsia have 4 times the incidence of seizures compared to women in their third decade of life.– Twenty-five percent of eclampsia cases occur

before labor (ie, antepartum).– Fifty percent of eclampsia cases occur during

labor (ie, intrapartum).– Twenty-five percent of eclampsia cases occur

after delivery (ie, postpartum).– Patients with severe preeclampsia are at greater

risk to develop seizures.– Twenty-five percent of patients with eclampsia

have only mild preeclampsia prior to the seizures

Causes:The cause of the seizures is not clear,

although several processes have been implicated in their development.– Areas of cerebral vasospasm may be

severe enough to cause focal ischemia, which may in turn lead to seizures.

– Pathologic alterations in cerebral blood flow and tissue edema induced by vasospasm may result in headaches, visual disturbances, and hypertensive encephalopathy, resulting in a seizure.

• Prior to the seizures, Symptoms include the following:– Headache (82.5%)– Hyperactive reflexes

(80%)– Marked proteinuria

(52%)– Generalized edema

(49%)– Visual disturbances

(44.4%)– Right upper quadrant

pain or epigastric pain (19%)

• Sometimes, there is:– Lack of edema (39%)– Absence of

proteinuria (21%)– Normal reflexes (20%)

Eclamptic seizure

– The patient may have 1 or more seizures.

– Seizures generally last 60-75 seconds.– The patient's face initially may become

distorted, with protrusion of the eyes.– The patient may begin foaming at the

mouth.– Respiration ceases for the duration of

the seizure.

• The seizure may be divided into 2 phases:– Phase 1 lasts 15-20 seconds and begins with facial twitching.

The body becomes rigid, leading to generalized muscular contractions.

– Phase 2 lasts approximately 60 seconds. It starts in the jaw, moves to the muscles of the face and eyelids, and then spreads throughout the body. The muscles begin alternating between contracting and relaxing in rapid sequence.

• A coma or a period of unconsciousness follows phase 2.– Unconsciousness lasts for a variable period.– Following the coma phase, the patient may regain some

consciousness.– The patient may become combative and very agitated.– The patient has no recollection of the seizure.

• A period of hyperventilation occurs after the tonic-clonic seizure. This compensates for the respiratory and lactic acidosis that develops during the apneic phase.

• Seizure-induced complications may include tongue biting, head trauma, broken bones, or aspiration.

Documents

Hypertensive Disorders With Pregnancy