PREGNANCY INDUCED

Blood pressure reach 140/90mmHg or greater for the first time

after Midpregnancy but proteinuria is not identified. Half of
these patient subsequently develop preeclampsia syndrome.
HYPERTENSION Gestational hypertension is reclassified by some as “transient
Course Outline hypertension” if evidence for preeclampsia does not develop
and blood pressure returns to normal by 12 weeks postpartum.
❖ TYPES OF PIH
❖ DIAGNOSIS OF HYPERTENSIVE DISORDERS
PRE-ECLAMPSIA
❖ GESTATIONAL HYPERTENSION
❖ PRE-ECLAMPSIA Summary:
❖ PREECLAMPSIA SUPERIMPOSED ON CHRONIC
HYPERTENSION ▪ Hypertension, proteinuria, edema
❖ RISK FACTORS
▪ The new onset of htn and proteinuria or htn and end-
❖ ETIPATHOGENESIS
organ dysfunction with or without proteinuria.
❖ PHENOTYPIC EXPRESSION OF PREECLAMPSIA
SYNDROME ▪ Caused by placental and maternal vascular and always
❖ ETIOLOGY resolves after delivery
❖ PATHOGENESIS ▪ Increase risk of cardiovascular disease
❖ PATHOPHYSIOLOGY ▪ Increases in systolic and diastolic blood pressure can
❖ PREDICTIVE TESTS be either normal physiological changes or signs of
❖ ECLAMPSIA
developing pathology.
❖ OBSTETRIC MEASURE
❖ PREVENTION
It is described as pregnancy-specific that can affect virtually
❖ EARLY DIAGNOSIS OF PREECLAMPSIA
❖ EVALUATION OF PREECLAMPSIA every organ system. Much more than gestational hypertension
❖ CLINICAL MANAGEMENT OF PREECLAMPSIA with proteinuria, appearance of proteinuria remains an
❖ MANAGEMENT CONSIDERATIONS OF important diagnostic criterion. Other diagnostic criteria are the
PREECLAMPSIA following: thrombocytopenia, renal dysfunction, hepatocellular
❖ LONGTERM CONSEQUENCES necrosis, CNS perturbations, and pulmonary edema.

TYPES OF PIH: INDICATORS OF PREECLAMPSIA SEVERITY

(1) Preeclampsia and eclampsia syndrome
(2) Chronic hypertension of any etiology
(3) Preeclampsia superimposed on chronic hypertension
(4) Gestational hypertension
DIAGNOSIS OF HYPERTENSIVE DISORDERS
Hypertension is diagnosed when blood pressure exceeds
140mmHg systolic or 90mmHg diastolic. Eclamptic seizures
develop in some whose blood pressure have stayed below
140/90mmHg. A sudden rise in mean arterial pressure but still
in normotensive – “delta hypertension” – may signify
preeclampsia
Delta Hypertension is when there is an acute rise in blood
pressure. Some women will go on to have obvious
preeclampsia, and some develop eclamptic seizures or HELLP
while still in normotensive.
GESTATIONAL HYPERTENSION
Preeclampsia does not develop and hypertension resolves by
12th week postpartum.
✓ Headaches or visual disturbances such as scotomata
can precede eclampsia
✓ Epigastric pain or RUQ pain accompanies
hepatocellular necrosis, ischemia, and edema.
Accompanied by elevated serum hepatic transaminase
levels.
✓ Thrombocytopenia. Represents platelet activation and
aggregation as well as microangiopathic hemolysis.
✓ Renal or cardiac involvement
✓ Obvious fetal-growth restriction
✓ Early-onset disease.
PREECLAMPSIA SUPERIMPOSED ON CHRONIC
HYPERTENSION
▪ Chronic underlying hypertension is diagnosed in women
with documented blood pressure > 140/90mmHg before
pregnancy or before 20 weeks gestation or both
▪ Blood pressure normally drops during second and early
third trimesters in both normotensive & chronically
hypertensive women.
▪ During third trimester BP return to their originally
hypertensive levels, it may be difficult to determine
whether hypertension is chronic or induced by pregnancy.
▪ Chronic hypertension, BP rises to abnormal levels typically
after 24wks of gestation. If new-onset or worsening
baseline hypertension is accompanied by new-onset
proteinuria, then superimposed preeclampsia is
diagnosed.
▪ Superimposed preeclampsia is commonly diagnosed
earlier in pregnancy. It tends to be more severe and more
often accompanied by fetal-growth restriction.
RISK FACTORS
❖ Older women are at greater risk for chronic
hypertension with superimposed preeclampsia
❖ African-American women [black women have greater
morbidity]
❖ Multiparas
❖ Pregnancies with male fetus.
❖ Smoking during pregnancy
❖ HIV
❖ Seropositivity
❖ Sleep-disordered breathing
ETIOPATHOGENESIS
➢ Exposed to chorionic villi for the first time
➢ Exposed to superabundance of chorionic villi, as with
twins or hydatidiform mole
➢ Preexisting conditions associated with endothelial cell
activation or inflammation
➢ Genetically predisposed to hypertension developing
during pregnancy.
➢ Regardless of those precipitating etiology,
preeclampsia is characterized by abnormalities
resulting in systemic vascular endothelial damage with
resultant vasospasms, transudation of plasma, and
ischemic and thrombotic sequelae.
PHENOTYPIC EXPRESSION OF PREECLAMPSIA
SYNDROME
TWO-STAGE DISORDER THEORY OF PREECLAMPSIA
Stage 1: caused by endovascular trophoblastic remodeling that
downstream causes the stage 2 clinical syndrome.
Stage 2: modified by preexisting maternal conditions that are
also manifest endothelial cell activation or inflammation and
are listed in the third prior bullet.
ETIOLOGY
(1) Placental implantation with abnormal trophoblastic
invasion of uterine vessels
(2) Immunological maladaptive tolerance between
maternal, paternal, and fetal tissues.
(3) Maternal maladaptation to cardiovascular or
inflammatory changes of normal pregnancy
(4) Genetic factors including inherited predisposing genes
and epigenetic influences.
PATHOGENESIS
VASOSPASMS. Caused by systemic endothelial activation that
increase resistance to produce hypertension subsequently.
Systemic endothelial cell injury promotes interstitial leakage, &
blood constituents, including platelets & fibrinogen are
deposited subendothelially. With diminished blood flow due to
maldistribution from vasospasm and interstitial leakage,
ischemia to the surrounding tissues can lead to necrosis,
hemorrhage, and other end-organ disturbances characteristics.
ENDOTHELIAL CELL INJURY. Centerpiece of preeclampsia
pathogenesis. Protein factor(s), secreted into maternal
circulation & produce activation & dysfunction of systemic
vascular endothelium. Activated or injured endothelial cells
produce less nitric oxide & may secrete substances that
promote coagulation & greater sensitivity vasopressors.
Endothelial activation includes characteristics alteration in
glomerular capillary endothelial morphology, greater capillary
permeability, and elevated blood concentrations of substances
associated with endothelial activation.
INCREASED PRESSOR RESPONSES. Pregnant women
normally develop refractoriness to infused vasopressors. During
early preeclampsia, women have enhanced vascular reactivity
to infused norepinephrine and angiotensin II. Increased in
sensitivity in angiotensin II precedes the onset of gestational
hypertension. Nitric oxide is a vasodilator synthesized from l-
arginine by endothelial cells. Inhibition of nitric oxide raises
arterial pressure, lowers HR, and reverses the pregnancy-
induced refractoriness to vasopressors. Endothelins are 21-
amino-acid peptides & potent vasoconstrictors. ET-1 are
elevated in normotensive while highly elevated serum levels to
women with preeclampsia. They likely arise from systemic
endothelial activation. Magnesium sulfate lowers the levels of
ET-1
ANGIOGENIC & ANTIGIOGENIC PROTEINS. Placental
vasculogenesis is evident by 21 days after conception.
Angiogenic imbalance describes excessive amounts if
antigiogenic factors that are thought to be stimulated by
worsening hypoxia at the uteroplacental interface. Soluble fins-
like tyrosine kinase 1 (sFlt-1) is a receptor for VEGF. elevated
maternal sFlt- 1 levels inactivate and reduce circulating free
placental growth factor (PIGF) and VEGF concentrations,
leading to endothelial dysfunction. sFlt-1 levels begin to rise
maternal serum months before preeclampsia is evident. High
levels in 2nd trimester are associated with doubling risk for
preeclampsia.These factors are also operative in pregnancies
complicated by fetal-growth restriction. Soluble endogline
(sENG), inhibits transforming growth factor beta. Decreased
binding to endoglin diminishes endothelial nitric oxide-
dependent vasodilatation. It begin to rise months before
clinical preeclampsia develops, metformin reduces angiogenic
secretion from human tissue.
PATHOPHYSIOLOGY
These are thought to consequence of endothelial dysfunction,
vasospasms, and ischemia.
CARDIOVASCULAR SYSTEM
Common with preeclampsia syndrome related to:
(1) Greater cardiac afterload caused by hypertension.
(2) Cardiac preload
(3) Endothelial activation leading to interendothelial
extravasation of intravascular fluid into extracellular
space.
HEMODYNAMIC CHANGES AND CARDIAC FUNCTION
Cardiac output declines, due at least in part to greater
peripheral resistance. When assessing cardiac function in
preeclampsia, consideration is given to echo cardiographic
measures of myocardial function and to clinically relevant
ventricular function. blood loss incurred at delivery. Anemia
may also partially result from greater erythrocyte destruction
as subsequently described.
MATERNAL THROMBOCYTOPENIA
Platelet count <100,00/uL indicates severe disease. The lower
the platelet count the higher the maternal and fetal morbidity
and mortality. After the delivery, the platelet count may
continue to decline for the first day or so. The cause is
unknown, immunological process or simply platelet deposition
at sites of endothelial damage may be implicated. Low platelet
doesn’t develop in fetuses or neonates born to preeclamptic
patient despite of severe maternal thrombocytopenia.
HEMOLYSIS
Severe preeclampsia is accompanied by hemolysis that
manifests as elevated serum lactate dehydrogenase levels and
reduce haptoglobin levels. Microangiopathic hemolysis is
caused by endothelial disruption with platelet adherence and
fibrin disposition.
Hemolysis + thrombocytopenia = Abnormally elevated serum
liver transaminase levels that indicate hepatocellular necrosis.
COAGULATION CHANGES
There is a subtle change in coagulation and less often
erythrocyte destruction is commonly found with preeclampsia
and especially eclampsia. Abnormal coagulations are generally
mild and seldom clinically significant. Routine laboratory
assessments of coagulation, such as prothrombin time (PT) ,
activated partial thromboplastin time (aPTT) , and plasma
fibrinogen level, are not required in the management of
pregnancy-associated hypertensive disorders.
ENDOCRINE & HORMONAL ALTERATIONS
Renin, angiotensin II, angiotensin 1-, aldosterone,
deoxycorticosterone, and atrial natriuretic peptide (ANP) are
substantively augmented during normal pregnancy.
▪ ANP released during atrial wall stretching from
expansion of blood volume and it responds to cardiac
contractility. It rise in pregnancy and further enhanced
in preeclampsia.
▪ Proatrial natriuretic peptide, precursor, also increased.
▪ Vasopressin levels are still similar in nonpregnant,
normal pregnant, and preeclamptic women.
FLUID AND ELECTROLYTE ALTERATIONS
The volume of extracellular fluid, manifest as edema, usually
much greater than normal pregnant women. Generalized
edema & proteinuria have reduced plasma oncotic pressure
that create filtration imbalance. This displaces intravascular
fluid into the surrounding interstitial.
Eclamptic convulsion. The serum pH and bicarbonate
concentration are lowered due to lactic acidosis [metabolic
acidosis] and respiratory loss of carbon dioxide [respiratory
acidosis].
KIDNEY
Clinical importance, renal perfusion and glomerular filtration
are reduced. Levels that are much less than normal
nonpregnant values are infrequent and are the consequence of
severe disease. Urine sodium is elevated. Creatinine is also
elevated. Sodium-containing crystalloid infusion raises left
ventricular filling pressure, and although oliguria temporarily
improves, rapid infusions may cause clinically apparent
pulmonary edema. IV therapy is contraindicated to
preeclamptic patient with oliguria unless UO is diminished from
hemorrhage or fluid loss from vomiting or fever. Uric acid is
typically elevated that attributes to the reduction of GFR and
due to enhanced tubular reabsorption. Preeclampsia is also
associated with diminished urinary excretion of calcium.
PROTEINURIA. Proteinuria aids the establishment of diagnosis
of preeclampsia. 24-hour urinary excretion exceeding 300mmg
protein or 1+ dipstick. In urine dipstick assessment, the value
may show 1+ or 2+ from concentrated urine specimens from
women who excrete <300mg/dL. Proteinuria may develop late
and some women may already deliver or had seizure before it
appears. 10% to 15% of women with HELLP syndrome don’t
have presentation of proteinuria. 17% of eclamptic patient
didn’t have proteinuria.
ANATOMICAL CHANGES. Glomeruli are enlarged and
bloodless, capillary loops variable dilated and contracted.
Glomerular capillary endotheliosis (swollen endothelial cells).
Swollen cells block or partially block capillary lumen. Presence
of homogenous endothelial deposits of protein & fibrin-like
material.
ACUTE KIDNEY INJURY. Acute tubular necrosis is almost
invariably induced by comorbid hemorrhage with hypovolemia
and hypotension. caused by severe obstetrical bleeding-
especially placental abruption-coupled with inadequate blood
replacement. Renal cortical necrosis develops rarely.
MYOCARDIAL FUNCTION. Diastolic dysfunction occurs in 40
to 45 percent. When there is a dysfunction, ventricles don’t
relax properly and cannot fill properly. Diastolic dysfunction
stems from ventricular remodeling, which is judged to be an
adaptive response to maintain normal contractility despite the
increased afterload of preeclampsia. High levels of
antiangiogenic proteins may be contributory.
VENTRICULAR FUNCTION. Cardiac troponin levels are slightly
elevated, and amino-terminal pro-brain natriuretic peptide (Nt
pro-BNP) levels are elevated with severe preeclampsia. Filling
pressures are dependent on the volume of intravenous fluids.
Thus, aggressive hydration results in overtly hyperdynamic
ventricular function. Aggressive fluid administration to
otherwise normal women with severe preeclampsia
substantially elevates normal left sided filling pressures and
raises a physiologically normal cardiac output to hyperdynamic
levels.
BLOOD VOLUME
Hemoconcentration is hallmark of eclampsia. Women of
average size have a blood volume of 3000 mL, and during the
last several weeks of a normal pregnancy, this averages 4500
mL. In eclampsia, anticipated 1500mL excess is loss.
Hemoconcentration may result from generalized vasospasm >
endothelial activation + leakage of plasma into interstitial
space. In preeclamptic, depending on its severity,
hemoconcentration is usually not as marked.
LIVER
Hepatic lesions with eclampsia are regions or periportal
hemorrhage in the liver periphery. Some degree of hepatic
infarction accompanied hemorrhage in almost half of women
who died with eclampsia. Findings: elevated serum hepatic
transaminase levels. Hemolysis and thrombocytopenia with
eclampsia, this constellation of hemolysis, hepatocellular
necrosis, and thrombocytopenia was later termed HELLP
syndrome
LIVER INVOLVEMENT WITH PREECLAMPSIA SHOWS
THREE MANIFESTATIONS:
(1) Pain. RUQ or midepigastric pain and tenderness
(2) Serum elevations of AST & ALT.
(3) Hemorrhagic infarction may extend to form hepatic
hematoma.
HELLP SYNDROME. There’s no universally accepted strict
definition for HELLP syndrome. Complications included
eclampsia in 6 percent, placental abruption- 1 0 percent, acute
kidney injury-5 percent, and pulmonary edema- 1 0 percent.
Stroke, hepatic hematoma, coagulopathy, acute respiratory
distress syndrome, and sepsis were other serious complications
BRAIN
Headaches and visual symptoms are common with severe
preeclampsia and associated convulsions define eclampsia.
NEUROANATOMICAL LESIONS. Most death were from
pulmonary edema, and brain lesions were coincidental,
Autopsy of eclamptic women were cortical & subcortical
petechial hemorrhages. Other describes major lesions include
subcortical edema, multiple nonhemorrhagic areas of
“softening” throughout the brain, and hemorrhagic areas in the
white matter. Hemorrhage can also occur in the basal ganglia
or pons and sometimes there’s rupture into the ventricles.
CEREBROVASCULAR PATHOPHYSIOLOGY. Two general
theories to explain cerebral abnormalities with eclampsia. The
first theory suggests that in response to acute and severe
hypertension, cerebrovascular overregulation leads to
vasospasm. In this scheme, diminished cerebral blood low is
hypothesized to result in ischemia, cytotoxic edema, and
eventually tissue infarction. second theory is that sudden Purtscher retinopathy [retinal blindness], caused by retinal
elevations in systemic blood pressure exceed the normal artery occlusion and permanent.
cerebrovascular autoregulatory capacity. Regions of forced
vasodilation and vasoconstriction develop, especially in arterial CEREBRAL EDEMA. Symptoms ranged from lethargy,
boundary zones. At the capillary level, disruption of end- confusion, and blurred vision to obtundation and coma.
capillary pressure causes increased hydrostatic pressure, Consideration is given for treatment with mannitol or
hyperperfusion, and extravasation of plasma and red cells dexamethasone
through endothelial tight-junction openings. his leads to
vasogenic edema. Most likely, combination of two. Posterior PREDICTIVE TESTS
reversible encephalopathy, interendothelial cell leak develops ❖ Placental perfusion/vascular resistance.
at blood pressure (hydraulic) levels much lower than those that ❖ Fetal-placental unit endocrine dysfunction.
usually cause vasogenic edema and is coupled with a loss of ❖ Renal dysfunction.
upper-limit autoregulation. ❖ Endothelial dysfunction/oxidant stress
❖ Others.
CEREBRAL BLOOD FLOW. Autoregulation is a mechanism by
which cerebral blood flow remains despite changes in cerebral SEVERE PRE-ECLAMPSIA
perfusion pressure. cerebral perfusion pressure is the
difference between mean arterial pressure and intracranial ▪ BP: 160/110 mmHg
pressure. to explain eclamptic seizures, it was theorized that ▪ Proteinuria: 3+ / 4+
autoregulation must be altered by pregnancy. autoregulation is ▪ (+) extensive edema
unchanged across pregnancy in rodents. However, some ▪ Decrease UO: 400 to 600mL/24hrs
investigators have provided evidence of impaired auto ▪ Abdominal edema, ischemia to the liver and pancreas
regulation in women with preeclampsia. Greater cerebral blood = severe epigastric pain, nausea, and vomiting.
low in this trimester in women with severe preeclampsia ▪ Pulmonary edema = SOB
compared with that in normotensive pregnant women. ▪ Cerebral edema = blurred vision, seeing spots, severe
Eclampsia occurs when cerebral hyperperfusion forces capillary headache, hyperreflexia, ankle clonus.
fluid interstitially because of endothelial damage. This leak
leads to perivascular edema characteristic of the preeclampsia ECLAMPSIA
syndrome
▪ Cerebral edema > seizure
NEUROLOGICAL MANIFESTATIONS ▪ Can happen up to 2 days postpartum
▪ Cerebral edema (acute) = coma
▪ Headache & scotomata – arise from cerebrovascular ▪ 20% maternal mortality rate
perfusion. Don’t usually respond to traditional ▪ Poor fetal prognosis: hypoxia = fetal acidosis
analgesia but improve after magnesium sulfate ▪ Before seizure: increase BP and increase temperature
infusion. due to cerebral pressure.
▪ Convulsions – caused by excessive release of
excitatory neurotransmitters. Extended seizures can Tonic Phase: approximately 20 seconds and may bite tongue
cause significant brain injury and later brain and respirations halt
dysfunction.
Clonic Phase: up to minute, bladder and bowel muscles
▪ Blindness – rare but it complicates eclamptic
contract, and relax incontinence.
convulsions in up to 15% of women. It may develop up
to a week or more following a delivery.
▪ Generalized cerebral edema – vary from confusion to TREATMENT
coma. Dangerous because it can develop fatal (1) Prophylactic
transtentorial herniation. - Proper antenatal care
▪ Cognitive decline - Low dose aspirin
(2) Curative
VISUAL CHANGES AND BLINDNESS. Scotomata, blurry
- Delivery of fetus & placenta
vision, or diplopia are common with severe preeclampsia and
eclampsia. Improves with magnesium sulfate therapy or !!MUST CONSIDER MATURATION OF THE FETUS BEFORE
lowered blood pressure. Amaurosis [occipital blindness], lasted DELIVERY!!
from 4 hours to 8 days but it resolved completely in all cases.
!! LESS COMPLICATIONS = INCREASE MATURATION!! CARDIOVASCULAR DRUGS – diuretics, antihypertensive
drugs
MANAGEMENT CONSIDERATIONS
ANTIOXIDANTS – ascorbic acid, alpha tocopherol [vitamin E],
(i) Severe htn vitamin D
(ii) Fluid therapy
(iii) Plasma volume expansion ANTITHROMBOTIC DRUGS – low dose of aspirin, aspirin/
(iv) Neuroprophylaxis dipyridamole, aspirin + heparin, aspirin + ketanserin
(v) Analgesia anesthesia
(vi) Blood loss delivery EARLY DIAGNOSIS OF PREECLAMPSIA
(vii) Persistent severe postpartum htn
▪ Prenatal visits aid the early detection of preeclampsia.
(viii) Plasma exchange
▪ Women without overt hypertension, but in whom
early developing preeclampsia is suspected during
OBSTETRIC MEASURES
routine prenatal visits, are seen more frequently.
(1) Timing of Delivery ▪ Overt hypertension, proteinuria, headache, visual
▪ > 37 terminate disturbances, or epigastric pain supervenes.
▪ < 37 expectant management at least 34 ▪ New-onset hypertension-either diastolic pressures >90
weeks mm Hg or systolic pressures >1 40 mmHg-are admitted
▪ Unstable conditions: to determine if the increase is due to preeclampsia,
- Stabilized > deliver > start seizure prophylaxis and and if so, to evaluate its severity
steroids if < 34 weeks
(2) Method of Delivery EVALUATION OF PREECLAMPSIA
▪ Vaginal birth = vertex
 Clinical findings such as headache, visual disturbances,
▪ Amniotomy + oxytocin = induction cervix
epigastric pain, and rapid weight gain.
▪ PGE2: cervix (x)
 Daily weight measurement
▪ C.S.: fetal distress, late deceleration, failure
 Quantification of proteinuria and creatinine ratio
induction of labor, contracted pelvis,
 Blood pressure readings
malpresentations.
 Measurement of plasma or serum creatinine and
(Immediate Delivery)
hepatic transaminase levels and a hemogram.
▪ ER setting: control BP and seizures
Measurement of uric acid and lactate dehydrogenase
▪ Don’t wait, don’t hesitate and withing 6hr…
levels and coagulation.
terminate
 Fetal size and well-being and amniotic fluid volume
(3) Intrapartum Care
evaluation
▪ Close monitoring of the fetus
▪ Proper analgesic to the mother
▪ Anti-htn prn
CLINICAL MANAGEMENT OF MIDTRIMESTER
▪ 2nd stage of labor shortened thru forceps PREECLAMPSIA
(4) Postpartum Care NURSING MANAGEMENT FOR SEVERE ECLAMPSIA
▪ NO methergine [SMDOA]
▪ Continue observation for 48 hours
▪ Anti-htn until 48hrs  Support bed rest
▪ Prophylactic treatment: Magnesium sulfate  Monitor maternal & fetal well being
▪ Lorazepam and phenytoin: 2nd line agents for  Diet moderate CHON & low Na
refractory seizures.  O2 pn, large bore IV
 Anti htn medications and Magnesium sulfate and
PREVENTION calcium gluconate
DIETARY MANIPULATION – low salt diet, calcium or fish oil MEDICAL MANAGEMENT FOR SEVERE PREECLAMPSIA
supplementation FOR < 34 WEEKS
EXERCISE – physical activity, stretching
 Admit to L&D
 Maternal and fetal assessment
  Consider magnesium sulfate
 Treat dangerous hypertension
➢ CONTRAINDICATION TO CONSERVATIVE MANAGEMENT
o Persistent symptoms or severe hypertension
o Eclampsia, pulmonary edema, HELLP syndrome
o Significant renal dysfunction, coagulopathy
o Abruption
o Previable fetus
o Fetal compromise
➢ ABSENCE OF CONTRAINDICATIONS
▪ Corticosteroids for lung maturation
▪ Frequent evaluation: vital signs, UOP
▪ Daily lab evaluation for HELLP syndrome
➢ ONGOING INPATIENT MANAGEMENT
▪ Daily maternal assessment
▪ Serial lab evaluation of renal function and for
HELLP syndrome
▪ Daily fetal assessment and evaluation of serial
growth and amniotic fluid.
➢ DELIVER AT 34 WEEKS
ECLAMPSIA NURSING MANAGEMENT (MAKRA)
 Maintain patent airway
 Administer O2 via mask
 Keep NPO
 Rx: Magnesium sulfate, Diazepam
 Assess fetal well being
ECLAMPSIA MEDICAL MANAGEMENT
o Magnesium sulfate to control convulsions
o Intermittent administration of antihypertensive drugs
o Avoid diuretics unless pulmonary edema is present
o Limit IV fluid administration unless there’s fluid loss
o Delivery of fetus to resolve preeclampsia
MANAGEMENT CONSIDERATIONS FOR ECLAMPSIA
SEVERE HYPERTENSION MANAGEMENT
Severe hypertension can cause cerebral hemorrhage,
hypertensive encephalopathy and can provoke convulsions.
Placental abruption and congestive heart disease can also
trigger.
❖ Hydralazine
- Severe gestational hypertension
- Intravenously
- Recommend labetalol if 2nd dose of hydralazine is
not working
- Proven remarkably effective to prevent cerebral
hemorrhage
-Note: fetal response to diminished uterine
perfusion and may result in unnecessary &
potentially dangerous emergency.
❖ Labetalol
- Some prefer this medication because of few side
effects
- Intravenous
- Hydralazine causes more maternal tachycardia
and palpitations while labetalol leads to maternal
bradycardia and hypotension
- Contraindicated to asthmatic women
❖ Nifedipine
- Orally administered
- Popular due to efficacy to control acute
pregnancy-related hypertension.
- Sublingual is not recommended because of
dangerous rapid and extensive effect
FLUID THERAPY
Lactated ringer solution is administered routinely at rate of 60
to 120mL per hour. Controlled, conservative fluid
administration is preferred for typical women with severe
preeclampsia who already has excessive extracellular fluid that
is inappropriately distributed between intravascular and
extravascular spaces. Infusion of large fluid volumes enhances
the maldistribution and thereby appreciably elevates the risk
for pulmonary and cerebral edema. For patient with anuria,
small incremental boluses can be given to maintain urine
output above 30mL.
❖ Pulmonary Edema
- Aspiration of gastric contents may be the result of
convulsions, anesthesia, or over sedation should
be excluded.
- Three common causes: (1) pulmonary capillary
permeability edema (2) cardiogenic edema and/
or (3) combination of two
- If given vigorous fluid replacement – will have
mild pulmonary congestion secondary to
permeability.
❖ Invasive Hemodynamic Monitoring
- Ironically, usually vigorous treatment of the
former that results in most cases of the latter.
- Such monitoring is best reserved for severely
preeclamptic women with accompanying cardiac
disease, renal disease, or both or with refractory
hypertension, oliguria, and pulmonary edema.
BLOOD VOLUME EXPANSION
Due to association to hemoconcentration, infusion of various PLASMA EXCHANGE
fluids, starch polymers, albumin concentrates, or combinations
Severe preeclampsia-eclampsia persists despite delivery. They
thereof to expand blood volume. It is not recommended due to
advocate single or multiple plasma exchange for these women.
serious maternal morbidity and substantive perinatal mortality
rate accompanied their expectant management. REVERSIBLE CEREBRAL VASOCONSTRICTION SYNDROME

NEUROPROPHYLAXIS Another cause of persistent hypertension, “thunderclap”

headache, seizures, and central nervous system findings.
Magnesium sulfate was reported to be superior to the Reversible cerebral vasoconstriction syndrome is characterized
comparator agent to prevent eclampsia. Magnesium sulfate by diffuse segmental constriction of cerebral arteries and may
was superior to phenytoin to prevent eclamptic women with be associated with ischemic and hemorrhagic strokes. It is
gestational hypertension or preeclampsia.
common in women and in some cases, if vasoconstriction is
severe it can be the cause of cerebral ischemia and infarction.
ANALGESIA AND ANESTHESIA
Use of conduction of analgesia for women with preeclampsia LONG-TERM CONSEQUENCES
syndrome has proven ideal. The initial problem in this method
includes hypotension and diminished uterine perfusion caused FUTURE PREGNANCIES
by sympathetic blockade in preeclamptic women. Rapid
Lack of deep placentation is linked with preeclampsia, placental
infusion of large volume of crystalloids or colloid corrects
abruption, fetal-growth restriction, and preterm birth.
hypotension from neural blockage. Maternal hypotension
Gestational hypertension or preeclampsia also contributes to
resulting from regional analgesia was managed with judicious
developing hypertension in the future. Recurrence of risk for
IV fluid administration. Undergoing general anesthesia,
preeclampsia is elevated further in women with metabolic
maternal blood pressure was managed to avoid severe
syndrome. Nulliparas diagnosed with preeclampsia before
hypertension.
30wks had a recurrence risk as high as 4015 during subsequent
pregnancy.
BLOOD LOSS AT DELIVERY
Fall in blood pressure soon after delivery most often means LONG TERM MORBIDITY AND MORTALITY
excessive blood loss and not sudden resolution of vasospasm
Preeclampsia is a marker for subsequent long-term
and endothelial damage. Oliguria follows delivery, hematocrit
cardiovascular and related morbidity and mortality.
should be evaluated frequently to aid detection of excessive
Hypertension attributable to pregnancy should resolve withing
blood loss. If identified, hemorrhage should be treated
12 weeks of delivery.
appropriately by crystalloid and blood transfusion.

CARDIOVASCULAR MORBIDITY
PERSISTENT SEVERE POSTPARTUM HYPERTENSION
Any hypertension is a marker for morbidity and mortality in
Severe PP hypertension usually follows labor and delivery
later life. The prevalence of ischemic heart disease and stroke
complicated by hypertension. If intravenous hydralazine or
were increased in women who had gestational hypertension
labetalol are being used repeatedly, oral regimens can be given.
compared with normotensive controls. Diastolic dysfunction is
Administration of NSAIDs may aggravate PP hypertension in
also more common and preeclampsia is also a risk for coronary
those with preeclampsia syndrome. Women with chronic
artery calcification and idiopathic cardiomyopathy. Women
hypertension and left-ventricular hypertrophy, severe PP
with pregnancy-associated hypertension are at increased risk
hypertension can cause pulmonary edema from cardiac failure.
for type 2 diabetes. Preeclampsia is a risk factor for later
Nifedipine plus furosemide or nifedipine alone can treat severe
diabetic retinopathy and retinal detachment.
postpartum eclampsia and significantly lowered the need for
additional antihypertensive. Long term adverse outcomes: metabolic syndrome, diabetes,
obesity, dyslipidemia, atherosclerosis.
Women with severe preeclampsia often have immediate PP
weight in excess of their last prenatal weight. If this weight In later life, patient who had preeclampsia will develop chronic
increases and associated with severe persistent PP hypertension and have an increased ventricular mass before
hypertension, diuresis with IV furosemide is helpful in becoming hypertensive.
controlling blood pressure.
RENAL SEQUELAE
Preeclampsia is a marker for subsequent renal disease. 15% of
previously preeclamptic patient have renal dysfunction.
Women with recurrent preeclampsia have higher risk for renal
sequelae.

CENTRAL NERVOUS SYSTEM SEQUELAE

Eclamptic seizures were believed to have no significant long-
term sequelae. All eclamptic women have multifocal areas of
perivascular edema and some areas have cerebral infarction.

Temporal lobe white matter changes and reduced cortical

volume in previously preeclamptic women. Formerly
preeclamptic women at approximately 10 years had lower
vision-related quality of life compared with control subjects,
Elevated risk for retinopathy. A cause versus an effect of these
white matter lesions remains unknown.