Seminar
on
Definition
• “Hypertension develops as a direct
result of the gravid state in which
the women does not have a history
of previous hypertension or
evidence of it.”
-Annamma
Jacob (2009)
Hypertensive Disease
Associated with Pregnancy
• Gestational Hypertension
• Preeclampsia
• Eclampsia
• HELLP Syndrome
• Chronic Hypertension
Hypertensive Disease
Associated with Pregnancy
 Chronic HypertensionChronic Hypertension
Gestational Hypertension
◦ Criteria
 Develops after 20 weeks of gestation
 Proteinuria is absent
 Blood pressures return to normal postpartum
◦ Morbidity is directly related to the degree
of hypertension
 PreeclampsiaPreeclampsia
 EclampsiaEclampsia
 HEELP SyndromeHEELP Syndrome
Hypertensive Disease
Associated with Pregnancy
 Chronic HypertensionChronic Hypertension
 Gestational HypertensionGestational Hypertension
Preeclampsia
◦ Criteria
 Develops after 20 weeks
 Blood pressure elevated on two occasions
at least 6 hours apart
 Associated with proteinuria and edema
 May occur less than 20 weeks with gestational
trophoblastic neoplasia
 EclampsiaEclampsia
 HEELP SyndromeHEELP Syndrome
Hypertensive Disease
Associated with Pregnancy
 Chronic HypertensionChronic Hypertension
 Gestational HypertensionGestational Hypertension
 PreeclampsiaPreeclampsia
Eclampsia
◦ Diagnosis of preeclampsia
◦ Presence of convulsions not explained
by a neurologic disorder
 Grand mal seizure activity
◦ Occurs in 0.5 to 4% or patients with
preeclampsia
 HEELP SyndromeHEELP Syndrome
Hypertensive Disease
Associated with Pregnancy
 Chronic HypertensionChronic Hypertension
 Gestational HypertensionGestational Hypertension
 PreeclampsiaPreeclampsia
 EclampsiaEclampsia
HELLP Syndrome
◦ A distinct clinical entity with:
 Hemolysis, Elevated Liver enzymes, Low
Platelets
◦ Occurs in 4 to 12 % of patients with
severe preeclampsia
 Microangiopathic hemolysis
 Thrombocytopenia
 Hepatocellular dysfunction
PRE ECLAMPSIA
Preeclampsia vs. Severe
Preeclampsia
Criteria for
Preeclampsia
• Previously
normotensive woman
• > 140 mmHg systolic
• > 90 mmHg diastolic
• Proteinuria > 300 mg in
24 hour collection
• Nondependent edema
Criteria for Severe
Preclampsia
 BP > 160 systolic or >110
diastolic
 > 5 gm of protein in 24 hour urine
or > 3+ on 2 dipstick urines
greater than 4 hours apart
 Oliguria < 500 mL in 24 hours
 Cerebral or visual distrubances
(headache, scotomata)
 Pulmonary edema or cyanosis
 Epigastric or RUQ pain
 Evidence of hepatic dysfunction
 Thrombocytopenia
 Intrauterine growth restriciton
(IUGR)
Risk Factors for
Preeclampsia
• Primi gravida
• Multifetal gestations
• Maternal age over 35
• Preeclampsia in a
previous pregnancy
• Chronic hypertension
• Pregestational diabetes
• Placental abnormalities
• Vascular and
connective tissue
disorders
• Nephropathy
• Antiphospholipid
syndrome
• Obesity
• African-American race
Risk Factors
FACTOR RISK RATIO
Primi parity 3:1
Age > 40 3:1
African American 1.5:1
Chronic hypertension 10:1
Renal disease 20:1
Antiphospholipid syndrome 10:1
Diagnostic criteria
• Hypertension
• An absolute rise of BP of at least 140/90 mm/Hg or
rise in systolic 30mm/Hg or rise in diastolic 15mm/Hg
or a rise of Mean arterial pressure of 20 mm/Hg or
the Mean arterial pressure is >105 mm/Hg.
• Oedema
• Pitting oedema over the ankles after 12 hours of bed
rest.
• Rapid gain in weight of more than 2.5 kg a week
• Proteinuria
• Presence of total protein in 24hour urine of more
than 0.3gm
incidence
• INCIDENCE:
• It may vary from 5 – 15%
• Primigravidae - 10%
• Multigravidae - 5%
Patho physiology
• Endothelial dysfunction
• Intense vasospasm
• Increased circulating pressor substances (or)
appearances of a new pressor agent (factor x)
• Vascular system is sensitized.
• Trophoblast invasion and uterine vascular
changes
• Diminished vascular refractoriness to the normal
circulating pressor substances.
IN PRE ECLAMPSIA
• There is an imbalance in different components of
prostaglandins. Absolute deficiency of vasodilator
prostaglandin (PGI2 ) from vascular endothelium and
increased synthesis of thromboxane a potent
vasoconstrictor in platelets.
• There is increased vascular sensitivity to the
Pressor agent angiotensin II
• Nitric oxide:
It significantly relaxes vascular smooth muscle
inhibits platelet aggregation and prevents intervillous
thrombosis. Deficiency of nitric oxide contributes
to the development of hypertension.
Contd…
• Endothelin - I
Is synthesized by endothelial cells and it is
a potent vaso constrictor compared to
angiotensin II. Endothelin I also contributes to
the cause of hypertension
• Inflammatory Mediators.
Cytokines derived from activated leukocytes
cause endothelial injury.
• Abnormal lipid metabolism :
Results in more oxidative stress. Hence,
Pre eclampsia is characterized by endothelial
dysfunction and vasopasm.
.
Patho physiology
Pathophysiology of
edema
• Increased oxidative stress →
endothelial injury→
increased capillary permeability.
(Leaky capillaries and decreased
blood osmotic pressure).
Pathophysiology of proteinuria
Pathophysiologic
Changes
• Cardiovascular effects
• Hematologic effects
• Neurologic effects
• Pulmonary effects
• Renal effects
• Fetal effects
Pathophysiologic
Changes
Cardiovascular effects
◦ Hypertension
◦ Increased cardiac output
◦ Increased systemic vascular
resistance
 Hematologic effects
 Neurologic effects
 Pulmonary effects
 Renal effects
 Fetal effects
Pathophysiologic
Changes
 Cardiovascular effectsCardiovascular effects
Hematologic effects
◦ Volume contraction/Hypovolemia
◦ Elevated hematocrit
◦ Thrombocytopenia
◦ Microangiopathic hemolytic anemia
◦ Third spacing of fluid
◦ Low oncotic pressure
 Neurologic effectsNeurologic effects
 Pulmonary effectsPulmonary effects
 Renal effectsRenal effects
 Fetal effectsFetal effects
Pathophysiologic
Changes
 Cardiovascular effectsCardiovascular effects
 Hematologic effectsHematologic effects
Neurologic effects
◦ Hyperreflexia
◦ Headache
◦ Cerebral edema
◦ Seizures
 Pulmonary effectsPulmonary effects
 Renal effectsRenal effects
 Fetal effectsFetal effects
Pathophysiologic
Changes
 Cardiovascular effectsCardiovascular effects
 Hematologic effectsHematologic effects
 Neurologic effectsNeurologic effects
Pulmonary effects
◦ Capillary leak
◦ Reduced colloid osmotic pressure
◦ Pulmonary edema
 Renal effectsRenal effects
 Fetal effectsFetal effects
Pathophysiologic
Changes
 Cardiovascular effectsCardiovascular effects
 Hematologic effectsHematologic effects
 Neurologic effectsNeurologic effects
 Pulmonary effectsPulmonary effects
Renal effects
◦ Decreased glomerular filtration rate
◦ Glomerular endotheliosis
◦ Proteinuria
◦ Oliguria
◦ Acute tubular necrosis
 Fetal effectsFetal effects
Pathophysiologic
Changes
 Cardiovascular effectsCardiovascular effects
 Hematologic effectsHematologic effects
 Neurologic effectsNeurologic effects
 Pulmonary effectsPulmonary effects
 Renal effectsRenal effects
Fetal effects
◦ Placental abruption
◦ Fetal growth restriction
◦ Oligohydramnios
◦ Fetal distress
◦ Increased perinatal morbidity and
mortality
Clinical features
• Head ache
Swelling over ankles, face,
abdominal wall, vulva and even
the whole body.
Weight gain-sudden onset
• Disturbed sleep
• Decreased urine output
• Epigastric pain
• Eye symptoms-blurring, diminished
vision
• Pulmonary edema
investigations
• Urine analysis
• Opthalmoscopic examination
• Blood values
– Serum uric acid level
– Serum urea
– Serum creatinine
– Liver function test
– Coagulation profile
Antenatal fetal monitoring
– Clinical examination
– daily fetal kick count,
– USG for fetal growth and liquor
pockets,
– Cardio Toco Graphy
– Bio physical profile
Management
• The ultimate cure is delivery
• Assess gestational age
• Assess cervix
• Fetal well-being
• Laboratory assessment
• Rule out severe disease!!
Principles of management
• Anti seizure prophylaxis with mgso4 is started.
• Careful assessment of maternal and fetal
status followed by delivery is done.
• Administeration of cortico steroid improves
perinatal and maternal out come.
• Cesearean section is the common mode of
delivery.
• Platelet transfusion should be given if the
count is less than 50,000/mm3
.
• Patient should be managed in an ICU until
there is improvement in platelet count,urine
out put,BP, and liver enzymes
• Recurrence risk is 3- 10%
Hypertensive
Emergencies
• Fetal monitoring
• IV access
• IV hydration
• The reason to treat is maternal, not
fetal
• May require ICU
Medical management
Seizure Prophylaxis
• Magnesium sulfate
• 4-6 g bolus
• 1-2 g/hour
• Monitor urine output and Deep
Tendon Reflexes
• With renal dysfunction, may
require a lower dose
Magnesium Sulfate
• Is not a hypotensive agent
• Works as a centrally acting
anticonvulsant
• Also blocks neuromuscular
conduction
• It increases the seizure thereshold
in the nerve terminals
• Serum levels: 6-8 mg/dL
Toxicity
• Respiratory rate < 12
• DTR’s not detectable
• Altered sensorium
• Urine output < 25-30 ml/hour
• Antidote: 10 ml of 10% solution of
calcium gluconate IV over 3
minutes
Mgso4 regimen
Anti hypertensive
therapy
• Hydralazine
• Labetalol
• Nifedipine
• Nitroprusside
• Diazoxide
• Clonidine
Hydralazine
• Dose: 5-10 mg
• Onset: 10-20 minutes
• Duration: 3-8 hours
• Side effects: headache, flushing,
tachycardia, lupus like symptoms
• Mechanism: peripheral vasodilator
Labetalol
• Dose: 20mg, then 40, then 80 every
20 minutes, for a total of 220mg
• Onset: 1-2 minutes
• Duration: 6-16 hours
• Side effects: hypotension
• Mechanism: Alpha and Beta
blocker
Nifedipine
• Dose: 10 mg po, not sublingual
• Onset: 5-10 minutes
• Duration: 4-8 hours
• Side effects: chest pain, headache,
tachycardia
• Mechanism: Calcium channel
blockers.
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: hypotension
• Mechanism: direct vasodilator
Corticosteroids for
fetal lung maturation
• If birth is considered likely within 7 days in
women with pre-eclampsia:
• give two doses of betamethasone 12 mg
intramuscularly 24 hours apart in women
between 24 and 34 weeks
Contd..
• REST: It increases the renal blood flow,
uterine blood flow and reduces the BP.
• DIET: The diet should contain adequate
amount of protein (100gm).usual salt intake is
not restricted. Fluids need not be restricted.
Total calories requirement is 1600calories
/day.
• Sedative: Diazepam 5mg at bed time.
• Diuretics: It should not be used injudiciously
as they cause harm to the baby by diminishing
placental perfusion and by electrolytic
imbalance. The most potent diuretic commonly
used is frusemide (Lasix) 40mg given orally
after break fast for 5 days in a week.
• METHOD OF TERMINATION :
• By induction or by cesaerean
section.
MANAGEMENT DURING
LABOR• The patient should be in bed
• Liberal sedatives should be given in the
form of pethidine 75-100 mg IM
• Anti hypertensive drug may be given if
the BP is too high
• BP and urine output are to be noted
regularly
• Careful monitoring of the fetus is
mandatory
Contd..
• Labor duration is curtailed by low
rupture of membrane in the I stage and
forceps or ventouse in the II stage
• IV Ergometrine following the delivery of
the anterior shoulder is withheld as it
may cause further rise of BP
• The patient should be sedated
immediately following delivery of the
baby with IM morphine 15 mg to prevent
post partum eclampsia
PUERPERIUM:
• The patient is to be watched closely for 48
hours ,the period during which convulsions
usually occurs
• Tab. Phenobarbitone 60 mg in repeated dose
can produce effective sedation
• Hypotensive drugs is to continue if the
diastolic pressure is raised beyond 100 mmhg
• The patient is to be kept in hospital till the BP is
brought down to safe level and proteinuria
disappears.
Follow up
• Advise the woman to come for a check-
up twice a week regularly.
• Monitor her blood pressure, her urine for
the presence of proteins, and the fetal
condition.
• Encourage her to take rest.
• Encourage her to take a normal diet. She
should not be advised to restrict her
intake of salt and fluids.
• Advise her to go for an institutional delivery.
• Inform her family members to take her urgently
to the hospital if there are danger signs such
as:
• Headache (increasing in frequency and
duration)
• Visual disturbances (blurring, double vision,
blindness)
• Oliguria (passing less than 400 ml urine in 24
hours)
• Upper abdominal pain
• Oedema, especially of the face, sacrum/lower
back
Complications
Immediate complications
Remote complication
ECLAMPSIA
The term eclampsia is derived
from a greek word, meaning “like
flash of lightening”. It may occur
quite abruptly, without any warning
manifestations.
• Pre eclampsia when complicated
with convulsion and/or coma is
called Eclampsia
Causes of convulsions
• Anoxia-
• spasm of the cerebral vessels following
hypertension -increased cerebro
vascular resistance - fall in cerebral
O2consumption – anoxia
• Cerebral oedema- May contribute to
irritation
• Cerebral dysrhythmia - Increases
following anoxia or oedema.
Eclamptic convulsions
• Premonitory stage:
• The convulsive movements usually begin
about the mouth in the form of facial twitching
last few seconds or half a minute.
• The tonic stage:
• The entire body become rigid in a generally
muscular contraction, the features are
distorted, the arms flexed and the hands
clenched, the body being in a condition of tonic
spasm, persist for 15 to 20 seconds.
• re her awakeness.
• The clonic stage:
There is alternate contraction and relaxation
of the muscles suddenly, the jaws begin to open
and close violently followed by eyelids. The facial
and other muscle contract and relax in rapid
succession.
• Coma:
Convulsive movements cease. The patient
lies quiet, breather seriously coma supervenes.
The duration of coma after a convulsion in
variable. The patient wakes after a short time
and is not conscious of anything. In severe
cases, the coma persists from one convulsion to
another and death may result be
THE FIRST THING TO DO
AT A SEIZURE IS TO TAKE
YOUR OWN PULSE!
Management
General management
• Should be nursed in a quiet dark room.
• Handling of the patients should be
minimum.
• Examination of the patient must be
gentle and quick and done after the
patient is under the effect of a sedative
• The throat should be kept clear of
mucous
• Vital signs - half hour and hourly
Contd..
• The bladder is catheterized to monitor urine
output and proteinuria
• Oxygen should be at hand all measures to treat
asphyxia should be available.
• Careful nursing and attention to prevent injury
during a fit are imperative. A soft firm mouth
gag introduced in time will save injury to the
tongue.
• Proper maintenance of fluid balance to
prevent fluid over load.
• Antibiotics given to prevent infection.
Control of convulsions
Alternate
Anticonvulsants
• Have not been shown to be as
efficacious as magnesium sulfate
and may result in sedation that
makes evaluation of the patient
more difficult
– Diazepam 5-10 mg IV
– Sodium Amytal 100 mg IV
– Pentobarbital 125 mg IV
– Dilantin 500-1000 mg IV infusion
After the Seizure
• Assess maternal status
• Fetal well-being
• Effect delivery
• Transport when indicated
• No need for immediate cesarean
delivery
Obstetric management
Other Complications
• Pulmonary edema
• Oliguria
• Persistent hypertension
• DIC
Pulmonary Edema
• Fluid overload
• Reduced colloid osmotic pressure
• Occurs more commonly following
delivery as colloid oncotic
pressure drops further and fluid is
mobilized
Treatment of Pulmonary
Edema
• Avoid over-hydration
• Restrict fluids
• Lasix 10-20 mg IV
• Usually no need for albumin or
Hetastarch (Hespan)
Oliguria
• 25-30 cc per hour is acceptable
• If less, small fluid boluses of 250-
500 cc as needed
• Lasix is not necessary
• Postpartum diuresis is common
• Persistent oliguria almost never
requires a PA cath
Persistent Hypertension
• BP may remain elevated for several
days
• Diastolic BP less than 100 do not
require treatment
• By definition, preeclampsia
resolves by 6 weeks
Disseminated Intravascular
Coagulopathy
• Rarely occurs without abruption
• Low platelets is not DIC
• Requires replacement blood
products and delivery
Anesthesia Issues
• Continuous lumbar epidural is
preferred if platelets normal
• Need adequate pre-hydration of
1000 ml
• Level should always be advanced
slowly to avoid low BP
• Avoid spinal with severe disease
HELLP Syndrome
• He-hemolysis
• EL-elevated liver enzymes
• LP-low platelets
HELLP Syndrome
• Is a variant of severe preeclampsia
• Platelets < 100,000
• LFT’s - 2 x normal
• May occur against a background of
what appears to be mild disease
Conservative
Management
• Controversial
• Steroids
• Requires tertiary care
• Must have stable laboratory and
reassuring fetal status
• May use antihypertensives
Prevention
• Low dose ASA ineffective in patients at
low risk
• Calcium supplementation is ineffective
(2.0 g of calcium gluconate per day)
• No compelling evidence that either are
harmful
• Recent study done with antioxidant
(1,000mg VitC and 400mg VitE).
– Small study that needs to be confirmed.
Hypertensive Disease
Associated with Pregnancy
Chronic Hypertension
◦ Diagnosed before the 20th
week or
present before the pregnancy
◦ Mild hypertension
 > 140-180 mmHg systolic
 > 90-100 mmHg diastolic
 Gestational HypertensionGestational Hypertension
 PreeclampsiaPreeclampsia
 EclampsiaEclampsia
 HEELP SyndromeHEELP Syndrome
NURSING DIAGNOSES
• Ineffective airway clearance
• Risk for fetal injury
• Risk for maternal injury related to
convulsion
• Impaired cerebral perfusion
• Ineffective elimination related to oliguria
and proteinuria
• Risk for infection
Contd…
• Risk for aspiration
• Anticipatory grieving
• Altered family process
• Health seeking behaviour
• Fear and anxiety related to pregnancy
outcome
• Fluid volume excess related to edema
• Impaired tissue integrity related to edema
• Impaired body image related to edema of face
and limbs
PPH

PPH

  • 1.
  • 2.
    Definition • “Hypertension developsas a direct result of the gravid state in which the women does not have a history of previous hypertension or evidence of it.” -Annamma Jacob (2009)
  • 3.
    Hypertensive Disease Associated withPregnancy • Gestational Hypertension • Preeclampsia • Eclampsia • HELLP Syndrome • Chronic Hypertension
  • 4.
    Hypertensive Disease Associated withPregnancy  Chronic HypertensionChronic Hypertension Gestational Hypertension ◦ Criteria  Develops after 20 weeks of gestation  Proteinuria is absent  Blood pressures return to normal postpartum ◦ Morbidity is directly related to the degree of hypertension  PreeclampsiaPreeclampsia  EclampsiaEclampsia  HEELP SyndromeHEELP Syndrome
  • 5.
    Hypertensive Disease Associated withPregnancy  Chronic HypertensionChronic Hypertension  Gestational HypertensionGestational Hypertension Preeclampsia ◦ Criteria  Develops after 20 weeks  Blood pressure elevated on two occasions at least 6 hours apart  Associated with proteinuria and edema  May occur less than 20 weeks with gestational trophoblastic neoplasia  EclampsiaEclampsia  HEELP SyndromeHEELP Syndrome
  • 6.
    Hypertensive Disease Associated withPregnancy  Chronic HypertensionChronic Hypertension  Gestational HypertensionGestational Hypertension  PreeclampsiaPreeclampsia Eclampsia ◦ Diagnosis of preeclampsia ◦ Presence of convulsions not explained by a neurologic disorder  Grand mal seizure activity ◦ Occurs in 0.5 to 4% or patients with preeclampsia  HEELP SyndromeHEELP Syndrome
  • 7.
    Hypertensive Disease Associated withPregnancy  Chronic HypertensionChronic Hypertension  Gestational HypertensionGestational Hypertension  PreeclampsiaPreeclampsia  EclampsiaEclampsia HELLP Syndrome ◦ A distinct clinical entity with:  Hemolysis, Elevated Liver enzymes, Low Platelets ◦ Occurs in 4 to 12 % of patients with severe preeclampsia  Microangiopathic hemolysis  Thrombocytopenia  Hepatocellular dysfunction
  • 8.
  • 9.
    Preeclampsia vs. Severe Preeclampsia Criteriafor Preeclampsia • Previously normotensive woman • > 140 mmHg systolic • > 90 mmHg diastolic • Proteinuria > 300 mg in 24 hour collection • Nondependent edema Criteria for Severe Preclampsia  BP > 160 systolic or >110 diastolic  > 5 gm of protein in 24 hour urine or > 3+ on 2 dipstick urines greater than 4 hours apart  Oliguria < 500 mL in 24 hours  Cerebral or visual distrubances (headache, scotomata)  Pulmonary edema or cyanosis  Epigastric or RUQ pain  Evidence of hepatic dysfunction  Thrombocytopenia  Intrauterine growth restriciton (IUGR)
  • 10.
    Risk Factors for Preeclampsia •Primi gravida • Multifetal gestations • Maternal age over 35 • Preeclampsia in a previous pregnancy • Chronic hypertension • Pregestational diabetes • Placental abnormalities • Vascular and connective tissue disorders • Nephropathy • Antiphospholipid syndrome • Obesity • African-American race
  • 11.
    Risk Factors FACTOR RISKRATIO Primi parity 3:1 Age > 40 3:1 African American 1.5:1 Chronic hypertension 10:1 Renal disease 20:1 Antiphospholipid syndrome 10:1
  • 12.
    Diagnostic criteria • Hypertension •An absolute rise of BP of at least 140/90 mm/Hg or rise in systolic 30mm/Hg or rise in diastolic 15mm/Hg or a rise of Mean arterial pressure of 20 mm/Hg or the Mean arterial pressure is >105 mm/Hg. • Oedema • Pitting oedema over the ankles after 12 hours of bed rest. • Rapid gain in weight of more than 2.5 kg a week • Proteinuria • Presence of total protein in 24hour urine of more than 0.3gm
  • 13.
    incidence • INCIDENCE: • Itmay vary from 5 – 15% • Primigravidae - 10% • Multigravidae - 5%
  • 14.
    Patho physiology • Endothelialdysfunction • Intense vasospasm • Increased circulating pressor substances (or) appearances of a new pressor agent (factor x) • Vascular system is sensitized. • Trophoblast invasion and uterine vascular changes • Diminished vascular refractoriness to the normal circulating pressor substances.
  • 15.
    IN PRE ECLAMPSIA •There is an imbalance in different components of prostaglandins. Absolute deficiency of vasodilator prostaglandin (PGI2 ) from vascular endothelium and increased synthesis of thromboxane a potent vasoconstrictor in platelets. • There is increased vascular sensitivity to the Pressor agent angiotensin II • Nitric oxide: It significantly relaxes vascular smooth muscle inhibits platelet aggregation and prevents intervillous thrombosis. Deficiency of nitric oxide contributes to the development of hypertension.
  • 16.
    Contd… • Endothelin -I Is synthesized by endothelial cells and it is a potent vaso constrictor compared to angiotensin II. Endothelin I also contributes to the cause of hypertension • Inflammatory Mediators. Cytokines derived from activated leukocytes cause endothelial injury. • Abnormal lipid metabolism : Results in more oxidative stress. Hence, Pre eclampsia is characterized by endothelial dysfunction and vasopasm. .
  • 17.
  • 19.
    Pathophysiology of edema • Increasedoxidative stress → endothelial injury→ increased capillary permeability. (Leaky capillaries and decreased blood osmotic pressure).
  • 20.
  • 21.
    Pathophysiologic Changes • Cardiovascular effects •Hematologic effects • Neurologic effects • Pulmonary effects • Renal effects • Fetal effects
  • 22.
    Pathophysiologic Changes Cardiovascular effects ◦ Hypertension ◦Increased cardiac output ◦ Increased systemic vascular resistance  Hematologic effects  Neurologic effects  Pulmonary effects  Renal effects  Fetal effects
  • 23.
    Pathophysiologic Changes  Cardiovascular effectsCardiovasculareffects Hematologic effects ◦ Volume contraction/Hypovolemia ◦ Elevated hematocrit ◦ Thrombocytopenia ◦ Microangiopathic hemolytic anemia ◦ Third spacing of fluid ◦ Low oncotic pressure  Neurologic effectsNeurologic effects  Pulmonary effectsPulmonary effects  Renal effectsRenal effects  Fetal effectsFetal effects
  • 24.
    Pathophysiologic Changes  Cardiovascular effectsCardiovasculareffects  Hematologic effectsHematologic effects Neurologic effects ◦ Hyperreflexia ◦ Headache ◦ Cerebral edema ◦ Seizures  Pulmonary effectsPulmonary effects  Renal effectsRenal effects  Fetal effectsFetal effects
  • 25.
    Pathophysiologic Changes  Cardiovascular effectsCardiovasculareffects  Hematologic effectsHematologic effects  Neurologic effectsNeurologic effects Pulmonary effects ◦ Capillary leak ◦ Reduced colloid osmotic pressure ◦ Pulmonary edema  Renal effectsRenal effects  Fetal effectsFetal effects
  • 26.
    Pathophysiologic Changes  Cardiovascular effectsCardiovasculareffects  Hematologic effectsHematologic effects  Neurologic effectsNeurologic effects  Pulmonary effectsPulmonary effects Renal effects ◦ Decreased glomerular filtration rate ◦ Glomerular endotheliosis ◦ Proteinuria ◦ Oliguria ◦ Acute tubular necrosis  Fetal effectsFetal effects
  • 27.
    Pathophysiologic Changes  Cardiovascular effectsCardiovasculareffects  Hematologic effectsHematologic effects  Neurologic effectsNeurologic effects  Pulmonary effectsPulmonary effects  Renal effectsRenal effects Fetal effects ◦ Placental abruption ◦ Fetal growth restriction ◦ Oligohydramnios ◦ Fetal distress ◦ Increased perinatal morbidity and mortality
  • 28.
  • 29.
    Swelling over ankles,face, abdominal wall, vulva and even the whole body.
  • 30.
  • 31.
    • Disturbed sleep •Decreased urine output • Epigastric pain • Eye symptoms-blurring, diminished vision • Pulmonary edema
  • 32.
    investigations • Urine analysis •Opthalmoscopic examination • Blood values – Serum uric acid level – Serum urea – Serum creatinine – Liver function test – Coagulation profile
  • 33.
    Antenatal fetal monitoring –Clinical examination – daily fetal kick count, – USG for fetal growth and liquor pockets, – Cardio Toco Graphy – Bio physical profile
  • 34.
    Management • The ultimatecure is delivery • Assess gestational age • Assess cervix • Fetal well-being • Laboratory assessment • Rule out severe disease!!
  • 35.
    Principles of management •Anti seizure prophylaxis with mgso4 is started. • Careful assessment of maternal and fetal status followed by delivery is done. • Administeration of cortico steroid improves perinatal and maternal out come. • Cesearean section is the common mode of delivery. • Platelet transfusion should be given if the count is less than 50,000/mm3 . • Patient should be managed in an ICU until there is improvement in platelet count,urine out put,BP, and liver enzymes • Recurrence risk is 3- 10%
  • 36.
    Hypertensive Emergencies • Fetal monitoring •IV access • IV hydration • The reason to treat is maternal, not fetal • May require ICU
  • 37.
  • 38.
    Seizure Prophylaxis • Magnesiumsulfate • 4-6 g bolus • 1-2 g/hour • Monitor urine output and Deep Tendon Reflexes • With renal dysfunction, may require a lower dose
  • 39.
    Magnesium Sulfate • Isnot a hypotensive agent • Works as a centrally acting anticonvulsant • Also blocks neuromuscular conduction • It increases the seizure thereshold in the nerve terminals • Serum levels: 6-8 mg/dL
  • 40.
    Toxicity • Respiratory rate< 12 • DTR’s not detectable • Altered sensorium • Urine output < 25-30 ml/hour • Antidote: 10 ml of 10% solution of calcium gluconate IV over 3 minutes
  • 41.
  • 42.
    Anti hypertensive therapy • Hydralazine •Labetalol • Nifedipine • Nitroprusside • Diazoxide • Clonidine
  • 43.
    Hydralazine • Dose: 5-10mg • Onset: 10-20 minutes • Duration: 3-8 hours • Side effects: headache, flushing, tachycardia, lupus like symptoms • Mechanism: peripheral vasodilator
  • 44.
    Labetalol • Dose: 20mg,then 40, then 80 every 20 minutes, for a total of 220mg • Onset: 1-2 minutes • Duration: 6-16 hours • Side effects: hypotension • Mechanism: Alpha and Beta blocker
  • 45.
    Nifedipine • Dose: 10mg po, not sublingual • Onset: 5-10 minutes • Duration: 4-8 hours • Side effects: chest pain, headache, tachycardia • Mechanism: Calcium channel blockers.
  • 46.
    Clonidine • Dose: 1mg po • Onset: 10-20 minutes • Duration: 4-6 hours • Side effects: unpredictable, avoid rapid withdrawal • Mechanism: Alpha agonist, works centrally
  • 47.
    Nitroprusside • Dose: 0.2– 0.8 mg/min IV • Onset: 1-2 minutes • Duration: 3-5 minutes • Side effects: hypotension • Mechanism: direct vasodilator
  • 48.
    Corticosteroids for fetal lungmaturation • If birth is considered likely within 7 days in women with pre-eclampsia: • give two doses of betamethasone 12 mg intramuscularly 24 hours apart in women between 24 and 34 weeks
  • 49.
    Contd.. • REST: Itincreases the renal blood flow, uterine blood flow and reduces the BP. • DIET: The diet should contain adequate amount of protein (100gm).usual salt intake is not restricted. Fluids need not be restricted. Total calories requirement is 1600calories /day. • Sedative: Diazepam 5mg at bed time. • Diuretics: It should not be used injudiciously as they cause harm to the baby by diminishing placental perfusion and by electrolytic imbalance. The most potent diuretic commonly used is frusemide (Lasix) 40mg given orally after break fast for 5 days in a week.
  • 50.
    • METHOD OFTERMINATION : • By induction or by cesaerean section.
  • 51.
    MANAGEMENT DURING LABOR• Thepatient should be in bed • Liberal sedatives should be given in the form of pethidine 75-100 mg IM • Anti hypertensive drug may be given if the BP is too high • BP and urine output are to be noted regularly • Careful monitoring of the fetus is mandatory
  • 52.
    Contd.. • Labor durationis curtailed by low rupture of membrane in the I stage and forceps or ventouse in the II stage • IV Ergometrine following the delivery of the anterior shoulder is withheld as it may cause further rise of BP • The patient should be sedated immediately following delivery of the baby with IM morphine 15 mg to prevent post partum eclampsia
  • 53.
    PUERPERIUM: • The patientis to be watched closely for 48 hours ,the period during which convulsions usually occurs • Tab. Phenobarbitone 60 mg in repeated dose can produce effective sedation • Hypotensive drugs is to continue if the diastolic pressure is raised beyond 100 mmhg • The patient is to be kept in hospital till the BP is brought down to safe level and proteinuria disappears.
  • 54.
    Follow up • Advisethe woman to come for a check- up twice a week regularly. • Monitor her blood pressure, her urine for the presence of proteins, and the fetal condition. • Encourage her to take rest. • Encourage her to take a normal diet. She should not be advised to restrict her intake of salt and fluids.
  • 55.
    • Advise herto go for an institutional delivery. • Inform her family members to take her urgently to the hospital if there are danger signs such as: • Headache (increasing in frequency and duration) • Visual disturbances (blurring, double vision, blindness) • Oliguria (passing less than 400 ml urine in 24 hours) • Upper abdominal pain • Oedema, especially of the face, sacrum/lower back
  • 56.
  • 57.
  • 59.
  • 60.
    ECLAMPSIA The term eclampsiais derived from a greek word, meaning “like flash of lightening”. It may occur quite abruptly, without any warning manifestations. • Pre eclampsia when complicated with convulsion and/or coma is called Eclampsia
  • 61.
    Causes of convulsions •Anoxia- • spasm of the cerebral vessels following hypertension -increased cerebro vascular resistance - fall in cerebral O2consumption – anoxia • Cerebral oedema- May contribute to irritation • Cerebral dysrhythmia - Increases following anoxia or oedema.
  • 62.
    Eclamptic convulsions • Premonitorystage: • The convulsive movements usually begin about the mouth in the form of facial twitching last few seconds or half a minute. • The tonic stage: • The entire body become rigid in a generally muscular contraction, the features are distorted, the arms flexed and the hands clenched, the body being in a condition of tonic spasm, persist for 15 to 20 seconds. • re her awakeness.
  • 63.
    • The clonicstage: There is alternate contraction and relaxation of the muscles suddenly, the jaws begin to open and close violently followed by eyelids. The facial and other muscle contract and relax in rapid succession. • Coma: Convulsive movements cease. The patient lies quiet, breather seriously coma supervenes. The duration of coma after a convulsion in variable. The patient wakes after a short time and is not conscious of anything. In severe cases, the coma persists from one convulsion to another and death may result be
  • 64.
    THE FIRST THINGTO DO AT A SEIZURE IS TO TAKE YOUR OWN PULSE!
  • 65.
  • 66.
    General management • Shouldbe nursed in a quiet dark room. • Handling of the patients should be minimum. • Examination of the patient must be gentle and quick and done after the patient is under the effect of a sedative • The throat should be kept clear of mucous • Vital signs - half hour and hourly
  • 67.
    Contd.. • The bladderis catheterized to monitor urine output and proteinuria • Oxygen should be at hand all measures to treat asphyxia should be available. • Careful nursing and attention to prevent injury during a fit are imperative. A soft firm mouth gag introduced in time will save injury to the tongue. • Proper maintenance of fluid balance to prevent fluid over load. • Antibiotics given to prevent infection.
  • 68.
  • 69.
    Alternate Anticonvulsants • Have notbeen shown to be as efficacious as magnesium sulfate and may result in sedation that makes evaluation of the patient more difficult – Diazepam 5-10 mg IV – Sodium Amytal 100 mg IV – Pentobarbital 125 mg IV – Dilantin 500-1000 mg IV infusion
  • 70.
    After the Seizure •Assess maternal status • Fetal well-being • Effect delivery • Transport when indicated • No need for immediate cesarean delivery
  • 71.
  • 73.
    Other Complications • Pulmonaryedema • Oliguria • Persistent hypertension • DIC
  • 74.
    Pulmonary Edema • Fluidoverload • Reduced colloid osmotic pressure • Occurs more commonly following delivery as colloid oncotic pressure drops further and fluid is mobilized
  • 75.
    Treatment of Pulmonary Edema •Avoid over-hydration • Restrict fluids • Lasix 10-20 mg IV • Usually no need for albumin or Hetastarch (Hespan)
  • 76.
    Oliguria • 25-30 ccper hour is acceptable • If less, small fluid boluses of 250- 500 cc as needed • Lasix is not necessary • Postpartum diuresis is common • Persistent oliguria almost never requires a PA cath
  • 77.
    Persistent Hypertension • BPmay remain elevated for several days • Diastolic BP less than 100 do not require treatment • By definition, preeclampsia resolves by 6 weeks
  • 78.
    Disseminated Intravascular Coagulopathy • Rarelyoccurs without abruption • Low platelets is not DIC • Requires replacement blood products and delivery
  • 79.
    Anesthesia Issues • Continuouslumbar epidural is preferred if platelets normal • Need adequate pre-hydration of 1000 ml • Level should always be advanced slowly to avoid low BP • Avoid spinal with severe disease
  • 80.
    HELLP Syndrome • He-hemolysis •EL-elevated liver enzymes • LP-low platelets
  • 81.
    HELLP Syndrome • Isa variant of severe preeclampsia • Platelets < 100,000 • LFT’s - 2 x normal • May occur against a background of what appears to be mild disease
  • 82.
    Conservative Management • Controversial • Steroids •Requires tertiary care • Must have stable laboratory and reassuring fetal status • May use antihypertensives
  • 83.
    Prevention • Low doseASA ineffective in patients at low risk • Calcium supplementation is ineffective (2.0 g of calcium gluconate per day) • No compelling evidence that either are harmful • Recent study done with antioxidant (1,000mg VitC and 400mg VitE). – Small study that needs to be confirmed.
  • 84.
    Hypertensive Disease Associated withPregnancy Chronic Hypertension ◦ Diagnosed before the 20th week or present before the pregnancy ◦ Mild hypertension  > 140-180 mmHg systolic  > 90-100 mmHg diastolic  Gestational HypertensionGestational Hypertension  PreeclampsiaPreeclampsia  EclampsiaEclampsia  HEELP SyndromeHEELP Syndrome
  • 85.
    NURSING DIAGNOSES • Ineffectiveairway clearance • Risk for fetal injury • Risk for maternal injury related to convulsion • Impaired cerebral perfusion • Ineffective elimination related to oliguria and proteinuria • Risk for infection
  • 86.
    Contd… • Risk foraspiration • Anticipatory grieving • Altered family process • Health seeking behaviour • Fear and anxiety related to pregnancy outcome • Fluid volume excess related to edema • Impaired tissue integrity related to edema • Impaired body image related to edema of face and limbs