Hypertensive crisis in pregnancy can occur at any stage and is a leading cause of maternal and fetal morbidity and mortality worldwide. It is defined as severe hypertension (systolic BP >160 or diastolic BP >110) accompanied by acute end organ damage. It requires immediate treatment to prevent further complications. Common end organ effects include pulmonary edema, acute kidney injury, liver dysfunction, cerebral hemorrhage or infarction. Immediate treatment involves careful blood pressure control, monitoring for organ dysfunction, and delivery of the fetus and placenta when stable to ultimately resolve the condition.

1. Presenter: DR SHIVANI
OBSTETRICS AND GYNAECOLOGY
HYPERTENSIVE CRISIS IN PREGNANCY

2. INTRODUCTION
 Hypertensive disorders of
pregnancy constitute one of the
leading causes of maternal and
perinatal morbidity and mortality
worldwide.
 Hypertensive crisis is an obstetric
emergency
 It can occur at any time during
treatment of patient regardless of
history or diagnosis

3. Incidence of hypertensive disorders: 5-10% of
all pregnancy
Preeclampsia: 2-8% globally
Eclampsia: 1 in 1500 to 1 in 2000, 1-5% in India
Hypertensive crisis complicates around 2% of
all pregnancies.
Maternal mortality in hypertensive disorders
of pregnancy worldwide, including India: 13%
EPIDEMIOLOGY

4. Hypertensive crisis
HYPERTENSIVE CRISIS
HYPERTENSIVE
URGENCY
1. No end organ damage
2. Less rapid reduction in
BP
HYPERTENSIVE
EMERGENCY
1. End organ damage
2. Immediate treatment
required(within 30-60 min)

5. DEFINITION
Hypertensive emergency is described by ACOG as PERSISTENT (lasting 15
minutes or more), ACUTE ONSET SEVERE HYPERTENSION, defined as
SYSTOLIC BP>160 mm Hg, or DIASTOLIC BP> 110 mm Hg in the setting of
PREECLAMPSIA or ECLAMPSIA associated with acute and ongoing
ORGAN DAMAGE to kidney, brain, heart and vascular system .
ACOG, 2019

6. Measurement of BLOOD PRESSURE
 MERCURY SPHYGMOMANOMETER- GOLD
STANDARD
 Patient sitting or semi-recumbent position with
back supported
 an appropriate size cuff should be used
(length 1.5 times upper arm circumference or
a cuff with a bladder that encircles 80% or
more of the arm)
 10-minute or longer rest period.
 No intake of caffeine or tobacco 30 min prior
 The diastolic pressure is recorded in
Korotkoff phase V.

7. Diagnostic criteria for preeclampsia
 BLOOD PRESSURE
o SBP>140 mm Hg or DBP>90
mm Hg on two occasions 4
hours apart after 20 weeks
gestation in a previously
normotensive patient.
OR
o SBP>160 mm Hg or
DBP>110 mm Hg or more.
AND
 PROTEINURIA
 300 mg per 24 hr urine
collection
 Protein/Creatinine ratio of 0.3
mg/dL
 Dipstick reading 2+ or more
ACOG, 2019

8. In the absence of proteinuria, new onset hypertension with the new
onset of any of the following:
 THROMBOCYTOPENIA: Platelet count< 100,000*109/L
 SERUM CREATININE CONCENTRATION > 1.1mg/dL or doubling
of its concentration in absence of renal disease
 Impaired liver function: blood transaminase concentration more
than twice the upper limit
 Pulmonary edema
 New onset headache
ACOG, 2019

9. Severe features
o SBP>160 mm Hg or DBP>110 mm Hg or more on two
occasions 4 hours apart(unless antihypertensive therapy
is initiated before this time)
 THROMBOCYTOPENIA: Platelet count< 100,000*109/L
 SERUM CREATININE CONCENTRATION > 1.1mg/dL or
doubling of its concentration in absence of renal disease
 Impaired liver function: blood transaminase concentration
more than twice the upper limit or severe right upper
quadrant /epigastric pain
 Pulmonary edema
 New onset headache unresponsive to medications
 Visual disturbances
ACOG, 2019

10. Eclampsia
 Convulsive manifestation of hypertensive disorders of pregnancy
 Defined by new onset tonic-clonic focal or multifocal seizure in absence of
other causative conditions such as epilepsy, cerebral artery ischaemia and
infarction, ICH, or drug use.
 Cause unknown. Theories of etiology:
 Cerebral vasospasm, hemorrhage, ischaemia,edema microthrombi causing
cerebral blood vessel occlusion
 Excessive release of excitatory neurotransmitter- glutamate; massive
depolarization of network neurons; burst of action potentials
 Hypertensive encephalopathy

11. PREMONITORY
SYMPTOMS AND
SIGNS OF
ECLAMPSIA
Severe
and
persistent
headache
Blurred
vision
Altered
mental
status
Photopho
bia
Restlessn
ess
agitation
Nausea,
vomiting
Oliguria
Epigastric
pain

13. What causes end organ damage
Abnormal trophoblastic implantation
Endothelial dysfunction and vasospasm
Proangiogenic and antiangiogenic proteins
Immunological intolerence
Genetic Imprinting
Oxidative stress

15. 2 stage model for preeclampsia

16. CARDIOVASCULAR CHANGES IN
PREGNANCY
PHYSIOLOGICAL CHANGES PATHOLOGICAL CHANGES IN
PREECLAMPSIA
Cardiova
scular
changes
Increased
cardiac
output Increased
plasma
volume
Increase
heart rate
Increased
stroke
volume
Reduced
arterial
pressure
Reduced
peripheral
resistanc
e
 increased cardiac afterload
caused by hypertension;
 Cardiac preload, which is affected
negatively by pathologically
diminished hypervolemia of
pregnancy and is increased by
intravenous crystalloid or oncotic
solutions
 endothelial activation with
interendothelial extravasation of
intravascular fluid into the
extracellular space and
importantly, into the lungs
 Low intravascular volume

17. CARDIOVASCULAR CRISES
 Impaired regulation of coronary blood flow and marked increase in
ventricular wall stress may result in-
ANGINA
MYOCARDIA
L
INFARCTION
CONGESTIV
E HEART
FAILURE
MALIGNANT
VENTRICULAR
ARRHYTHMIA
DISSECTING
AORTIC
ANEURYSM
PULMONARY
EDEMA

18. PULMONARY EDEMA
Non cardiogenic permeability
edema
Acute systolic
hypertension
Diastolic dysfunction
Concentric ventricular
hypertrophy
Cardiogenic pulmonary
edema
Cardiogenic edema
Preeclampsia associated
endothelial activation with
capillary-alveolar leakage
Increased capillary
permeability
Non cardiogenic
permeability edema

19. PULMONARY EDEMA
Management
Fig: Non cardiogenic pulmonary edema in a
severe preeclampsia patient
 Upright position
 Maintain airway
 O2 inhalation via nasal prongs @ up to
4L/min
 Frusemide 20-40 mg intravenous
injection
 Control severe hypertension
 Nitroglycerine to reduce cardiac
preload
 Intubation and mechanical ventilation
may be required
 Termination of pregnancy after

20. Renal changes during pregnancy
PHYSIOLOGICAL CHANGES
PATHOLOGICAL CHANGES IN
PREECLAMPSIA
Renal changes
Increased
kidney size
Increased
renal plasma
flow
Increased
GFR
Decreased
serum
creatinine:
(0.5-0.7 mg/dl)
Non-
significant
proteinuria
Maintenance
of acid base
and electrolyte
balance
 Morphological changes
 Glomerular capillary
endotheliosis
 Decreased GFR
 Elevated creatinine
 Plasma uric acid elevation
 Decreased calcium
excretion
 Significant proteinuria
 Acute kidney injury

21. Glomerular capillary endotheliosis

22. Acute kidney injury-Acute tubular necrosis
 In the scenario of preeclampsia, it is
seen in-
 placental abruption
 HELLP syndrome
 Acute tubular necrosis may be either
oliguric (urine output < 400 mL/day)
or non- oliguric ( > 400 mL/day)
LABS:
 elevated serum creatinine (>3
mg/dL)
 Urinalysis: urinary granular cast,
ingreased fractional sodium
excretion, proteinuria, red blood
cell casts, hematuria
Necrosis
of the
afferent
arterioles
of the
glomerulu
s
Hemorrhag
es of the
cortex and
medulla
Fibrinoid
necrosis
Proliferativ
e
endarteritis

23. Acute kidney Injury
 Rare
 Seen in multipara, multifetal pregnancies and
placental abruptions
 Presents as severe oliguria/anuria, gross hematuria,
flank pain
 CT scan shows radioluscent rim in the cortex
 Recovery may take months, usually incomplete.
Renal cortical necrosis:
• Fluid resuscitation/restriction depending on
cause
• Vasopressors if hypotension develops
• Treatment of acidosis
• Antibiotics
• Adequate nutrition, protein intake restriction
• Dialysis if required
Treatment
of AKI

24. CHANGES IN LIVER DURING
PREGNANCY
PHYSIOLOGICAL CHANGES
PATHOLOGICAL CHANGES IN
PREECLAMPSIA
liver
Increased
hepatic
arterial
and
portal
venous
blood
flow
Increased
alkaline
phosphat
ase
Lower
levels of
AST, ALT,
GGT,
Bilirubin
Decrease
d serum
albumin
concentra
tion
fibrinogen
,
caerulopl
asmin,
transferri
n and
binding
proteins
increased
Portal
vein
pressure
increased
in late
pregnanc
y,
 The characteristic lesions were
regions of periportal hemorrhage in
the liver periphery along with some
degree of hepatic infarction
 HELLP syndrome
 symptomatic involvement
 elevated levels of serum
aminotransferases AST>ALT
 hepatic failure- shock liver in
obstetrical hemorrhage from
abruption
 Hepatic hematoma
 Hepatic rupture

25. HELLP SYNDROME
 Coined by Louis Weinstein in 1982
 Most severe form of preeclampsia
 Incidence: 0.2-0.6% of all pregnancies
 Third trimester; 30% may occur or progresses postpartum
 Increased maternal (1%) and perinatal mortality (10% to 60%)
SYMPTOMS AN SIGNS:
 Vague; malaise, nausea, vomiting, epigastric pain, headache, mucosal
bleed, hypertension, petechial hemorrhage, jaundice
LABS:
 LDH: > 600IU/L
 AST/ALT > Twice the upper limit
 THROMBOCYTOPENIA: Platelet count< 100,000*109/L
 PBS: Schistocytes,echinocytes,burr cells
 Elevated indirect bilirubin, Low serum haptoglobin.
D/D: acute fatty liver of
pregnancy, TTP, HUS

26. HELLP SYNDROME
Effects of HELLP syndrome on
pregnancy
 Abruptio placentae
 Subcapsular liver haematoma
 AKI
 Massive hepatic necrosis
 Liver rupture
 DIC
 Maternal death
MANAGEMENT:
 A: Maintenance of airway, breathing and
circulation
 Antihypertensives
 Magnesium sulphate
 Assessment and correction of maternal
coagulation abnormalities:FFP and vitamin K
 Platelet transfusion reserved for active
bleeding or prior to surgery or regional
anaesthesia/analgesia if the platelet count is
below 50 × 109/L.
 Corticosteroids for fetal lung maturity
 Delivery

27. HELLP SYNDROME
Abdominal CT imaging performed postpartum in a woman with severe HELLP syndrome and right-
upper quadrant pain. A large subcapsular hematoma (asterisk) is seen confluent with intrahepatic
infarction and hematoma (arrowhead). Numerous flame-shaped hemorrhages are seen at the
hematoma interface (arrows).

28. Central nervous system
Pathological
changes
Cerebral edema
Cerebral,
ventricular and
subarachnoid
hemorrhage
Petechial
hemorrhage and
local edema
Basal ganglion
infarcts
Cerebral infarcts

29. Cerebral autoregulation
Normal cerebral blood flow-
 50 mL per 100 g tissue per minute.
 When the BP falls, cerebral arterioles normally dilate, whereas when BP
increases, they constrict to maintain constant cerebral blood flow.
 Works between 60 and 120 mm Hg diastolic BP
With severe hypertension (130 to 150 mm Hg cerebral perfusion
pressure)
 BREAKTHROUGH THEORY: cerebral blood vessels constrict as much as
possible and then reflex cerebral vasodilatation occurs overperfusion,
damage to small blood vessels, cerebral edema, and increased intracranial
pressure.
 OVERREGULATION THEORY: exaggerated vasoconstrictive response of the
arterioles resulting in cerebral ischemia

30. Hypertensive Encephalopathy
 Untreated hypertension progresses to a hypertensive crisis in up to 1% to
2% of cases.
 systolic BP above 220 mm Hg or a diastolic BP above 130 mm Hg
 Derangement autoregulation of cerebral arterioles
 other evidence for end-organ damage may be present
 Treatment: Prevention is the goal
 confirmation of diagnosis is prompt response of the patient to antihypertensive
therapy. The headache and sensorium often clear within 1 to 2 hours after the
treatment.
 Hospitalization and bedrest
 Infusion of normal saline during the first 24 to 48 hours to achieve volume
expansion
 Antihypertensives
 Repletion of potassium losses

31. Hypertensive Encephalopathy
 Drug of choice: sodium nitroprusside
 arterial and venous relaxation
 Dose: iv infusion of 0.25 to 3 mcg/kg per
minute.
 Onset of action: immediate, and its effect
may last 3 to 5 minutes after
discontinuing the infusion.
 Risk: cyanide poisoning
 When it is infused at less than 2 mcg/kg
per minute, cyanide toxicity is unlikely.
 Treatment of toxicity: 3% sodium nitrite
@ < 5 mL/min, up to a total dose of 15
mL. Then, infusion of 12.5 g of sodium
thiosulfate in 50 mL of 5% dextrose in
Signs of
toxicity
anorexia
disorient
ation
headach
e
fatigue
restlessne
ss
tinnitus
Delirium
and
hallucination
s
nausea,
vomiting
Metaboli
c

32. Cerebrovascular accidents
 Severe hypertension may cause cerebral hemorrhage and stroke
 Systolic hypertension more predictive of cerebral injury
 CVA may be due to intracerebral hemorrhage, ruptured intracranial
aneurysm, cerebral thrombosis

33. Posterior reversible
encephalopathy
syndrome(PRES)
Reversible Cerebral
Vasoconstriction Syndrome
 Presents with vision loss or deficit,
seizure, headache, and altered
sensorium or confusion.
 Most affected region:
parietooccipital cortex—the
boundary zone of the anterior,
middle, and posterior cerebral
arteries.
 MRI: presence of vasogenic
edema and hyperintensities in the
posterior aspects of the brain
 reversible multifocal narrowing of
the arteries of the brain
 Constituted by thunderclap
headache and, less commonly,
focal neurologic deficits related to
brain edema, stroke, or seizure.
•control of hypertension
• antiepileptic medication
• long-term neurologic follow-up
Treatment:

34. Ophthalmological manifestation
 Due to impaired organ perfusion and loss of autoregulation of blood flow
 Ischemia of the retina(with flame-shaped retinal hemorrhages, retinal
infarcts, or papilledema) may occur, causing decreased visual acuity
 Blindness is less common, is usually reversible, and may arise from three
potential areas- visual cortex of the occipital lobe, the lateral geniculate
nuclei, and the retina.
 Serous retinal detachment is usually unilateral and seldom causes total
visual loss. Asymptomatic serous retinal detachment is relatively
common.
 permanent blindness may result from a combination of retinal infarctions
and bilateral lesions inthe lateral geniculate nuclei.

35. Cranial magnetic resonance imaging performed 3
days postpartum in a woman with eclampsia and
HELLP syndrome. Neurovisual defects persisted
at 1 year, causing job disability.
Purtscher retinopathy caused by choroidal
ischemia and infarction in preeclampsia
syndrome.

36. Basic Management Objectives
Termination of pregnancy
with the least possible
trauma to mother and fetus.
Birth of an infant who
subsequently thrives, and
Complete restoration of
health to the mother

37. GOALS OF TREATMENT OF HYPERTENSIVE
EMERGENCIES
 WITHIN 1-2 HOURS-
 REDUCE MAP 20-25%
 CONTROLLED ENVIRONMENT
 IV/IMMEDIATE RELEASE MEDICATIONS
NEED TO DECREASE BP QUICKLY AND
EFFECTIVELY
 SINGLE DRUG IN SMALL INTERMITTENT
DOSE IS PREFERRED, COMBINATION OF
DRUGS ENHANCES SIDE EFFECTS

38.  In the event of hypertensive crisis, with
prolonged uncontrolled hypertension,
maternal stabilization should occur before
delivery.
 If diagnosed in office setting, refer to
hospital/tertiary centre for treatment after
stabilization of BP and administration of
magnesium sulphate for seizure
prophylaxis.
GOALS OF TREATMENT OF HYPERTENSIVE
EMERGENCIES

39. First line drugs for hypertensive emergencies
Intravenous
Labetelol
Intravenous
hydralazine
Immediate release
nifedipine oral

41. DRUG DOSAGE ALGORITHM
LABETELOL
20 mg
labetelol iv
over more
than 2 min
40 mg
labetelol iv
over more
than 2 min
80 mg
labetelol iv
over more
than 2 min
10 mg
hydralazin
e iv for
more than
2min
CONSULT
NIFEDIPINE
10 mg oral
nifedipine
20 mg oral
nifedipine
20 mg oral
nifedipine
20 mg
labetelol iv
for more
than 2min
CONSULT
HYDRALAZINE
5 or 10 mg
hydralazin
e iv over
more than
2 min
10 mg
hydralazin
e iv over
more than
2 min
20 mg
labetelol iv
over more
than 2 min
40 mg
labetelol iv
for more
than 2min
CONSULT

42. Treatment of resistant hypertension
 When all the first line drugs fail to relieve acute onset severe
hypertension-- emergent consultation with anaesthesiologist,
maternal-fetal medicine subspecialist or critical care specialist
to discuss second line intervention recommended
 Drugs that can be used are:
 Nicardipine
 Esmolol
 Sodium nitroprusside(only for extreme emergencies)

43. Goal of antihypertensive therapy
 DON’T NORMALIZE BP:
140-150 mm Hg SBP and 90-100 DBP
HOW OFTEN TO CHECK BP AFTER ANTIHYPERTENSIVE
THERAPY?
ONCE THE ABOVE MENTIONED BP ACHIEVED RECHECK BP-
EVERY 10 MIN FOR 1 HOUR
EVERY 15 MIN FOR 1 HOUR
EVERY 30 MIN FOR 1 HOUR
THEN EVERY HOUR FOR 4 HOURS

44. Magnesium sulphate
 Drug of choice for seizure prophylaxis and treatment
 It is recommended regardless of whether the patient has
gestational hypertension with severe features, preeclampsia or
eclampsia.(ACOG, 2019)
Vasculature
Ca2+ antagonist
Smooth muscle
relaxant
Relieve vasospasm
Decreased vascular
resistance
Cerebral endothelium
Ca2+ antagonist
Decreased stress fibre
contraction
Decreased
paracellular BBB
permeability
Limits cerebral edema
Anticonvulsant
NMDA antagonist
Decreases effect of
glutamate
Limits neuronal
depolarization
Increases seizure
threshold
MECHANISM OF ACTION:

45. Magnesium sulphate
What to look for if toxicity?
 Urine output
 patellar reflexes
 respiratory rate
 serum magnesium in case of
renal dysfunction
What to do if toxicity
 Calcium gluconate is administered as a 1g dose
(10mL of a 10% solution) IV over a period of 2min
 oxygen therapy
 endotracheal intubation if required
Contraindications:
 Myaesthenia gravis
 Renal failure

46. :
WHEN MgSO4 is contraindicated
USE OF DIURETICS
 ANTICONVULSANTS
USED:
 LORAZEPAM
 DIAZEPAM
 PHENYTOIN INDICATIONS:
CONGESTIVE LEFT
VENTRICULAR FAILURE
ACUTE PULMONARY
EDEMA
INCREASED
INTRACRANIAL
PRESSURE
RENAL FAILURE

47. FLUID THERAPY
 Controlled, conservative fluid administration is preferred for the
typical woman with severe preeclampsia
 Lactated Ringer Solution @ 60-125ml/hr unless excessive fluid
loss.
 For preeclamptic woman with anuria, small incremental bolus
to be given to maintain the urine output >30 ml/hr.
 For labor analgesia with neuraxial analgesia, crystalloid
solutions are infused slowly in graded amounts.

48. When to deliver?
 At or beyond 34 0/7 weeks: Delivery following maternal stabilization
 At less than 34 0/7 weeks: maternal and fetal condition if stable,
expectant management may be considered with strict maternal and fetal
monitoring.
 If fetus is previable: termination of pregnancy.
 In eclampsia, delivery should be prompt, preferably within 12 hours.
Mode of delivery
 Labor induction and vaginal delivery
 Caeserean section
Delivery should not be delayed for the administration of steroids in the late preterm
period

49. Conditions Precluding Expectant Management∗
Uncontrolled severe-range blood pressures
Persistent headaches, refractory to treatment
Epigastric pain or right upper pain unresponsive to repeat analgesics
Visual disturbances, motor deficit or altered sensorium
Stroke
Myocardial infarction
HELLP syndrome
New or worsening renal dysfunction (serum creatinine greater than 1.1
mg/dL or twice baseline)
Pulmonary edema
Eclampsia
Suspected acute placental abruption or vaginal bleeding in the absence
of placenta previa
Materna
l:

50. Conditions Precluding Expectant
Management∗
Abnormal fetal testing
Fetal death
Fetus without expectation for survival at the time of maternal
diagnosis (eg, lethal anomaly, extreme prematurity)
Persistent reversed end-diastolic flow in the umbilical artery
∗In some cases, a course of antenatal steroids can be considered depending on gestational age and maternal
severity of illness.
Fetal:

51. PRINCIPLES OF MANAGEMENT
 A: Assessing the airway (A)
 Assessing breathing (B) and circulation (C): if seizure occurs- Left lateral
position and oxygen
 Antihypertensives
 magnesium sulphate
 continuous fetal monitoring
 Management of fluid balance
 VITALS AND URINE OUTPUT MONITORING
 ANTIBIOTICS
 Delivery should follow stabilization of the maternal condition
 PREVENTION OF RECURRENT SEIZURES
 TREATMENT OF COMPLICATIONS

52. INTRAPARTUM CARE
 Strict monitoring of vitals including heart rate, blood pressure, respiration,
reflexes and urine output hourly
 Continuous fetal heart rate monitoring
 Maintain iv access, maintain strict fluid balance chart
 Provide maintenance dose of manesium sulfate and antihypertensives
 Carefully monitor progress of labour
 If vaginal delivery: 2nd stage can be cut short using forceps or vaccuum
 Active management of 3rd stage of labour with oxytocin
 choice of anaesthesia: Epidural anaesthesia is of choice
Avoidance of acute hypovolemia
Prevention of PPH:
Use of uterotonics
Avoid ergomentrine

53. Postpartum care
 Careful monitoring in first 48 hours due to risk of convulsions
 Anticonvulsants for 24 hours of delivery or the last convulsion whichever
occurs later
 Antihypertensive to continue till DBP< 110 mm Hg
 Persistent Severe Postpartum Hypertension: due to mobilization of
pathological interstitial fluid and redistribution into the intravenous
compartment, underlying chronic hypertension, or usually both-
 Antihypertensives
 Frusemide
 Plasma exchange
 After discharge: post natal visit at 6 weeks, if BP still high, refer to

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