HYPERTENSIVE DISORDERS OF PREGNANCY 33.ppt

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1. by dr. chaltu R

2. Hypertensive disorders represent the most
common medical complications of pregnancy
Incidence between 5 and 10 percent
One of the major causes of maternal
morbidity-mortality leading to 10–15% of
maternal deaths especially in the developing
areas of the world.

3. Hypertension is defined as a BP >140 mm Hg
systolic or >90 mm Hg diastolic.
The HTN should be present on at least two
occasions, at least 4 hours apart, but within
a maximum of a 1-week period.
A single BP record greater than or equal to
160/110 is considered sufficient to diagnose
HTN

4. 1.Sitting position for ambulatory pts and
semi recumbent for admitted patients
after 10’ rest
2.Right arm used consistently
3.Measurement taken at the level of the
heart
4.The 5
th
Korotkoff sound used for diagnosis

5. 5 classes of hypertensive disorders were
identified according to the latest
classification system
Differentiating between these groups is
mandatory regarding the determination of
best management strategies.

6. 1. Gestational Hypertension
2. Preeclampsia
3. eclampsia
4. chronic hypertension
5. superimposed Preeclampsia

7. Is the development of an elevated BP during
pregnancy(after 20 weeks gestational age)
Or in the first 24 hours postpartum
Without other signs or symptoms of
preeclampsia or preexisting hypertension
The BP must return to normal within 6
weeks after delivery.

8. The commonest hypertensive disorder of
pregnancy
Incidence 6-29% in nulliparous and 2% -4% in
multiparous women
Some women with gestational hypertension may
have undiagnosed chronic hypertension
Some women may progress to develop
preeclampsia
Usually develops after 37 weeks

9. Favorable pregnancy outcome if mild
gestational HTN
Higher rate of induction and caesarean
section
High risk of preeclampsia if gestational
hypertension develops early (before 35
weeks)
Worse prognosis if severe gestational HTN

10. Complicates 5-7% of pregnancies
More common in black race
Primarily defined as gestational hypertension plus proteinuria
Elevated BP is the traditional hallmark for diagnosis of the
disease.
Mild preeclampsia:the diastolic BP remains below 110 mm Hg
and the systolic BP below 160 mm Hg.
Proteinuria is defined as:
concentration >0.1 g/L in >2 random urine specimens collected
>4 hours apart
Or 0.3 g (300 mg) in a 24-hour period

11. In the absence of proteinuria preeclampsia should be
considered:
Gestational hypertension plus
persistent cerebral symptoms
Epigastric or right upper quadrant pain plus nausea
or vomiting
IUGR
Abnormal laboratory tests such as thrombocytopenia
and elevated liver enzymes.

12. Atypical Preeclampsia
Development of Preeclampsia earlier than 20
weeks, and late postpartum period (>48
hours postpartum).

13. Age of the woman (<20yrs? or >35yrs)
Nulliparity
Family history of preeclampsia
Obesity
Spouse change
Multifetal gestation
Preeclampsia in previous pregnancy
Poor outcome in previous pregnancy
Preexisting medical—genetic conditions :
Chronic hypertension
Renal disease
Type 1DM
Thrombophilias

14. >one of the following criteria is present:
BP >160 mm Hg systolic or >110 mm Hg
Cerebral or visual disturbances
Progressive renal insufficiency cr >1.1mg/dl

15. Pulmonary edema
Epigastric or right upper-quadrant pain
Elevated liver enzymes
Thrombocytopenia (plt < 100000)

16. the amount of proteinuria, presence of
oliguria, and (IUGR)removed as criteria
for the diagnosis of severe disease.

17. Etiology remains unknown
Possible etiologies:
Abnormal trophoblasticinvasion
Coagulation abnormalities
Vascular endothelial damage
Cardiovascular maladaptation
Immunologic phenomena
Genetic predisposition
Dietary deficiencies or excesses
Imbalance in angiogenesis
Increased oxidative stress

18. Heart: Generally unaffected; cardiac
decompensation in the presence of preexisting
heart disease.
Kidney:Renal lesions (glomerular endotheliosis);
GFR and renal blood flow decrease;
hyperuricemia; proteinuria may appear late in
clinical course; hypocalciuria; alterations in
calcium regulatory hormones; impaired sodium
excretion; suppression of renin angiotensin
system.

19. Coagulation System: Thrombocytopenia; low
antithrombin III; higher fibronectin.
Liver:HELLP syndrome (hemolysis, elevated ALT
and AST, and low platelet count).
CNS:Fibrinoid necrosis, thrombosis,
microinfarcts, and petechial hemorrhages,
primarily in the cerebral cortex, and Cerebral
edema may be observed
Lungs: Pulmonary edema as a result of capillary
leak, fluid overload (iatrogenic), postpartum
refill or CHF

20. 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.
Epigastricpain 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.

21. Mild lower extremity edema is common
in normal pregnancy (80% of pregnancies)
Rapidly increasing or nondependent
edema may be a signal of developing
preeclampsia
This signal theory remains controversial
and has been removed from 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.

22. Blood Pressure
Right upper quadrant (RUQ) abdominal
tenderness
Bibasilar creptations
Brisk, or hyperactive deep tendon
reflexes
A sudden change in dependent edema,
edema in nondependent areas such as the
face and hands
Rapid weight gain during serial weight
measurement

23. Hemolysis
Elevated Liver enzymes
Low Platelets
0.2 to 0.6 % of all pregnancies
Complicates 10% of cases of severe PE and up to 50% of
cases of eclampsia
Maternal mortality has been estimated to be as high as 2-24%
Perinatal mortalityis equally high, ranging from 9 –
39 %.
RUQ pain, nausea, vomiting, and malaise are common.
The hallmark of the disorder is microangiopathic
hemolysis

24. The elevated liver enzyme levels in the
syndrome are thought to be secondary to
obstruction of hepatic blood flow by fibrin
deposits in the sinusoids.
This obstruction leads to periportal necrosis
and, in severe cases, intrahepatic hemorrhage,
subcapsular hematoma formation or hepatic
rupture

25. Rupture of a subcapsular hematoma of the
liver is a life threatening complication & it
needs emergency surgical intervention.
Even with appropriate treatment, maternal
and fetal mortality is almost 50%.
Mortality associated with exsanguination
with coagulopathy and sepsis.
The thrombocytopenia has been attributed
to increased consumption and/or destruction
of platelets.

27. 90%of patients present with generalized
malaise
65 % with epigastric pain,
30 % with nausea and vomiting,
31 percent with headache
Because of the variable nature of the
clinical presentation, the diagnosis of
HELLP syndrome is generally delayed
Usually present with complications

28. Hemolysis(as least two of these):
• Peripheral smear (schistocytes, burr cells
• Serum bilirubin(≥1.2 mg/dL)
• Low serum haptoglobin
Severe anemia unrelated to blood loss
Elevated liver enzymes
• Aspartatetransaminaseor alanine
transaminaseat least twice the ULN
• Lactate dehydrogenasetwice or more of the
Low platelet count
Platelet count < 100 000/mm3

29. Class 1defined as a platelet nadir below
50,000/mm3,
class 2 as a platelet nadir between 50,000
and 100,000/mm3,
class 3as a platelet nadir between
100,000 and 150,000/mm3.

30. Acute fatty liver in pregnancy.
Hepatitis
Thrombocytopenia purpura
Hemolytic Uremic syndrome
Diabetic Ketoacidosis
Kidney stones
Peptic ulcer disease

31. Eclampsia is defined as the development of
convulsions or unexplained coma during
pregnancy or postpartum in patients with signs
and symptoms of PE.
Should not be attributed to other causes
The seizures are GTC
May appear before (50%), during (25%), or after
labor (25%).

32. Eclamptic fit stages ( 4 stages):
Premonitory stage (1/2 minute):
Eye rolled up
Twitches of the face and hands
Tonic stage (1/2 minute):
Generalized tonic spasm with
episthotonus.
Cyanosis
Tongue may be bitten between the
clenched teeth

33. Clonic stage (1-2 minutes):
Convulsions
Tongue may be bitten
face is congested and cyanosed
conjunctival congestion
blood stained froth from the mouth
Stertorous breathing
temperature may rise
involuntary passage of urine or stool
Gradually convulsions stop

34. Coma:
Variable duration due to respiratory and
metabolic acidosis.
Deep coma may occurs (cerebral
hemorrhage).
Labor usually starts shortly after the fit.

35. Sometimes labor does not start and
convulsions recur again ‘intercurrent
eclampsia’and carries a bad prognosis.
Atypical eclampsia when eclampsia develops
before 20 weeks of gestation or after 48hours
postpartum
Usually associated with GTD and
antiphopholipid antibody syndrome
Other possible causes should be excluded

36. Hypertensive
encephalopathy
Seizure disorder
Hypoglycemia,
Hyponatremia
Vasculitis/angiopathy
Amniotic fluid embolism
Cerebrovascular accidents
Hemorrhage
Meningitis/ encephlitis
Ruptured aneurysm or
malformation
Arterial embolism,
thrombosis
Venous thrombosis
Hypoxic ischemic
encephalopathy
Angiomas

37. Hypertension present before the pregnancy
HTN that is diagnosed before the 20
th
week
of gestation unless there is GTD
Hypertension that persists for more than 42
days postpartum

38. Development of new-onset proteinuria
Proteinuria defined when more than
500mg in 24 hours
Severe exacerbation in hypertension
Development of symptoms or
thrombocytopenia and abnormal liver
enzymes/deranged renal functions.

39. Baseline investigations:
Complete blood count
Urine albumin
Renal function tests
Liver function tests
Uric acid level
Ultra sound ( fetal growth and BPP)

40. Special Investigations:
Coagulation profile (if thrombocytopenia or elevated
liver enzymes)
Peripheral morphology if HELLP syndrome suspected
Serum electrolytes in eclampsia
Chest x-ray
ECG in patients with pulmonary edema and/or CHF
CT or MRI in patients with prolonged coma

41. Gestational Hypertension
At risk for progression to either severe
hypertension, preeclampsia, or eclampsia
The risks are increased with a lower GA at
the time of diagnosis(< 35 weeks)
Close observation of maternal and fetal
conditions

42. Maternal evaluations:
Weekly prenatal visits
Education about reporting preeclamptic symptoms
Evaluation of complete blood count, and liver
enzymes.
Fetal evaluation
Amniotic fluid volume & fetal weight
Weekly nonstress testing

43. Restriction of dietary salt & physical activity
has not proven beneficial
Antihypertensive drugs does not improve
pregnancy outcome
Do not require seizure prophylaxis because
the rate of eclampsia in these women is less
than 1 in 500.

44. Basic management objectives:
Termination of pregnancy with the least
possible trauma to mother and fetus.
Birth of an infant who subsequently thrives.
Complete restoration of health to the
mother.

45. Out patient management :
Women with DBP between 90-100 or SBP
between 140-160mmHg
Compliant patient
No Fetal jeopardy
No severity features

46. Follow up during out pt management of PE includes:
Urine protein daily
BP measurement daily
Fetal movement count daily
ANC follow up twice weekly
CBC and liver enzymes during each ANC visit
NST and serial fetal growth and amniotic fluid
evaluation

47. The patient should report the following :
Decreased urine output
Sudden increase in weight and generalized
edema
Persistent headache
Blurring of vision
Right upper quadrant or epigastric pain
Decreased fetal movement
Vaginal bleeding
Convulsion or loss of consciousness

48. PREECLAMPSIA WITHOUT SEVERE FEATURES
gestational age >40 weeks delivery is
indicated
37–40 weeks, cervical status is assessed and, if
favorable, induction is initiated
Prophylactic intrapartum magnesium sulfate
to prevent convulsions is indicated
PREECLAMPSIA WITH SEVERE FEATURES
mandates hospitalization

49. Contraindications to continued expectant
management
The gestational age >34 weeks
Fetal pulmonary maturity is confirmed
Imminent eclampsia (persistent severe symptoms)
Multiorgan dysfunction
Severe IUGR
Abruptio placentae/Labor/rupture of membrane
Nonreassuring fetal testing
Pulmonary edema
HELLP/partial HELLP syndrome

50. Acute blood pressure control:
hydralazine5 to 10 mg iv every 20 minutes
for a maximal dose of 25 mg in 60 minutes.
labetalol20 to 80 mg iv every 10 minutes
for a maximal dose of 300 mg
nifedipineis 10 to 20 mg orally every 20
minutes for a maximal dose of 50 mg within
60 minutes.
Maintenance antihypertensive:
Methyl dopaup to 4gm PO in divided doses
Nifedipine10-20mg PO every 6 hours

51. Anticonvelsants prophylaxysis:
Magnesium sulfate is the drug of choice to
prevent convulsions.

52. Vaginal delivery is the preferred approach
Seizure prophylaxis
Urine output monitoring
Total IV fluids should not exceed 100
mL/hour
Epidural, Spinal, or combined techniques of
regional anesthesia is the method of choice
during cesarean delivery
Aspiration and failed intubation
Increases in systemic and cerebral pressures
during intubation and extubation.

53. Postpartum
Seizure prophylaxis for at least 24 hours
Antihypertensive drug treatment
Monitoring

54. Seizures are self-limited
Ensure that the airway is clear
Prevent injury
Prevent aspiration of gastric contents
anticonvulsant to prevent and manage
seizure
Immediate delivery
CS for obstetric indications
Strict fetomaternal monitoring

55. Magnesium sulfate seizure prophylaxis IV loading dose of
4–6 g over 20 minutes, maintenance dose of 1–2 g/hour.
UOP & Creatinine level are monitored, and the magnesium
dose is adjusted
Patellar reflexes and respiratory rate
Depressed DTR discontinue magnesium sulphate.
In the presence of patellar reflexes, serum magnesium
levels usually are unnecessary.
Calcium gluconate (10 mL of 10% solution) should be
available in the event of hypermagnesemia.

56. In practice we use:
Magnesium sulphate 20% 4gm IV over 20 min
5gm IM in each buttock( 50% )
2gm IV over 5 min if convulsion recur( 50% )
5gm 50% magnesium sulphate every 4 hrs
Continue for 24 hours

57. Other anticonvulsants:
Diazepam
Phenytoin
Lytic cocktail

58. In general, the rate of PE in subsequent
pregnancies is about 20%, with significantly
higher rates if the onset of HELLP syndrome
is during the second trimester.
The rate of recurrent HELLP syndrome ranges
from 2% to 19%, and the most reliable data
suggest a recurrence risk of less than 5%.

59. Women with a history of eclampsia are at
increased risk for all forms of PE in
subsequent pregnancies.
PE in subsequent pregnancies25%, with
substantially higher rates if the onset of
eclampsia was in the second trimester.
The rate of recurrent eclampsia is about 2%.