PRegnancy indiced hypertension lecture one.ppt

PRegnancy indiced hypertension lecture one.ppt

1. Hypertensive Disorders With
Pregnancy

2. •Complicates 7-10% of pregnancies
–70% Preeclampsia-eclampsia
–30% Chronic hypertension
–Eclampsia 0.05% incidence
•20% of Maternal Deaths
•Cause of 10% of Preterm birth
•Etiology unknown

3. •Young female 3 fold increased risk
•African American 2 fold increased risk
•Multifetal pregnancies
–Twins
–Triplets
•Hypertension
•Diabetes Mellitus
•Renal Disease
•Collagen Vascular Disease

4. Hypertension during Pregnancy: Classification
•Pregnancy-induced hypertension
–Hypertension without proteinuria/edema
–Preeclampsia
•mild
•severe
–Eclampsia
•Coincidental HTN: preexisting or persistent
•Pregnancy-aggravated HTN
–superimposed preeclampsia
–superimposed eclampsia
•Transient HTN: occurs in 3rd trimester, mild

5. Preeclampsia: Definition
1.1*HTN (new onset > 20 weeks) + proteinuria
• OR
•2.* HTN (new onset > 20 wks) + multisystemicsigns
• -CNS
• -pulmonary edema
• -renal dysfunction
• -liver impairment
• -thrombocytopenia
•* Proteinuriais not required for diagnosis

6. Criteria for Severe Preeclampsia
•SBP > 160 mm Hg
•DBP > 110 mm Hg
•Proteinuria > 5 g/24 hr.
or 3-4+ on dipstick
•Oliguria < 500 cc/24 hr.
•serum
creatinine(›1.1mg/dl or
double)
•Pulmonary edema or
cyanosis
•CNS symptoms (HA, vision
changes)
•Abdominal (RUQ) pain
•Any feature of HELLP
–hemolysis
–liver enzymes(2x of
normal)
–Thrombocytopenia(platlate
˂100,0000)
•IUGR or oligohydramnios

7. Preeclampsia: Risk Factors
•primipaternity
•Chronic renal disease
•Chronic hypertension
•Multiple gestation
•Family or personal history of preeclampsia
•Age > 40 years
•African-American race
•Diabetes mellitus

8. Etiology
•Etiology is unknown.
•Many theories:
–genetic
–immunologic
–dietary deficiency (calcium, magnesium, zinc)
•supplementation has not proven effective
–placental source (ischemia)

9. Pathogenesis
•The normal conversion of the fibro-elastic
spiral arteries of the non-pregnant uterus to
the low-pressure, high-flow circulation
necessary for fetal well-being fails to occur.
•Subsequently the fetus will fail to grow and
may even develop oligohydramnios.
•Evidence suggesting the presence of either of
these two factors is a defining feature of
severe pre-eclampsia.

10. Pathogenesis
Endothelial Dysfunction
•In pre-eclampsia there is widespread
endothelial dysfunction leading to placental
ischaemia and multi-organ dysfunction.
•The endothelium is an important barrier that
controls movement between the intra-
vascular and extra-cellular compartments. It
is also a highly active metabolic organ.

11. Pathogenesis
•Therefore, the synthesis of many
substances including nitric oxide (NO)
and prostacyclin (PGI2) may be
decreased in pre-eclampsia. This leads
to a major effect on smooth muscle
reactivity and platelet adhesion.

13. Etiology and Prevention
•A major underlying defect is a relative
deficiency of prostacyclin vs thromboxane
•Normally (non-preeclamptic) there is an 8-10
fold in prostacyclin with a smaller in
thromboxane
–prostacyclin salutatory effects dominate
•vasodilation, platelet aggregation, uterine tone
•In preeclampsia, thromboxane’s effects
dominate
–thromboxane (from platelets, placenta)
–prostacyclin (from endothelium, placenta)

14. Preeclampsia Prophylaxis: Aspirin
•Aspirin has been extensively studied as a
targeted therapy to thromboxane
production

15. Preeclampsia: Mechanism
•At this time the most widely accepted
proposed mechanism for preeclampsia is:
Global Endothelial Cell Dysfunction
•Endothelial cell dysfunction is just one
manifestation of a broader intravascular
inflammatory response
–present in normal pregnancy
–excessive in preeclampsia
–Proposed source of inflammatory stimulus:
placenta

16. Pathophysiology
Of importance, and distinguishing preeclampsia
from chronic or gestational hypertension, is
that preeclampsia is more than hypertension; it
is a systemic syndrome, and several of its
“non-hypertensive”complications can be life-
threatening when blood pressure elevations
are quite mild.

17. Pathophysiology: Cardiovascular
•In severe preeclampsia, typically
hyperdynamic with normal-high CO, normal-
mod. high SVR, and normal PCWP and CVP.
•Despite normal filling pressures,
intravascular fluid volume is reduced (30-
40% in severe PIH)
•Variations in presentation depending on
prior treatment and severity and duration of
disease
•Total body water is increased (generalized
edema)

18. Pathophysiology: Cardiovascular
•Preeclamptic patients are prone to develop
pulmonary edemadue to reduced colloid
oncotic pressure (COP), which falls further
postpartum:
Colloid oncotic pressure:
Antepartum Postpartum
Normal pregnancy:22 mm Hg 17 mm Hg
Preeclampsia: 18 mm Hg 14 mm Hg

19. Pathophysiology
•Respiratory:
–Airway is edematous; use smaller ET tube (6.5)
–risk of pulmonary edema; 70% postpartum
•Renal:
–Renal blood flow & GFR are decreased
–Renal failure due to plasma volume or renal
artery vasospasm
–Proteinuria due to glomerulopathy
•glomerular capillary endothelial swelling with subendothelial
protein deposits
–Renal function recovers quickly postpartum

20. Pathophysiology: Hepatic
•RUQ pain is a serious complaint
–needs imaging, especially when accompanied
by liver enzymes
–caused by liver swelling, periportal
hemorrhage, subcapsular hematoma, hepatic
rupture (30% mortality)
•HELLP syndrome occurs in ~ 20% of
severe preeclamptics.

21. Pathophysiology
•Coagulation:
–Generally hypercoagulable with evidence of
platelet activation and increased fibrinolysis
–Thrombocytopenia is common, but fewer than
10% have platelet count < 100,000
–DIC may occur,
•Acutely esp. with placental abruption
•Neurologic:
–Symptoms: headache, visual changes, seizures
–Hyperreflexia is usually present
–Eclamptic seizures may occur even w/out BP
•Possible causes: hypertensive encephalopathy, cerebral edema,
thrombosis, hemorrhage, vasospasm

22. Clinical Implications of
Preeclampsia
•Preeclampsia ranges from mild to severe.
•Progression may be slow or rapid –hours to
days to weeks.
For clinical management, preeclampsia should
be over diagnosed to prevent maternal and
perinatal morbidity and mortality –primarily
through timing of delivery.

23. Differential Diagnosis
•Documentation of HBP before conception
or before gestational week 20 favors a
diagnosis of chronic hypertension
(essential or secondary).
•HBP presenting at midpregnancy (weeks
20 to 28) may be due to early
preeclampsia, transient hypertension, or
unrecognized chronic hypertension.

24. Laboratory Tests
High-risk patients presenting with normal
BP:
•Hematocrit
•Hemoglobin
•Serum uric acid
•If 1+ protein by routine urinalysis (clean catch)
present obtain a timed collection for protein and
creatinine
•Accurate dating and assessment of fetal growth
•Baseline sonogram at 25 to 28 weeks

25. Preeclampsia: Treatment
•Goal is to prevent eclampsia and other severe
complications.
•Attempts to treat preeclampsia by natriuresis
or by lowering BP may exacerbate pathologic
changes.
•Palliate maternal condition to allow fetal
maturation and cervical ripening.

26. Preeclampsia: Treatment
Maternal Evaluation
•Goals:
–Early recognition of preeclampsia
–Observe progression, both to prevent
maternal complications and protect well-
being of fetus.
•Early signs:
–BP rises in late second and early third trimesters.
–Initial appearance of proteinuria is important.

27. Indication of Delivery

28. Obstetric Management
•Medical management while awaiting
delivery:
–use of steroids if fetus < 34 wks
–antihypertensives to maintain DBP b/n 105-110
–magnesium sulfate for seizure prophylaxis
–monitor fluid balance, u/O, daily weights,
symptoms, reflexes, HCT, plts, LFT’s, proteinuria

29. Obstetric Management
•Indications for expediteddelivery:
–fetal distress
–BP despite aggressive Rx
–worsening end-organ function
–development or worsening of HELLP syndrome
–development of eclampsia

30. Antihypertensive Therapy
•Most commonly, for acute control: hydralazine,
labetolol
•Nifedipine may be used, but unexpected
hypotension may occur when given with MgSO
4
•For refractory hypertension: nitroglycerin or
nitroprusside may be used
–Nitroprusside dose and duration should be limited
to avoid fetal cyanide toxicity
–Usually require invasive arterial pressure monitoring
•Angiotensin-converting enzyme (ACE) inhibitors
contraindicated due to severe adverse fetal
effects

31. Seizure Prophylaxis
•Evidence is strong that magnesium
sulfate is indicated for
–seizure treatment in eclamptics
–seizure prophylaxis in severe preeclamptics
•Role of magnesium prophylaxis in mild
preeclamptics is less clear

32. Magnesium Sulfate
•Is not a hypotensive agent
•Works as a centrally acting
anticonvulsant
•Also blocks neuromuscular conduction
•Serum levels: 6-8 mg/dL

33. Magnesium Sulfate
•Magnesium sulfate has many effects; its
mechanism in seizure control is not clear.
–NMDA (N-methyl-D-aspartate) antagonist
–vasodilator
•Brain parenchymal vasodilation demonstrated in
preeclamptics by Doppler ultrasonography
–increases release of prostacyclin
•Potential adverse effects:
–toxicity from overdose (respiratory, cardiac)
–bleeding
–hypotension with hemorrhage
–uterine contractility

34. Magnesium Sulfate
•Renally excreted
•Preeclamptics prone to renal failure
•Magnesium levels must be monitored frequently
either clinically (patellar reflexes, urinary output) or
by checking serum levels q 6-8 hours
•Therapeutic level: 4-7 meq/L
•Patellar reflexes lost: 8-10 meq/L
•Respiratory depression: 10-15 meq/L
•Respiratory paralysis: 12-15 meq/L
•Cardiac arrest: 25-30 meq/L

35. •MgSO4 may also increase the likelihood
of hypotension during regional
anaesthesia and will tend to blunt the
response to vasoconstrictors

36. Magnesium Toxicity
•Respiratory rate < 12
•Deep Tendon Reflex’s not detectable
•Altered sensorium
•Urine output < 25-30 cc/hour
•ECG changes occur (P–Q interval prolonged,
QRS complex widened) which may progress
to conduction defects and cardiac arrest.

37. Mx of magnesium toxicity
•stop MgSO4
•IV calcium
•manage airway
•Antidote: 10 ml of 10% solution of
calcium gluconate iv over 3 minutes

38. Antihypertensive Therapy
•Patients with chronic hypertension should continue
on their pre-pregnancy medication if NOT
contraindicated with pregnancy.
•The usual cut off to prescribe Antihypertensives
with pregnancy is 150/100.
•Care should be taken NOT to compromise the fetal
circulation by bringing the blood pression down to
normal.

39. Alpha-methyl Dopa
•The most commonly used and
presumably the safest with pregnancy.
•The usual dose starts with 250mg tds to
be increased up to 2 grams per day.
•It blocks the adrenaline release at post
synaptic sites.

40. Hydralazine
•Dose: 5-10 mg every 20 minutes
•Onset: 10-20 minutes
•Duration: 3-8 hours
•Side effects: headache, flushing,
tachycardia, lupus like symptoms
•Mechanism: peripheral vasodilator

41. Labetalol
•Dose:
–IV:20mg, then 40, then 80 every 20 minutes, for a
total of 220mg
–Oral 100 mg bid to be increased up to 200 mg qid.
( maximum 2400mg daily)
•Onset: 1-2 minutes
•Duration: 6-16 hours
•Side effects: hypotension
•Mechanism: Alpha and Beta block

42. Nifedipine
•Dose: 10 mg po, not sublingual
•Onset: 5-10 minutes
•Duration: 4-8 hours
•Side effects: chest pain, headache,
tachycardia
•Mechanism: CA channel block

43. Clonidine
•Dose: 1 mg po
•Onset: 10-20 minutes
•Duration: 4-6 hours
•Side effects: unpredictable, avoid rapid
withdrawal
•Mechanism: Alpha agonist, works
centrally

44. Nitroprusside
•Dose: 0.2 –0.8 mg/min IV
•Onset: 1-2 minutes
•Duration: 3-5 minutes
•Side effects: cyanide accumulation,
hypotension
•Mechanism: direct vasodilator

45. Eclampsia
•Women older than 40 years with preeclampsia
have 4 times the incidence of seizures compared to
women in their third decade of life.
–25% of eclampsia cases occur before labor (ie,
antepartum).
–50%of eclampsia cases occur during labor (ie,
intrapartum).
–25% percent of eclampsia cases occur after delivery (ie,
postpartum).
–Patients with severe preeclampsia are at greater risk to
develop seizures.
–25% of patients with eclampsia have only mild
preeclampsia prior to the seizures

46. Causes:
The cause of the seizures is not clear,
although several processes have been
implicated in their development.
–Areas of cerebral vasospasm may be severe
enough to cause focal ischemia, which may in
turn lead to seizures.
–Pathologic alterations in cerebral blood flow and
tissue edema induced by vasospasm may result
in headaches, visual disturbances, and
hypertensive encephalopathy, resulting in a
seizure.

47. •Prior to the seizures,
Symptoms include the
following:
–Headache (82.5%)
–Hyperactive reflexes (80%)
–Marked proteinuria (52%)
–Generalized edema (49%)
–Visual disturbances (44.4%)
–Right upper quadrant pain or
epigastric pain (19%)
•Sometimes, there is:
–Lack of edema (39%)
–Absence of proteinuria
(21%)
–Normal reflexes (20%)

48. Eclamptic seizure
–The patient may have 1 or more seizures.
–Seizures generally last 60-75 seconds.
–The patient's face initially may become
distorted, with protrusion of the eyes.
–The patient may begin foaming at the
mouth.
–Respiration ceases for the duration of the
seizure.

49. •The seizure may be divided into 2 phases:
–Phase 1 lasts 15-20 seconds and begins with facial
twitching. The body becomes rigid, leading to
generalized muscular contractions.
–Phase 2 lasts approximately 60 seconds. It starts in
the jaw, moves to the muscles of the face and eyelids,
and then spreads throughout the body. The muscles
begin alternating between contracting and relaxing in
rapid sequence.

50. Cont…
•A coma or a period of unconsciousness follows phase
2.
–Unconsciousness lasts for a variable period.
–Following the coma phase, the patient may regain
some consciousness.
–The patient may become combative and very
agitated.
–The patient has no recollection of the seizure.

51. Cont…
•A period of hyperventilation occurs after
the tonic-clonic seizure. This
compensates for the respiratory and
lactic acidosis that develops during the
apneic phase.
•Seizure-induced complications may
include tongue biting, head trauma,
broken bones, or aspiration.

52. Treatment of Eclampsia
•Seizures are usually short-lived.
•If necessary, small doses of barbiturate or
benzodiazepine (thiopenton,50 mg, or midazolam, 1-
2 mg) and supplemental oxygen by mask.
•If seizure persists or patient is not breathing, rapid
sequence induction with cricoid pressure and
intubation should be performed.
•Patient may be extubated once she is completely
awake, recovered from neuromuscular blockade, and
magnesium sulfate has been administered.

53. HELLP Syndrome
•Weinstein regarded signs and
symptoms to constitute an entity
separate from severe preeclampsia and
in 1982 named the condition HELLP
•H = Haemolysis
•EL = Elevated Liver enzymes
•LP = Low Platelets
•currently regarded as a variant of
severe preeclampsia or a complication .

54. •The HELLP syndrome occurs in about
0.5 to 0.9% of all pregnancies and in 10
to 20% of cases with severe
preeclampsia

55. •70% of the cases develops before
delivery with a peak frequency
between the 27th and 37th gestational
weeks
•10% occur before the 27th week
•20% beyond the 37th gestational week

56. •HELLP syndrome usually develops within
the first 48 hours in women who have
had proteinuriaand hypertension prior to
delivery

57. •The triad signs of haemolysis, elevated
liver enzymes and thrombocytopenia

58. •Haemolysis, one of the major
characteristics of the disorder, is due to
a microangiopathic, haemolytic anaemia

59. Normal peripheral blood smear

60. Microangiopathic smear

61. H(hemolysis)
•unconjugated bilirubin
•low or undetectable haptoglobin
concentration is a more specific
indicator.
•Low haptoglobin concentration (< 1 g/L
–< 0.4 g/L)

62. Elevated Liver enzymes(EL)
•Elevation of liver enzymes may reflect
the haemolytic process as well as liver
involvement.
•enhanced asparate aminotransferase
(AST) and alanine aminotransferase
(ALAT) levels are mostly due to liver
injury

63. Low platelet(LP)
•Thrombocytopenia < 150·10
9
/L)
•caused by gestational thrombocytopenia (GT) (59%)
•immune thrombocytopenic purpura (ITP) (11%)
•preeclampsia (10%)
•HELLP syndrome (12%).
•PLTs < 100·10
9
/L are relatively rare in preeclampsia
and gestational thrombocytopenia, frequent in ITP
and obligatory in the HELLP syndrome

64. Differential diagnosis
•viral hepatitis
•cholangitis and other acute disease
•ITP
•acute fatty liver of pregnancy (AFLP)
•haemolytic uremic syndrome (HUS)
•thrombotic thrombocytopenic purpura
(TTP)
•systemic lupus erythematosus (SLE)

65. Management of pregnant women
with HELLP syndrome
•Immediate delivery
•> 34 weeks' gestation or later
•Nonreassuring tests of fetal status
•Presence of severe maternal disease:
multiorgan dysfunction, DIC, liver infarction
or hemorrhage, renal failure, or abruptio
placenta

66. •before 24 weeks' gestation, termination
of pregnancy should be strongly
considered

67. Method of Delivery
•Vaginal
•Cesarean section

68. Anesthesia Management
•As oxygen consumption increases
during pregnancy, the maternal
cardiovascular system adapts to meet
the metabolic demands of a growing
fetus.
•Airway edema may be particularly
severe in women with preeclampsia, in
patients placed in the Trendelenburg
position for prolonged periods

69. •A rapid-sequence induction of anesthesia,
application of cricoid pressure, and intubation
with a cuffed endotracheal tube are required
for all pregnant women receiving general
anesthesia after the first trimester.
•The driving force for placental drug transfer is
the concentration gradient of free drug
between the maternal and fetal blood.

70. •By virtue of age and gender, as well as
reduced epidural pressure after delivery,
pregnant women are at a higher risk for
developing post-dural puncture headache
(PDPH).
•Pregnancy and parturition are considered as
high risk when accompanied by conditions
unfavorable to the well-being of the mother,
fetus, or both.

71. •For cesarean section, the choice of anesthesia
depends on the urgency of the procedure, in
addition to the condition of the mother and
fetus.
•Fetal asphyxia develops as a result of
interference with maternal or fetal perfusion
of the placenta.
•Hypertensive diseases of pregnancy are a
common cause of maternal death

72. •Pre-eclampsia is associated with widespread
endothelial dysfunction leading to placental
ischaemia and multi-organ dysfunction.
•The main concerns to the anaesthetist are
those of an oedematous airway and
dysfunction of the cardiorespiratory, cerebro-
vascular and coagulation systems.
•Magnesium Sulphate is the anticonvulsant of
choice in prevention and treatment of
eclamptic fits.

73. Pre-anesthetic assessment
Fluid balance & Haemodynamics
•The presence of hypo-albuminaemia, increased
capillary permeability and a high hydrostatic pressure
(from the hypertension) leads to the risk of
pulmonary and pharyngolaryngeal oedema.
•However, judicious administration of fluid may be
necessary to avoid the pre renal oliguria that is
common with pre-eclamptic patients.
•With adequate treatment it is rare these days for the
oliguria to proceed to chronic renal dysfunction

74. •It is recommended for each department
to have a protocol to guide the
treatment of these patients in a
consistent way.
•Frusemide may be used to treat
persistent oliguria in the presence of an
adequately filled circulation.

75. Anaesthesia technique
•The advantages of regional over general
anaesthesia for Caesarean section include
–avoidance of the hypertensive response to
laryngoscopy
–a blunting of the neuro-endocrine response
to surgery
–prevention of the transient neonatal
depression associated with general
anaesthesia.

76. Spinal anesthesia
•Spinal anesthesia may not be ideal choice for
emergency CS for preeclamsia as LP could be
associated with subdural hematoma and its
preparation and procedure is time consuming,
•However, if chosen the ideal drugs available
are lidocaine 5%, bupivacaine 0.5%,

77. Spinal anesthesia
•Intravascular hypovolemia associated
with preeclampsia, use of
antihypertensive medications, and
administration of magnesium for seizure
prophylaxis may augment the
hypotension produced by neuraxial
techniques.

78. Coagulation
•There is no absolute level of platelet count
that accurately predicts the occurrence of
bleeding associated with regional
anaesthesia.
•thromboelastographic evidence show for the
assertion that there may be increasing risk
from regional blockade as the platelet count
falls below 75 to 80X10
3
/ml

79. •If the platelet count is less than 80,000
mm
-3
then further assessment of the
coagulation status is justified. The
results of the PT, APTT can be
compared with the normal range for
pregnant patients
•fresh-frozen plasma may reduce the risk
of maternal hemorrhage

80. •When responding pharmacologically to
hypotension, restraint is advocated
because patients with hypertensive
disorders may be have an exuberant
response. Small doses of vasopressors
(i.e., ephedrine 5 mg or phenylephrine
20–40 microgram) should be given
initially

81. •Judicious fluid management
•smaller possible dose of local anesthetic

82. General anesthesia
•May be necessary and difficult
intubation should be anticipated, the
main concerns are
–mucosal oedema of the upper airway,
therefore, prepare range of endotracheal
tubes down to a size 5.5-6.5 mm internal
diameter and a variety of laryngoscopes
and other aids
–severe hypertensive responses to noxious
stimuli

83. •Drugs used to attenuate the
hypertensive response to laryngoscopy
include the pre-induction use of
–Hydralazine, magnesium, labetalol,
–nitrates, nitroprusside,
–lidocaine
–parenteral opioids.

84. Summary
•Pre-eclampsia is a heterogeneous
multisystem disorder of pregnancy.
Controversies still exist with regard to
its aetiology, diagnosis and treatment.
•Careful control of the blood pressure in
a high dependency setting is
paramount.

85. Summary
•The main concerns to the obstetric
anaesthetist are those of the potential
problems with the airway and the
effects of organ dysfunction particularly
those of the cardiorespiratory, cerebral
and coagulation systems

86. Team work

88. •Thank you