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1
OUTLINE
1. Objective
2. Introduction
3. Classification
4. Definition
5. Etiology
6. Risk factors
7. Pathophysiology
8. Clinical presentation
9. Diagnosis
10.Treatment (goal of therapy, pharmacologic and non-pharmacologic therapy)
11.Follow-up (outcome evaluation) 1/2/2024 2
OBJECTIVE
 Define Hypertensive disorders in pregnancy
 Understand the:
pathophysiology,
sign & symptoms,
diagnosis and
management of Preeclampsia and eclampsia
1/2/2024 3
INTRODUCTION
Hypertension is the most common medical complication encountered
during pregnancy.
Complicating up to 10% of pregnancies.
Increased maternal and perinatal morbidity and mortality.
1/2/2024 4
CLASSIFICATION
1/2/2024 5
Hypertension in
Pregnancy
Pregnancy Induced
Hypertension
Gestational
Hypertension
Preeclampsia Eclampsia
Chronic
Hypertension
DEFINITION
During pregnancy, hypertension is defined as:
SBp ≥140 mmHg and/or DBp ≥90 mmHg on at least 2 occasions 4hrs apart.
Severe hypertension – SBp ≥160 mmHg and/or DBp ≥110 mmHg.
Chronic Hypertension:
Hypertension detected pre-pregnancy or before 20 weeks of gestation.
1/2/2024 6
CONT.
Gestational hypertension:
Hypertension without proteinuria or other signs/symptoms of preeclampsia.
Develops after 20 weeks of gestation.
 Up to 50 percent of these patients may ultimately develop signs and symptoms of
preeclampsia.
True gestational hypertension should resolve by 12 weeks postpartum.
1/2/2024 7
CONT.
Preeclampsia:
 Refers to the new onset of hypertension and proteinuria or significant end-
organ dysfunction with or without proteinuria.
After 20 weeks of gestation or postpartum.
1/2/2024 8
CONT.
Eclampsia:
Occurrence of a tonic-clonic seizure in a patient with preeclampsia in the
absence of other neurologic conditions that could account for the seizure.
1/2/2024 9
PREECLAMPSIA
Preeclampsia is a multisystem progressive disorder characterized by:
 The new onset of hypertension and proteinuria
or the new onset of hypertension plus significant end-organ dysfunction with
or without proteinuria,
 typically presenting after 20 weeks of gestation or Postpartum.
1/2/2024 10
CONT.
Superimposed Preeclampsia:
Preeclampsia occurs in patients with chronic hypertension.
Characterized by:
Acutely worsening hypertension
Resistance hypertension
New onset or sudden increase proteinuria
And/or new systemic/organ features in patients with CHTN
1/2/2024 11
ETIOLOGY
The etiology or exact cause of preeclampsia is not fully understood.
But it is thought to be caused by abnormalities in the development of
placenta.
The placenta not developing properly due to a problem with the blood vessels
supplying it.
1/2/2024 12
RISK FACTORS
Nulliparity
Multifetal gestation
Preeclampsia in previous pregnancy
Family history of preeclampsia
Age > 40 or < 18
Obesity
Chronic hypertension
Chronic kidney disease
Diabetes mellitus
Vascular disease
Autoimmune diseases
1/2/2024 13
PATHOPHYSIOLOGY
1/2/2024 14
The pathophysiology of
preeclampsia likely involves both
maternal and fetal/placental
factors.
1/2/2024 15
CLINICAL PRESENTATION
Sign/symptoms
Hypertension - All patients with
preeclampsia have hypertension
Persistent and/or severe headache
Visual abnormalities (photophobia,
blurred vision, or temporary blindness
Seizure
Altered mental status (confusion,
altered behavior [agitation])
RUQ, retrosternal, or epigastric
pain
New dyspnea, orthopnea
Oliguria
1/2/2024 16
CONT.
Potential laboratory findings
Proteinuria
Elevated creatinine
Thrombocytopenia
Elevated liver enzymes
1/2/2024 17
DIAGNOSIS
Preeclampsia is diagnosed with measured BP and presence of one or more
end organ dysfunction features.
Measured BP:
SBp ≥140 mmHg and/or DBp ≥90 mmHg (at least 2 occasions 4 hours apart).
1/2/2024 18
End organ dysfunction features:
Proteinuria ≥0.3 g in a 24-hour
urine
Platelet count <100,000/microL
Serum creatinine >1.1 mg/dL
Liver transaminases at least 2x the
UNL
Pulmonary edema
New-onset and persistent headache
Visual symptoms - blurred vision
1/2/2024 19
Severe Preeclampsia/ Preeclampsia with severe features
Diagnosis is with the presence of one or more of the following:
SBp ≥160 mmHg and/or DBp ≥110 mmHg
Symptoms of CNS
 New onset visual disturbance
 Severe headache
1/2/2024 20
Hepatic abnormality
 Liver transaminases at least 2x the UNL
 Severe persistent RUQ or epigastric pain
Kidney function impairment
 Serum creatinine >1.1 mg/dL
Platelet count <100,000/microL
Pulmonary edema
1/2/2024 21
TREATMENT
Goal of therapy
 To Control elevated BP.
To prevent severe HTN.
To prevent complications.
1/2/2024 22
The definitive treatment of preeclampsia is delivery to prevent development
of maternal or fetal complications from the disease.
Timing of delivery is based upon gestational age, the severity of
preeclampsia, and maternal and fetal condition.
1/2/2024 23
TIMING OF DELIVERY IN WOMEN WITH
PREECLAMPSIA
1/2/2024 24
1/2/2024 25
1/2/2024 26
Antihypertensive therapy is required for the treatment of severe hypertension
to prevent stroke, heart failure and other complications.
Antihypertensive therapy to control non severe hypertension does not alter
the course of preeclampsia and avoided in most patients.
Antihypertensive therapy may be suggested in non severe hypertension that
the elevated BP is persists after multiple measurements if delivery is likely to
be delayed for several days or weeks.
1/2/2024 27
MANAGEMENT 0F SEVERE HTN IN PREECLAMPSIA
1/2/2024 28
1/2/2024 29
SEIZURE PROPHYLAXIS
Intrapartum and postpartum seizure prophylaxis is recommended for all
patients with preeclampsia with severe features.
MgSo4 is drug of choice
 Usually initiated at the onset of labor or induction, or prior to.
Loading dose 4 - 6 g of a 10% solution iv over 15 to 20 minutes followed by 1 –
2 g/hour as a continuous infusion
If Cr is 1.1 – 2.5 maintenance dose of 1g/hr. If >2.5 or magnesium toxicity no
maintenance dose.
1/2/2024 30
MgSo4 toxicity:
Loss of deep tendon reflexes
Respiratory paralysis
Altered cardiac conduction
Cardiac arrest
Antidote – calcium gluconate 15 to 30ml of 10% solution Iv over 2 to 5
minutes for severe cardiac toxicity. 10 ml of 10% solution for less severe.
Alternative calcium chloride 5 to 10 ml of 10% solution
1/2/2024 31
PREVENTION OF PREECLAMPSIA
Low dose aspirin prophylaxis:
For high risk patients.
Aspirin 81 mg daily is recommended. 100 – 150 mg can be suggested.
Initiate aspirin in the 12th or 13th wks. of gestation.
Continue until delivery
1/2/2024 32
ECLAMPSIA
Eclampsia refers to the occurrence of new onset generalized tonic-clonic
seizure in patients with preeclampsia.
It is the convulsive manifestation of preeclampsia and one of clinical
manifestation at the severe end of the preeclampsia spectrum.
1/2/2024 33
PATHOGENESIS OF SEIZURE
Risk factors for eclampsia are similar to those for preeclampsia.
The precise cause of eclamptic seizure is not clearly understood. Two models
have been proposed.
1. Hypertension causes a breakdown of the autoregulatory system of cerebral
circulation, leading to hypoperfusion, endothelial dysfunction, and vasogenic
and/or cytotoxic edema.
1/2/2024 34
2. Hypertension causes activation of the autoregulatory system, leading to
constriction of cerebral vessels, hypoperfusion, localized ischemia,
endothelial dysfunction, and vasogenic and/or cytotoxic edema.
1/2/2024 35
CHARACTERISTICS OF ECLAMPTIC SEIZURE
Generally manifested by self limiting tonic-clonic seizure.
At onset an abrupt loss of consciousness.
The muscles of arms, legs, chest and back become stiff. After approximately
one minute the muscles begin to jerk for additional 1 to 2 minutes
1/2/2024 36
DIAGNOSIS
Clinical diagnosis based on new onset tonic-clonic seizure in the absence of
other causative conditions typically in patients with hypertensive disorders of
pregnancy.
1/2/2024 37
MANAGEMENT
If seizure is witnessed, maintaining air way patency and preventing aspiration
are the initial priorities.
The tonic-clonic phase usually resolves within 2 minutes. However, if the
patient is actively seizing for > 5 minutes:
Lorazepam 4mg IV At maximum rate of 2 mg/min., may repeat at 2 to 5 min if
seizure continues
If IV access has not been established Midazolam 10mg IM is alternative
1/2/2024 38
MgSo4 Prophylaxis:
MgSo4 can initiated after first episode of seizure for prevention of recurrent
seizures.
In patients with recurrent seizures on maintenance magnesium therapy, can
be treated with an additional bolus of 2 to 4 g Mgso4 administered IV over 5
minutes with frequent monitoring of magnesium toxicity.
1/2/2024 39
REFERENCES
1. UpToDate 21.6
2. MSD Manual Professional Version
1/2/2024 40
41

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Pharmacotherapy of Hypertension and Pregnancy.pptx

  • 1. 1
  • 2. OUTLINE 1. Objective 2. Introduction 3. Classification 4. Definition 5. Etiology 6. Risk factors 7. Pathophysiology 8. Clinical presentation 9. Diagnosis 10.Treatment (goal of therapy, pharmacologic and non-pharmacologic therapy) 11.Follow-up (outcome evaluation) 1/2/2024 2
  • 3. OBJECTIVE  Define Hypertensive disorders in pregnancy  Understand the: pathophysiology, sign & symptoms, diagnosis and management of Preeclampsia and eclampsia 1/2/2024 3
  • 4. INTRODUCTION Hypertension is the most common medical complication encountered during pregnancy. Complicating up to 10% of pregnancies. Increased maternal and perinatal morbidity and mortality. 1/2/2024 4
  • 5. CLASSIFICATION 1/2/2024 5 Hypertension in Pregnancy Pregnancy Induced Hypertension Gestational Hypertension Preeclampsia Eclampsia Chronic Hypertension
  • 6. DEFINITION During pregnancy, hypertension is defined as: SBp ≥140 mmHg and/or DBp ≥90 mmHg on at least 2 occasions 4hrs apart. Severe hypertension – SBp ≥160 mmHg and/or DBp ≥110 mmHg. Chronic Hypertension: Hypertension detected pre-pregnancy or before 20 weeks of gestation. 1/2/2024 6
  • 7. CONT. Gestational hypertension: Hypertension without proteinuria or other signs/symptoms of preeclampsia. Develops after 20 weeks of gestation.  Up to 50 percent of these patients may ultimately develop signs and symptoms of preeclampsia. True gestational hypertension should resolve by 12 weeks postpartum. 1/2/2024 7
  • 8. CONT. Preeclampsia:  Refers to the new onset of hypertension and proteinuria or significant end- organ dysfunction with or without proteinuria. After 20 weeks of gestation or postpartum. 1/2/2024 8
  • 9. CONT. Eclampsia: Occurrence of a tonic-clonic seizure in a patient with preeclampsia in the absence of other neurologic conditions that could account for the seizure. 1/2/2024 9
  • 10. PREECLAMPSIA Preeclampsia is a multisystem progressive disorder characterized by:  The new onset of hypertension and proteinuria or the new onset of hypertension plus significant end-organ dysfunction with or without proteinuria,  typically presenting after 20 weeks of gestation or Postpartum. 1/2/2024 10
  • 11. CONT. Superimposed Preeclampsia: Preeclampsia occurs in patients with chronic hypertension. Characterized by: Acutely worsening hypertension Resistance hypertension New onset or sudden increase proteinuria And/or new systemic/organ features in patients with CHTN 1/2/2024 11
  • 12. ETIOLOGY The etiology or exact cause of preeclampsia is not fully understood. But it is thought to be caused by abnormalities in the development of placenta. The placenta not developing properly due to a problem with the blood vessels supplying it. 1/2/2024 12
  • 13. RISK FACTORS Nulliparity Multifetal gestation Preeclampsia in previous pregnancy Family history of preeclampsia Age > 40 or < 18 Obesity Chronic hypertension Chronic kidney disease Diabetes mellitus Vascular disease Autoimmune diseases 1/2/2024 13
  • 14. PATHOPHYSIOLOGY 1/2/2024 14 The pathophysiology of preeclampsia likely involves both maternal and fetal/placental factors.
  • 16. CLINICAL PRESENTATION Sign/symptoms Hypertension - All patients with preeclampsia have hypertension Persistent and/or severe headache Visual abnormalities (photophobia, blurred vision, or temporary blindness Seizure Altered mental status (confusion, altered behavior [agitation]) RUQ, retrosternal, or epigastric pain New dyspnea, orthopnea Oliguria 1/2/2024 16
  • 17. CONT. Potential laboratory findings Proteinuria Elevated creatinine Thrombocytopenia Elevated liver enzymes 1/2/2024 17
  • 18. DIAGNOSIS Preeclampsia is diagnosed with measured BP and presence of one or more end organ dysfunction features. Measured BP: SBp ≥140 mmHg and/or DBp ≥90 mmHg (at least 2 occasions 4 hours apart). 1/2/2024 18
  • 19. End organ dysfunction features: Proteinuria ≥0.3 g in a 24-hour urine Platelet count <100,000/microL Serum creatinine >1.1 mg/dL Liver transaminases at least 2x the UNL Pulmonary edema New-onset and persistent headache Visual symptoms - blurred vision 1/2/2024 19
  • 20. Severe Preeclampsia/ Preeclampsia with severe features Diagnosis is with the presence of one or more of the following: SBp ≥160 mmHg and/or DBp ≥110 mmHg Symptoms of CNS  New onset visual disturbance  Severe headache 1/2/2024 20
  • 21. Hepatic abnormality  Liver transaminases at least 2x the UNL  Severe persistent RUQ or epigastric pain Kidney function impairment  Serum creatinine >1.1 mg/dL Platelet count <100,000/microL Pulmonary edema 1/2/2024 21
  • 22. TREATMENT Goal of therapy  To Control elevated BP. To prevent severe HTN. To prevent complications. 1/2/2024 22
  • 23. The definitive treatment of preeclampsia is delivery to prevent development of maternal or fetal complications from the disease. Timing of delivery is based upon gestational age, the severity of preeclampsia, and maternal and fetal condition. 1/2/2024 23
  • 24. TIMING OF DELIVERY IN WOMEN WITH PREECLAMPSIA 1/2/2024 24
  • 27. Antihypertensive therapy is required for the treatment of severe hypertension to prevent stroke, heart failure and other complications. Antihypertensive therapy to control non severe hypertension does not alter the course of preeclampsia and avoided in most patients. Antihypertensive therapy may be suggested in non severe hypertension that the elevated BP is persists after multiple measurements if delivery is likely to be delayed for several days or weeks. 1/2/2024 27
  • 28. MANAGEMENT 0F SEVERE HTN IN PREECLAMPSIA 1/2/2024 28
  • 30. SEIZURE PROPHYLAXIS Intrapartum and postpartum seizure prophylaxis is recommended for all patients with preeclampsia with severe features. MgSo4 is drug of choice  Usually initiated at the onset of labor or induction, or prior to. Loading dose 4 - 6 g of a 10% solution iv over 15 to 20 minutes followed by 1 – 2 g/hour as a continuous infusion If Cr is 1.1 – 2.5 maintenance dose of 1g/hr. If >2.5 or magnesium toxicity no maintenance dose. 1/2/2024 30
  • 31. MgSo4 toxicity: Loss of deep tendon reflexes Respiratory paralysis Altered cardiac conduction Cardiac arrest Antidote – calcium gluconate 15 to 30ml of 10% solution Iv over 2 to 5 minutes for severe cardiac toxicity. 10 ml of 10% solution for less severe. Alternative calcium chloride 5 to 10 ml of 10% solution 1/2/2024 31
  • 32. PREVENTION OF PREECLAMPSIA Low dose aspirin prophylaxis: For high risk patients. Aspirin 81 mg daily is recommended. 100 – 150 mg can be suggested. Initiate aspirin in the 12th or 13th wks. of gestation. Continue until delivery 1/2/2024 32
  • 33. ECLAMPSIA Eclampsia refers to the occurrence of new onset generalized tonic-clonic seizure in patients with preeclampsia. It is the convulsive manifestation of preeclampsia and one of clinical manifestation at the severe end of the preeclampsia spectrum. 1/2/2024 33
  • 34. PATHOGENESIS OF SEIZURE Risk factors for eclampsia are similar to those for preeclampsia. The precise cause of eclamptic seizure is not clearly understood. Two models have been proposed. 1. Hypertension causes a breakdown of the autoregulatory system of cerebral circulation, leading to hypoperfusion, endothelial dysfunction, and vasogenic and/or cytotoxic edema. 1/2/2024 34
  • 35. 2. Hypertension causes activation of the autoregulatory system, leading to constriction of cerebral vessels, hypoperfusion, localized ischemia, endothelial dysfunction, and vasogenic and/or cytotoxic edema. 1/2/2024 35
  • 36. CHARACTERISTICS OF ECLAMPTIC SEIZURE Generally manifested by self limiting tonic-clonic seizure. At onset an abrupt loss of consciousness. The muscles of arms, legs, chest and back become stiff. After approximately one minute the muscles begin to jerk for additional 1 to 2 minutes 1/2/2024 36
  • 37. DIAGNOSIS Clinical diagnosis based on new onset tonic-clonic seizure in the absence of other causative conditions typically in patients with hypertensive disorders of pregnancy. 1/2/2024 37
  • 38. MANAGEMENT If seizure is witnessed, maintaining air way patency and preventing aspiration are the initial priorities. The tonic-clonic phase usually resolves within 2 minutes. However, if the patient is actively seizing for > 5 minutes: Lorazepam 4mg IV At maximum rate of 2 mg/min., may repeat at 2 to 5 min if seizure continues If IV access has not been established Midazolam 10mg IM is alternative 1/2/2024 38
  • 39. MgSo4 Prophylaxis: MgSo4 can initiated after first episode of seizure for prevention of recurrent seizures. In patients with recurrent seizures on maintenance magnesium therapy, can be treated with an additional bolus of 2 to 4 g Mgso4 administered IV over 5 minutes with frequent monitoring of magnesium toxicity. 1/2/2024 39
  • 40. REFERENCES 1. UpToDate 21.6 2. MSD Manual Professional Version 1/2/2024 40
  • 41. 41

Editor's Notes

  1. In severe hypertension confirmation within minutes is sufficient Chronic hypertension may be essential hypertension (ie, without a known secondary cause) or Secondary hypertension (ie, with a known secondary cause, e.g., kidney disease).
  2. Develops after 20 weeks of gestation in a patient with a previously normal blood pressure.
  3. Most patients have proteinuria, but it is important to emphasize that the diagnosis can be made in a pregnant patient with hypertension but no proteinuria if the new-onset hypertension is accompanied by specific signs or symptoms of significant end organ dysfunction
  4. Abnormalities in the development of placental vasculature early in pregnancy may result in = relative placental under perfusion/hypoxia/ischemia, = which then leads to release of antiangiogenic factors into the maternal circulation that alter maternal systemic endothelial function = and cause hypertension and other manifestations of the disease (hematologic, neurologic, cardiac, pulmonary, renal, and hepatic dysfunction)