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Hypertensive-Disorders-with-Pregnancy.ppt

C.G. is a 39-year-old pregnant woman presenting with increased blood pressure and swelling. At 28 weeks gestation, her blood pressure was 180/100. She was diagnosed with preeclampsia based on her gestational hypertension and proteinuria. Preeclampsia is a hypertensive disorder of pregnancy affecting 7-10% of pregnancies. It is characterized by new onset hypertension and proteinuria after 20 weeks of gestation. Symptoms can range from mild to severe, including headaches, visual disturbances, RUQ pain, and others. Progression of preeclampsia must be closely monitored to determine optimal timing of delivery to prevent maternal and fetal complications.

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Hypertensive Disorders With Pregnancy Hisham M. Gamal, MD lecturer of Anaesthesia and postoperative ICU Alexandria Faculty Of Medicine [hisham.gamal83@yahoo.com]
• C.G. is a 39 year old married white female gravida 2, para 0, with one spontaneous abortion who presented for prenatal care at 14 weeks gestation. Blood pressure at that time was 130/80. The patient had no significant medical history and her gynecologic history was significant only for oral contraceptive use several years ago. • The pregnancy had been unremarkable until approximately one month ago when the patient noted increased swelling of her hands and feet. A 6 Kg. weight gain in two weeks time was noted. Blood pressure at that time was 124/78. There was no urinary protein. On the day prior to admission, at 28 weeks, the patient presented with a blood pressure of 160/98 and had been sent home to bedrest with instructions to take a single baby aspirin daily. On the day following, the patient was noted at home to have a persistent blood pressure of 180/100.
Avant propos… • 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
• Young female 3 fold increased risk • African American 2 fold increased risk • Multifetal pregnancies – Twins – Triplets • Hypertension • Diabetes Mellitus • Renal Disease • Collagen Vascular Disease
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
Preeclampsia: Risk Factors • Nulliparity (or, more correctly, primipaternity) • Chronic renal disease • Angiotensinogen gene T235 • Chronic hypertension • Antiphospholipid antibody syndrome • Multiple gestation • Family or personal history of preeclampsia • Age > 40 years • African-American race • Diabetes mellitus
Etiology and Prevention • Etiology is unknown. • Many theories: – genetic – immunologic – dietary deficiency (calcium, magnesium, zinc) • supplementation has not proven effective – placental source (ischemia)
Dr.Hisham
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)
Preeclampsia Prophylaxis: Aspirin • Aspirin has been extensively studied as a targeted therapy to  thromboxane production • CLASP study, A multicenter RCT [CLASP Collaborative Group, Lancet 1994;343:619-29] – 9364 women, risk factors for PIH or IUGR or who had PIH or IUGR – 60 mg ASA daily vs. placebo – Small reduction (12%) in occurrence of PIH – Small reduction in preterm deliveries: 20 vs 22% – No difference in neonatal outcome
Preeclampsia Prophylaxis: Aspirin • NIH study of high-risk patients, RCT, 60 mg aspirin daily vs. placebo [Caritis, et al., N Engl J Med 1998;338:701-5] – pre-gestational DM (471 patients) – chronic hypertension (774 patients) – multifetal gestations (688 patients) – prior history of preeclampsia (606 patients) • No reduction in development of preeclampsia in any subgroup or groups in aggregate • No difference in perinatal death, preterm delivery, IUGR, maternal or fetal hemorrhagic complications
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
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.
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)
Pathophysiology: Cardiovascular • Preeclamptic patients are prone to develop pulmonary edema due 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
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 w/subendothelial protein deposits – Renal function recovers quickly postpartum
Pathophysiology: Hepatic • RUQ pain is a serious complaint – warrants 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.
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
Classification • Chronic hypertension • Preeclampsia-eclampsia • Preeclampsia Superimposed upon chronic hypertension or Renal Disease • Gestational hypertension (only during pregnancy) • Transient hypertension (only after pregnancy)
Chronic Hypertension Defined as hypertension diagnosed • Before pregnancy • Before the 20th week of gestation • During pregnancy and not resolved postpartum
Gestational Hypertension • Gestational Hypertension: –Systolic >140 –Diastolic>90 –No Proteinurea –25% Develop Pre-eclampsia
Gestational Hypertension Diagnosis of gestational hypertension: • Detected for first time after midpregnancy • No proteinuria • Only until a more specific diagnosis can be assigned postpartum If: • BP returns to normal by 12 weeks postpartum, diagnosis is transient hypertension. • BP remains high postpartum, diagnosis is chronic hypertension. • Proteinurea develops Superimposed Preeclampsia is diagnosed (25% incidence)
Preeclampsia-Eclampsia • Occurs after 20th week (earlier with trophoblastic disease) • Increased BP (gestational BP elevation) with proteinuria • ‘LL’ Edema is NOT part of this definition
Diagnosis of Preeclampsia-Eclampsia • Gestational Hypertension: –Systolic >140 –Diastolic>90 • Proteinuria is defined as urinary excretion – 0.3 g protein or greater in a 24-hour – +2 or greater on urine dip specimen
Classification of Preeclampsia- Eclampsia • Mild Pre-eclampsia • Severe Pre-eclampsia
Classification of Preeclampsia-Eclampsia • Criteria for Severe Preeclampsia (one or more) – Blood Pressure: >160 systolic, >110 diastolic – Proteinurea: >5gm in 24 hours, over 3+ urine dip – Oligurea: less than 400ml in 24 hours – CNS: Visual changes, headache, scotomata, mental status change – Pulmonary Edema – Epigastric or RUQ Pain: Usually indicates liver involvement
Classification of Preeclampsia- Eclampsia • Criteria for Severe Preeclampsia (one or more) – Impaired Liver Function tests – Thrombocytopenia: <100,000 – Intrauterine Growth Restriction: With or without abnormal doppler assessment – Oligohydramnios
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.
Symptoms of Preeclampsia • 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. • Epigastric pain 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.
Symptoms of preeclampsia • While mild lower extremity edema is common in normal pregnancy, rapidly increasing or nondependent edema may be a signal of developing preeclampsia. However, this signal theory remains controversial and recently has been removed from most 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.
Physical Findings in Preeclampsia • Blood Pressure • Proteinurea • Retinal vasospasm or Retinal edema • Right upper quadrant (RUQ) abdominal tenderness stems from liver swelling and capsular stretch
Physical findings in Preeclampsia – Brisk, or hyperactive, reflexes are common during pregnancy, but clonus is a sign of neuromuscular irritability that raises concern. – Among pregnant women, 30% have some lower extremity edema as part of their normal pregnancy. However, a sudden change in dependent edema, edema in nondependent areas such as the face and hands, or rapid weight gain suggests a pathologic process and warrants further evaluation
Eclampsia • Women older than 40 years with preeclampsia have 4 times the incidence of seizures compared to women in their third decade of life. – Twenty-five percent of eclampsia cases occur before labor (ie, antepartum). – Fifty percent of eclampsia cases occur during labor (ie, intrapartum). – Twenty-five percent of eclampsia cases occur after delivery (ie, postpartum). – Patients with severe preeclampsia are at greater risk to develop seizures. – Twenty-five percent of patients with eclampsia have only mild preeclampsia prior to the seizures
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.
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.
• 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. • 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. • 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.
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
Laboratory Tests Patients presenting with hypertension before gestation week 20: • Same tests as described for high-risk patients presenting with normal BP • Early baseline sonography for dating and fetal size
Laboratory Tests Patients presenting with hypertension after midpregnancy: • Quantification of protein excretion • Hemoglobin and hematocrit and platelet count • Serum creatinine, uric acid, and transaminase level • Serum albumin, LDH, blood smear, and coagulation profile
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.
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.
Preeclampsia: Treatment • Maternal Evaluation…When To Hospitalize? – Often, hospitalization recommended with new-onset preeclampsia to assess maternal and fetal conditions. – Hospitalization for duration of pregnancy indicated for preterm onset of severe gestational hypertension or preeclampsia. – Ambulatory management at home or at day-care unit may be considered with mild gestational hypertension or preeclampsia remote from term
Preeclampsia
Indication of Delivery
Preeclampsia • Antepartum Management of Preeclampsia – Little to suggest therapy alters the underlying pathophysiology of preeclampsia. – Restricted activity may be reasonable. – Sodium restriction and diuretic therapy appear to have no positive effect.
Obstetric Management • Classically “stabilize and deliver”
Preeclampsia • The “cure” for preeclampsia is delivery – The “cure” is always beneficial for the mother, although c-section might be needed – The “cure” may be deleterious for the fetus
Preeclampsia • Route of Delivery – Vaginal delivery is preferable. – Aggressive labor induction (within 24 hours). – Neuraxial (epidural, spinal, and combined spinal-epidural) techniques offer advantages. – Hydralazine, nitroglycerin, or labetalol may be used as pretreatment to reduce significant hypertension during delivery.
Obstetric Management • Medical management while awaiting delivery: – use of steroids X 48 hours if fetus < 34 wks – antihypertensives to maintain DBP < 105-110 – magnesium sulfate for seizure prophylaxis – monitor fluid balance, I/O, daily weights, symptoms, reflexes, HCT, plts, LFT’s, proteinuria
Obstetric Management • Indications for expedited delivery: – fetal distress –  BP despite aggressive Rx – worsening end-organ function – development or worsening of HELLP syndrome – development of eclampsia
Antihypertensive Therapy • Most commonly, for acute control: hydralazine, labetolol • Nifedipine may be used, but unexpected hypotension may occur when given with MgSO4 • 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
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
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
Nifedipine • Dose: 10 mg po, not sublingual(potent generalized vasodilatation) • Onset: 5-10 minutes • Duration: 4-8 hours • Side effects: chest pain, headache, tachycardia • Mechanism: CA channel block
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: cyanide accumulation, hypotension • Mechanism: direct vasodilator
Preeclampsia • Anticonvulsive Therapy – Indicated to prevent recurrent convulsions in women with eclampsia or to prevent convulsions in women with preeclampsia. – Parenteral magnesium sulfate reduces the frequency of eclampsia and maternal death. (Caution in renal failure.)
Seizure Prophylaxis & Treatment • Magnesium sulfate vs. phenytoin for seizure prophylaxis in preeclampsia Lucas, et al., N Engl J Med 1995;333:201-5. – 2138 patients (75% had mild PIH) – Maternal & fetal outcomes similar except 10 seizures in the phenytoin group (0 in MgSO4) • Mg vs. diazepam & Mg vs. phenytoin for preventing recurrent seizures in eclamptics Eclampsia Trial Collaborative Group, Lancet 1995;345:1455 – Mg pts were 52% or 67% less likely to have a recurrent seizure than diazepam or phenytoin pts
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 – awaits large, prospective, randomized, placebo-controlled trial
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
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 • Treatment of magnesium toxicity: – stop MgSO4, IV calcium, manage airway
Treatment of Eclampsia • Seizures are usually short-lived. • If necessary, small doses of barbiturate or benzodiazepine (STP, 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.
Anesthetic Goals of Labor Analgesia in Preeclampsia • To establish & maintain hemodynamic stability (control hypertension & avoid hypotension) • To provide excellent labor analgesia • To prevent complications of preeclampsia – intracerebral hemorrhage – renal failure – pulmonary edema – eclampsia • To be able to rapidly provide anesthesia for C/S
Regional vs. General Anesthesia in Preeclampsia • Epidural anesthesia would probably be preferred by many anesthesiologists in a severely preeclamptic pt in a non-urgent setting • For urgent cases it is reassuring to know that spinal is also safe • This allows us to avoid general anesthesia with the potential for encountering a swollen, difficult airway and/or labile hypertension
Regional vs. General Anesthesia in Preeclampsia • General anesthesia is a well-known hazard in obstetric anesthesia: – 16X more likely to result in anesthetic- related maternal mortality – Mostly due to airway/respiratory complications, which would only be exaggerated in preeclampsia Hawkins, Anesthesiology 1997;86:273
Platelets & Regional Anesthesia in Preeclampsia • Prior to placing regional block in a preeclamptic it is recommended to check the platelet count. • No concrete evidence at to the lowest safe platelet count for regional anesthesia in preeclampsia • Any clinical evidence of DIC would contraindicate regional anesthesia.
Hazards of General Anesthesia in Preeclampsia • Airway edema is common – Mandatory to reexamine the airway soon before induction – Edema may appear or worsen at any time during the course of disease • tongue & facial, as well as laryngeal • Laryngoscopy and intubation may  severe BP – Labetolol & NTG are commonly used acutely – Fentanyl (1 mcg/kg), alfentanil (10 mcg/kg), lidocaine may be given to blunt response
Hazards of General Anesthesia in Preeclampsia • Magnesium sulfate potentiates depolarizing & non-depolarizing muscle relaxants – Initial dose of succinylcholine is not reduced. – Neuromuscular blockade should be monitored & reversal confirmed.
Invasive Central Hemodynamic Monitoring in Preeclampsia • Usually reserved for patients with complications – oliguria unresponsive to modest fluid challenge (500 cc LR X 2) – pulmonary edema – refractory hypertension • may have increased CO or increased SVR • Poor correlation between CVP and PCWP in PIH – However, at most centers anesthesiologists would begin with CVP & follow trend • not arbitrarily hydrate to a certain number – If poor response, change to PA catheter
Conclusions • Preeclampsia is a serious multi-organ system disorder of pregnancy that continues to defy our complete understanding. • It is characterized by global endothelial cell dysfunction. • The cause remains unknown. • There is no effective prophylaxis.
Conclusions • Delivery is the only effective cure. • Magnesium sulfate is now proven as the best medication to prevent and treat eclampsia. • Epidural analgesia for labor pain management & regional anesthesia for C/S have many beneficial effects & are preferred.
Postpartum Counseling and Followup • Counseling for Future Pregnancies • Risk of recurrent preeclampsia increases with – Preeclampsia before 30 weeks (40%) – Multiparas as compared with nulliparas or new father – Risk of recurrent preeclampsia may be substantially greater in African Americans.
Hypertensive-Disorders-with-Pregnancy.ppt

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Hypertensive-Disorders-with-Pregnancy.ppt

  • 1.
    Hypertensive Disorders With Pregnancy HishamM. Gamal, MD lecturer of Anaesthesia and postoperative ICU Alexandria Faculty Of Medicine [hisham.gamal83@yahoo.com]
  • 2.
    • C.G. isa 39 year old married white female gravida 2, para 0, with one spontaneous abortion who presented for prenatal care at 14 weeks gestation. Blood pressure at that time was 130/80. The patient had no significant medical history and her gynecologic history was significant only for oral contraceptive use several years ago. • The pregnancy had been unremarkable until approximately one month ago when the patient noted increased swelling of her hands and feet. A 6 Kg. weight gain in two weeks time was noted. Blood pressure at that time was 124/78. There was no urinary protein. On the day prior to admission, at 28 weeks, the patient presented with a blood pressure of 160/98 and had been sent home to bedrest with instructions to take a single baby aspirin daily. On the day following, the patient was noted at home to have a persistent blood pressure of 180/100.
  • 3.
    Avant propos… • Complicates7-10% of pregnancies – 70% Preeclampsia-eclampsia – 30% Chronic hypertension – Eclampsia 0.05% incidence • 20% of Maternal Deaths • Cause of 10% of Preterm birth • Etiology unknown
  • 4.
    • Young female3 fold increased risk • African American 2 fold increased risk • Multifetal pregnancies – Twins – Triplets • Hypertension • Diabetes Mellitus • Renal Disease • Collagen Vascular Disease
  • 6.
    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
  • 7.
    Preeclampsia: Risk Factors •Nulliparity (or, more correctly, primipaternity) • Chronic renal disease • Angiotensinogen gene T235 • Chronic hypertension • Antiphospholipid antibody syndrome • Multiple gestation • Family or personal history of preeclampsia • Age > 40 years • African-American race • Diabetes mellitus
  • 8.
    Etiology and Prevention •Etiology is unknown. • Many theories: – genetic – immunologic – dietary deficiency (calcium, magnesium, zinc) • supplementation has not proven effective – placental source (ischemia)
  • 9.
  • 11.
    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)
  • 12.
    Preeclampsia Prophylaxis: Aspirin •Aspirin has been extensively studied as a targeted therapy to  thromboxane production • CLASP study, A multicenter RCT [CLASP Collaborative Group, Lancet 1994;343:619-29] – 9364 women, risk factors for PIH or IUGR or who had PIH or IUGR – 60 mg ASA daily vs. placebo – Small reduction (12%) in occurrence of PIH – Small reduction in preterm deliveries: 20 vs 22% – No difference in neonatal outcome
  • 13.
    Preeclampsia Prophylaxis: Aspirin •NIH study of high-risk patients, RCT, 60 mg aspirin daily vs. placebo [Caritis, et al., N Engl J Med 1998;338:701-5] – pre-gestational DM (471 patients) – chronic hypertension (774 patients) – multifetal gestations (688 patients) – prior history of preeclampsia (606 patients) • No reduction in development of preeclampsia in any subgroup or groups in aggregate • No difference in perinatal death, preterm delivery, IUGR, maternal or fetal hemorrhagic complications
  • 15.
    Preeclampsia: Mechanism • Atthis 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, anddistinguishing 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 • Insevere 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 • Preeclampticpatients are prone to develop pulmonary edema due 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: – Airwayis 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 w/subendothelial protein deposits – Renal function recovers quickly postpartum
  • 20.
    Pathophysiology: Hepatic • RUQpain is a serious complaint – warrants 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: – Generallyhypercoagulable 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.
    Classification • Chronic hypertension •Preeclampsia-eclampsia • Preeclampsia Superimposed upon chronic hypertension or Renal Disease • Gestational hypertension (only during pregnancy) • Transient hypertension (only after pregnancy)
  • 23.
    Chronic Hypertension Defined ashypertension diagnosed • Before pregnancy • Before the 20th week of gestation • During pregnancy and not resolved postpartum
  • 24.
    Gestational Hypertension • GestationalHypertension: –Systolic >140 –Diastolic>90 –No Proteinurea –25% Develop Pre-eclampsia
  • 25.
    Gestational Hypertension Diagnosis ofgestational hypertension: • Detected for first time after midpregnancy • No proteinuria • Only until a more specific diagnosis can be assigned postpartum If: • BP returns to normal by 12 weeks postpartum, diagnosis is transient hypertension. • BP remains high postpartum, diagnosis is chronic hypertension. • Proteinurea develops Superimposed Preeclampsia is diagnosed (25% incidence)
  • 26.
    Preeclampsia-Eclampsia • Occurs after20th week (earlier with trophoblastic disease) • Increased BP (gestational BP elevation) with proteinuria • ‘LL’ Edema is NOT part of this definition
  • 27.
    Diagnosis of Preeclampsia-Eclampsia •Gestational Hypertension: –Systolic >140 –Diastolic>90 • Proteinuria is defined as urinary excretion – 0.3 g protein or greater in a 24-hour – +2 or greater on urine dip specimen
  • 28.
    Classification of Preeclampsia- Eclampsia •Mild Pre-eclampsia • Severe Pre-eclampsia
  • 29.
    Classification of Preeclampsia-Eclampsia •Criteria for Severe Preeclampsia (one or more) – Blood Pressure: >160 systolic, >110 diastolic – Proteinurea: >5gm in 24 hours, over 3+ urine dip – Oligurea: less than 400ml in 24 hours – CNS: Visual changes, headache, scotomata, mental status change – Pulmonary Edema – Epigastric or RUQ Pain: Usually indicates liver involvement
  • 30.
    Classification of Preeclampsia- Eclampsia •Criteria for Severe Preeclampsia (one or more) – Impaired Liver Function tests – Thrombocytopenia: <100,000 – Intrauterine Growth Restriction: With or without abnormal doppler assessment – Oligohydramnios
  • 31.
    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.
  • 32.
    Symptoms of Preeclampsia •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. • Epigastric pain 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.
  • 33.
    Symptoms of preeclampsia •While mild lower extremity edema is common in normal pregnancy, rapidly increasing or nondependent edema may be a signal of developing preeclampsia. However, this signal theory remains controversial and recently has been removed from most 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.
  • 34.
    Physical Findings inPreeclampsia • Blood Pressure • Proteinurea • Retinal vasospasm or Retinal edema • Right upper quadrant (RUQ) abdominal tenderness stems from liver swelling and capsular stretch
  • 35.
    Physical findings inPreeclampsia – Brisk, or hyperactive, reflexes are common during pregnancy, but clonus is a sign of neuromuscular irritability that raises concern. – Among pregnant women, 30% have some lower extremity edema as part of their normal pregnancy. However, a sudden change in dependent edema, edema in nondependent areas such as the face and hands, or rapid weight gain suggests a pathologic process and warrants further evaluation
  • 36.
    Eclampsia • Women olderthan 40 years with preeclampsia have 4 times the incidence of seizures compared to women in their third decade of life. – Twenty-five percent of eclampsia cases occur before labor (ie, antepartum). – Fifty percent of eclampsia cases occur during labor (ie, intrapartum). – Twenty-five percent of eclampsia cases occur after delivery (ie, postpartum). – Patients with severe preeclampsia are at greater risk to develop seizures. – Twenty-five percent of patients with eclampsia have only mild preeclampsia prior to the seizures
  • 37.
    Causes: The cause ofthe 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.
  • 38.
    Eclamptic seizure – Thepatient 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.
  • 39.
    • The seizuremay 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. • 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. • 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.
  • 43.
    Laboratory Tests High-risk patientspresenting 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
  • 44.
    Laboratory Tests Patients presentingwith hypertension before gestation week 20: • Same tests as described for high-risk patients presenting with normal BP • Early baseline sonography for dating and fetal size
  • 45.
    Laboratory Tests Patients presentingwith hypertension after midpregnancy: • Quantification of protein excretion • Hemoglobin and hematocrit and platelet count • Serum creatinine, uric acid, and transaminase level • Serum albumin, LDH, blood smear, and coagulation profile
  • 46.
    Preeclampsia: Treatment • Goalis 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.
  • 47.
    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.
  • 48.
    Preeclampsia: Treatment • MaternalEvaluation…When To Hospitalize? – Often, hospitalization recommended with new-onset preeclampsia to assess maternal and fetal conditions. – Hospitalization for duration of pregnancy indicated for preterm onset of severe gestational hypertension or preeclampsia. – Ambulatory management at home or at day-care unit may be considered with mild gestational hypertension or preeclampsia remote from term
  • 49.
  • 50.
  • 51.
    Preeclampsia • Antepartum Managementof Preeclampsia – Little to suggest therapy alters the underlying pathophysiology of preeclampsia. – Restricted activity may be reasonable. – Sodium restriction and diuretic therapy appear to have no positive effect.
  • 52.
    Obstetric Management • Classically“stabilize and deliver”
  • 53.
    Preeclampsia • The “cure”for preeclampsia is delivery – The “cure” is always beneficial for the mother, although c-section might be needed – The “cure” may be deleterious for the fetus
  • 54.
    Preeclampsia • Route ofDelivery – Vaginal delivery is preferable. – Aggressive labor induction (within 24 hours). – Neuraxial (epidural, spinal, and combined spinal-epidural) techniques offer advantages. – Hydralazine, nitroglycerin, or labetalol may be used as pretreatment to reduce significant hypertension during delivery.
  • 55.
    Obstetric Management • Medicalmanagement while awaiting delivery: – use of steroids X 48 hours if fetus < 34 wks – antihypertensives to maintain DBP < 105-110 – magnesium sulfate for seizure prophylaxis – monitor fluid balance, I/O, daily weights, symptoms, reflexes, HCT, plts, LFT’s, proteinuria
  • 56.
    Obstetric Management • Indicationsfor expedited delivery: – fetal distress –  BP despite aggressive Rx – worsening end-organ function – development or worsening of HELLP syndrome – development of eclampsia
  • 57.
    Antihypertensive Therapy • Mostcommonly, for acute control: hydralazine, labetolol • Nifedipine may be used, but unexpected hypotension may occur when given with MgSO4 • 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
  • 58.
    Hydralazine • Dose: 5-10mg every 20 minutes • Onset: 10-20 minutes • Duration: 3-8 hours • Side effects: headache, flushing, tachycardia, lupus like symptoms • Mechanism: peripheral vasodilator
  • 59.
    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
  • 60.
    Nifedipine • Dose: 10mg po, not sublingual(potent generalized vasodilatation) • Onset: 5-10 minutes • Duration: 4-8 hours • Side effects: chest pain, headache, tachycardia • Mechanism: CA channel block
  • 61.
    Clonidine • Dose: 1mg po • Onset: 10-20 minutes • Duration: 4-6 hours • Side effects: unpredictable, avoid rapid withdrawal • Mechanism: Alpha agonist, works centrally
  • 62.
    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
  • 63.
    Preeclampsia • Anticonvulsive Therapy –Indicated to prevent recurrent convulsions in women with eclampsia or to prevent convulsions in women with preeclampsia. – Parenteral magnesium sulfate reduces the frequency of eclampsia and maternal death. (Caution in renal failure.)
  • 64.
    Seizure Prophylaxis &Treatment • Magnesium sulfate vs. phenytoin for seizure prophylaxis in preeclampsia Lucas, et al., N Engl J Med 1995;333:201-5. – 2138 patients (75% had mild PIH) – Maternal & fetal outcomes similar except 10 seizures in the phenytoin group (0 in MgSO4) • Mg vs. diazepam & Mg vs. phenytoin for preventing recurrent seizures in eclamptics Eclampsia Trial Collaborative Group, Lancet 1995;345:1455 – Mg pts were 52% or 67% less likely to have a recurrent seizure than diazepam or phenytoin pts
  • 65.
    Seizure Prophylaxis • Evidenceis 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 – awaits large, prospective, randomized, placebo-controlled trial
  • 66.
    Magnesium Sulfate • Magnesiumsulfate 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
  • 67.
    Magnesium Sulfate • Renallyexcreted • 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 • Treatment of magnesium toxicity: – stop MgSO4, IV calcium, manage airway
  • 68.
    Treatment of Eclampsia •Seizures are usually short-lived. • If necessary, small doses of barbiturate or benzodiazepine (STP, 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.
  • 69.
    Anesthetic Goals ofLabor Analgesia in Preeclampsia • To establish & maintain hemodynamic stability (control hypertension & avoid hypotension) • To provide excellent labor analgesia • To prevent complications of preeclampsia – intracerebral hemorrhage – renal failure – pulmonary edema – eclampsia • To be able to rapidly provide anesthesia for C/S
  • 70.
    Regional vs. GeneralAnesthesia in Preeclampsia • Epidural anesthesia would probably be preferred by many anesthesiologists in a severely preeclamptic pt in a non-urgent setting • For urgent cases it is reassuring to know that spinal is also safe • This allows us to avoid general anesthesia with the potential for encountering a swollen, difficult airway and/or labile hypertension
  • 71.
    Regional vs. General Anesthesiain Preeclampsia • General anesthesia is a well-known hazard in obstetric anesthesia: – 16X more likely to result in anesthetic- related maternal mortality – Mostly due to airway/respiratory complications, which would only be exaggerated in preeclampsia Hawkins, Anesthesiology 1997;86:273
  • 72.
    Platelets & RegionalAnesthesia in Preeclampsia • Prior to placing regional block in a preeclamptic it is recommended to check the platelet count. • No concrete evidence at to the lowest safe platelet count for regional anesthesia in preeclampsia • Any clinical evidence of DIC would contraindicate regional anesthesia.
  • 73.
    Hazards of GeneralAnesthesia in Preeclampsia • Airway edema is common – Mandatory to reexamine the airway soon before induction – Edema may appear or worsen at any time during the course of disease • tongue & facial, as well as laryngeal • Laryngoscopy and intubation may  severe BP – Labetolol & NTG are commonly used acutely – Fentanyl (1 mcg/kg), alfentanil (10 mcg/kg), lidocaine may be given to blunt response
  • 74.
    Hazards of GeneralAnesthesia in Preeclampsia • Magnesium sulfate potentiates depolarizing & non-depolarizing muscle relaxants – Initial dose of succinylcholine is not reduced. – Neuromuscular blockade should be monitored & reversal confirmed.
  • 75.
    Invasive Central Hemodynamic Monitoringin Preeclampsia • Usually reserved for patients with complications – oliguria unresponsive to modest fluid challenge (500 cc LR X 2) – pulmonary edema – refractory hypertension • may have increased CO or increased SVR • Poor correlation between CVP and PCWP in PIH – However, at most centers anesthesiologists would begin with CVP & follow trend • not arbitrarily hydrate to a certain number – If poor response, change to PA catheter
  • 80.
    Conclusions • Preeclampsia isa serious multi-organ system disorder of pregnancy that continues to defy our complete understanding. • It is characterized by global endothelial cell dysfunction. • The cause remains unknown. • There is no effective prophylaxis.
  • 81.
    Conclusions • Delivery isthe only effective cure. • Magnesium sulfate is now proven as the best medication to prevent and treat eclampsia. • Epidural analgesia for labor pain management & regional anesthesia for C/S have many beneficial effects & are preferred.
  • 82.
    Postpartum Counseling and Followup •Counseling for Future Pregnancies • Risk of recurrent preeclampsia increases with – Preeclampsia before 30 weeks (40%) – Multiparas as compared with nulliparas or new father – Risk of recurrent preeclampsia may be substantially greater in African Americans.