Preeclampsia and Eclampsia: Prepared by:Alia Ismail Group no.552

Plan: Types of hypertension during pregnancy. Preeclampsia. Criteria of preeclampsia. Causes and pathphysiology. Prevention and Management conclusion reference

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: Definition Hypertension > 140/90 relative  no longer considered diagnostic Proteinuria > 300 mg/24 hours or  1+ on urine dipstick not mandatory for diagnosis; may occur late Edema (non-dependent) so common & difficult to quantify it is rarely evoked to make or refute the diagnosis

and eclampsia: Severe preeclampsia : Preeclampsia with hypertension >160/110 or proteinuria >5g/24h or multiorgan involvement Eclampsia: Convulsions in any woman who has, or then presents with, hypertension in pregnancy of any cause.

Criteria for Severe Preeclampsia SBP > 160 mm Hg DBP > 110 mm Hg Proteinuria > 5 g/24° or 3-4+ on dipstick Oliguria < 500 cc/24°  serum creatinine Pulmonary edema or cyanosis CNS symptoms (HA, vision changes) Abdominal (RUQ) pain Any feature of HELLP hemolysis  liver enzymes thrombocytopenia IUGR or oligohydramnios

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

Fetal complications of severe preeclampsia Intrauterine growth retardation Premature delivery Abruptio placentae Fetal distress/fetal demise Associated maternal risks General/regional anesthesia DIC Hemorrhage

Maternal complications of severe preeclampsia Cardiovascular dysfunction (cardiac failure, hypertension) Renal dysfunction (oliguria, reduced GFR, elevated creatinine, acute tubular necrosis, cortical necrosis) Respiratory dysfunction (ARDS, pulmonary edema) Hepatic dysfunction (elevated liver enzymes, subcapsular hematoma, HELLP syndrome) Cerebral dysfunction (encephalopathy, ischemia, cortical blindness, retinal detachment, infarction, hemorrhage, eclampsia)

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

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

Preeclampsia: Mechanism At this time the most widely accepted proposed mechanism for preeclampsia is: global endothelial cell dysfunction Redman: 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: 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, 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

Obstetric Management Classically “stabilize and deliver” 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 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 mon Angiotensin-converting enzyme (ACE) inhibitors contraindicated due to severe adverse fetal effects

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) 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

Benefits of Regional Analgesia for Labor in Preeclampsia Superior pain relief over parenteral narcotics Beneficial hemodynamic effects: 20% reduction in blood pressure with a small reduction in SVR & maintenance of CI Doppler velocimetry shows epidural analgesia reduces the S-D flow ratio in the uterine artery by 25% to levels seen in non-preeclamptics  vascular resistance & relief of vasospasm

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 (2.5 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 Pre-curarization is not indicated. Initial dose of succinylcholine is not reduced. Neuromuscular blockade should be monitored & reversal confirmed.

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.

References: www.google.com www.wikipedia.com dutta book of gynecolgy