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  • 1. Dr.SREEJITH.H
  • 2.  Hypertensive disease is the 4th leading cause of maternal death  Preeclampsia complicates about upto 8% of pregnancies  In U.S preeclampsia complicates approx 7-10% of pregnancies  Eclampsia 1 in 10000-150000 pregnancies  Severe PIH contributes to 20-40% of maternal deaths & 20% of perinatal deaths
  • 3.  Pregnancy Induced Hypertension  Preeclampsia  Eclampsia  Chronic hypertension  Chronic hypertension with superimposed preeclampsia
  • 4.  Defined as a systolic BP >140 mm Hg or diastolic BP >90 mm Hg OR  a constant increase in systolic or diastolic BP by 30 mmHg & 15 mm Hg respectively above patient’s baseline
  • 5.  Classic Triad of Preeclampsia - Hypertension Proteinuria, Edema  Defined as hypertension occuring after 20 wks gestation or in early postpartum period & returned to normal within 3 months after delivery OR  Onset after 20wks gestation & atleast one of the following
  • 6.  Proteinuria >300 mg/24 hr  Oliguria /serum plasma creatinine ratio >0.09mmol/L  Headaches with hyperreflexia,eclampsia,clonus,or visual disturbances  Increased liver enzymes , plasma glutathione S-transferase – alpha 1-1, or serum alanine aminotransferase or right quadrant pain  Thrombocytopenia,increased LDH, haemolysis, DIC  Intrauterine growth retardation
  • 7.  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
  • 8.  Nulliparity(Elderly & young primigravida)  Chronic renal disease(Nephritis)  Angiotensin gene T235  Chronic hypertension  Antiphospholipid antibody syndrome  Multiple gestation  Family or personal history of preeclampsia  Age > 40 years  African-American race  Diabetes mellitus
  • 9.  DISEASE OF THEORIES  Etiology is unknown.  Many theories:  Abnormal Placentation  Endothelial cell dysfunction  Imbalance b/w TXA2 & PGI2  dietary deficiency (calcium, magnesium, zinc) ▪ supplementation has not proven effective
  • 10.  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)
  • 11.  Aspirin has been extensively studied as a targeted therapy to ↓ thromboxane production  CLASP study, 1994, multicenter, randomized 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
  • 12.  NIH study of high-risk patients, randomized, 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
  • 13.  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 Redman, et al., Am J Obstet Gynecol 1999;180:499-506  present in normal pregnancy  excessive in preeclampsia  Proposed source of inflammatory stimulus: placenta
  • 14.  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)
  • 15.  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
  • 16.  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
  • 17.  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.
  • 18.  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
  • 19.  Hemolysis – abnormal peripheral smear Increased bilirubin level  Elevated liver enzymes- SGOT>70U/L LDH>600U/L  Low platelet count<100000/mm3  Clinical features –Malaise(90%) , Epigastric pain(90%), Nausea & vomitting(50%), Flu like syndrome  Usually before 36 weeks  70% antepartum & 30% postpartum  Rapidly progress to DIC  Associated with high maternal & fetal mortality
  • 20.  LIKE A FLASH OF LIGHTENING  Preeclampsia complicated by convulsion /coma  Most common in primi & multiple pregnancy Cause of convulsion  Hypertensive encephalopathy  Vasospasm- ischemia  Infarction  Haemorrhage  Oedema
  • 21.  Antepartum – 50%,intrapartum-30% postpartum-20% 3 stages  Premonitory stage- unconsciousness, twitching of facial muscles  Tonic stage(30s) – tonic spasm, opisthotonm  Clonic stage (1-4 min)– frank convulsions
  • 22.  Differential Diagnosis Epilepsy,ICSOL,Meningitis,Hysteria Management  MgSO4 is the DOC for seizure control & prevention of recurrent eclamptic seizures  Reduces seizures by >50%  4g MgSO4 iv over 10 min followed by a maintanence infusion of 1g/hr  Mg also causes vasodilataion & increase in CO by reducing SVR  Narrow Therapeutic Index ,with serum Mg level b/w 2 & 3.5 mmol/L . Therapeutic level 4-6 mEq/L  If toxicity present 10 ml 10 % Ca gluconate given slow iv
  • 23. MATERNAL Eclampsia, Renal Failure, Pulmonary edema, CVA, Blindness, PPH, Sepsis, Residual HTN FETAL IUGR, IUD, RDS, Prematurity, Intracranial Haemorrhage CAUSES OF MATERNAL DEATH Eclampsia, Intracranial haemorrhage, ARF, Pulmonary edema, DIC, HELLP
  • 24. CS Fetal Distress Worsening of Biophysical Profile RAPID DELIVERY Eclampsia Severe HTN not responding to treatment Renal & Hepatic Dysfunction coagulopathy
  • 25.  Hospitilistaion & Bed Rest(Lt lateral position)  Adequate Hydration & Diet (avoid excess Na)  Antihypertensives  Anticonvulsants GENERAL PRINCIPLES  Minimise vasospasm  Improve circulation  Improve intravascular volume  Correct acid base & electrolyte imbalance  Decrease CNS irritability
  • 26.  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
  • 27.  Most commonly, for acute control: 1.)Hydralazine Arterial dilator, dose 5-10mg iv ,slow onset 20-30mtsDOA: 2-3 hrs 2) Labetolol 10-20mg iv, Improves placental blood flow ,Rapid onset of action 1-2mts DOA-2-3hrs CI- Bronchial asthma,CCF  Most common for chronic control: Alpha methyl dopa. Central alpha 2 agonist Dose – 250 mg bd DOC for chronic treatment
  • 28.  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
  • 29.  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
  • 30.  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
  • 31.  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
  • 32.  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.
  • 33.  Labor analgesia  Anaesthesia for CS & Obstertic complication  Neonatal resuscitation  To prevent complications of preeclampsia  intracerebral hemorrhage/convulsions  renal failure  pulmonary edema  Eclampsia
  • 34.  To establish & maintain hemodynamic stability (control hypertension & avoid hypotension)  To provide excellent labor analgesia  To prevent complications of preeclampsia  To be able to rapidly provide anesthesia for C/S  To avoid drug induced depression
  • 35.  Newer studies shows that degree of hypotension in spinal & epidural block is same in PIH pt  So we can use either spinal / epidural  Graded epidural in a preeclampsia patient  5ml (0.5% bupivacaine)loading dose to attain T10 level  Then 5 ml increment at 5 mt interval to attain T4 level  Fentanyl(50-100mcg) can be added to increase speed of onset , duration quality Advantages of epidural  Gradual onset of sympathetic blockade  Cardiovascular stability  Avoids neonatal depression
  • 36.  Hood, et al., Anesthesiology 1999;90:1276-82  Retrospective study  Lowest intraoperative blood pressures not different  Total ephedrine use was small & not different  Spinal group received 400 cc more IV fluid  No pulmonary edema attributable to intraop fluid  Maternal & infant outcomes were similar
  • 37.  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  In the absence of such signs, most anesthesiologists would proceed at plt count >100000, many would proceed at 80000-100000, <80000 some would proceed (esp. spinal)
  • 38.  When placing a regional block in a patient with a platelet count < 100000, the most important thing is to monitor resolution of block closely  Bleeding time has been discredited as an indicator of epidural bleeding risk and is not indicated. Channing-Rogers, Semin Thromb Hemost 1990;16:;1-30  Low-dose aspirin is not a contraindication to regional anesthesia in preeclampsia  CLASP study: 1422 women on aspirin received epidurals without any bleeding complications
  • 39.  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
  • 40.  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
  • 41.  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
  • 42.  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.
  • 43.  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
  • 44.  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.
  • 45.  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.