Dr. Veena Chatrath Professor & HOD Dept. of Anaesthesiology GMC Amritsar.

Preeclampsia complicates nearly 6% - 10%

of all pregnancies.

Maternal ICU admission. Leading cause of preterm delivery-NICU Birth of LBW babies- economic, social and medical burden.

Leading cause of maternal and fetal morbidity and

mortality.

The National high blood pressure education program (NHBPEP) working group classifies hypertensive diseases in pregnancy into four groups: 1. Gestational hypertension

New onset hypertension in pregnancy presenting after 20 weeks. No proteinuria. BP returns to normal less than 12 weeks post partum.

2. Chronic hypertension

BP>140/90 mm Hg before pregnancy or

diagnosed before 20 weeks gestation

Hypertension first diagnosed after 20

weeks gestation but persistent after 12

weeks postpartum.

3. Pre-eclampsia/Eclampsia

BP >140/90 mmHg after 20 weeks gestation in a women with previously normal BP. Proteinuria >0.3 gm urine protein in 24 hrs. Eclampsia is defined as seizures that cannot be attributed to other causes in a women with pre-eclampsia.

4. Superimposed pre-eclampsia (on chronic hypertension):

New onset proteinuria (>300 mg/24 hr) in a women with hypertension but no proteinuria before 20 weeks

gestation

A sudden increase in proteinuria or blood pressure, or platelet count less than 100,000 in women with hypertension and proteinuria before 20 weeks gestation.

Pre-eclampsia is a complex, multi-system disorder. Defined by: Hypertension Sustained > 140/90 mmHg. 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 no longer a diagnostic criterion

SBP > 160 mm Hg DBP > 110 mm Hg Proteinuria >5 g/24hr or 3-4 + on dipstick Oliguria<500 ml/24hr serum creatinine Pulmonary edema or cyanosis

CNS symptoms (Headache, vision changes) Abdominal(RUQ) pain Any feature of HELLP hemolysis liver enzymes thrombocytopenia IUGR or oligohydramnios

Nulliparity 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 Obesity (BMI > 30 kg/sq.m)

Exact etiology is unknown. Many theories:

Genetic. Immunologic. Dietary deficiency(calcium,magnesium,zinc)

Supplementation has not proven effective.

Placental ischemia due to endothelial dysfunction.

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 effects dominate vasodilation, platelet aggregation, uterine tone

In

preeclampsia, thromboxanes effects dominate

thromboxane (from platelets, placenta) prostacyclin (from endothelium, placenta)

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

In severe preeclampsia:
Initially hyperdynamic state. Later patient become hypovolaemic with lower cardiac output.

Despite normal filling pressures, intravascular fluid

volume is reduced (30-40% in severe PIH)

Total body water is increased (generalized edema)

 Preeclamptic

patients are prone to develop pulmonary edema due to reduced colloid oncotic pressure (COP), which falls further postpartum:

Colloid oncotic pressure: Antepartum Normal pregnancy: 22 mm Hg Pre-eclampsia: 18 mm Hg

Postpartum 17 mm Hg 14 mm Hg

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

Increased uric acid.

Increased urine protein:creatinine ratio. Oliguria Renal function recovers quickly postpartum

Right upper quadrant 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.

Diagnosis: 1.Hemolysis: -Peripheral smear - bilirubin >1.2mg/dL - LDH> 600 IU/L 2.Elevated liver enzymes: -SGOT> 70 IU/L -LDH> 600 IU/L 3.Low platelets: <1 lakh /mm3

HEMATOLOGICAL

CHANGES:

hypercoagulability.
platelet activation. increased fibrinolysis. Thrombocytopenia ( platelet count <100,000/cumm) DIC.

 NEUROLOGIC:

Symptoms :Headache. Visual disturbances. Seizures. Hyperreflexia.

Etiology

of neurological symptoms: Cerebral

vasospasm with reduced blood flow causing ischemia. Cerebral oedema may be another

cause.

Uteroplacental insufficiency. Fetal complications: -Hypoxia -IUGR -Prematurity -IUD -Placental abruption

Prophylaxis:
Low dose Aspirin has been found to be most effective method of prevention.

It inhibits platelet thromboxane A2 synthesis without affecting synthesis of vascular prostacyclin avoids imbalance in thromboxane and prostacyclin ratio.

(NICE clinical guidelines 107, August 2010)

Delivery The only definitive treatment. Preeclamptic patients are divided into three categories: Group A- Preeclampsia features fully subside Management: can wait till spontaneous onset of labor but never exceed Expected Date of Delivery.
Group B- partial control, BP maintains a steady high level Management: >37wk - terminate without delay <37wk - expectant management at least till 34wks

Group C- persistently increasing BP to

severe level or addition of other features.

Management : terminate irrespective of Period of gestation, start seizure prophylaxis and steroids if <34wks.

Non severe HT (mild-moderate):

SBP 140-159 mmHg and DBP 90-109mmHg. Risk of hemorrhagic stroke in presence of systolic hypertension- lowering of SBP to 140150mmHg and DBP to 80-100 mmHg is

recommended.

Oral labetalol is the drug of choice.

Severe hypertension
SBP > 160 mmHg or DBP > 110 mmHg, Must be treatedprevents maternal complications e.g. myocardial ischemia, hypertensive encephalopathy, cerebrovascular hemorrhage, CHF.

Avoid precipitous fall in BP to maintain uteroplacental perfusion and oxygen delivery to foetus.

BP lowered to systolic-140-150 mmHg/ Diastolic- 80100mmHg @ 10-20 mmHg every 10-20 mins.

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 and atenolol are contraindicated due to severe adverse fetal effects.

Magnesium sulphate is the agent of choice for prophylaxis of severe eclampsia. Evidence is strong that magnesium sulfate is indicated for seizure treatment in eclamptics. seizure prophylaxis in severe preeclamptics. (given loading dose of 4-6 gm followed by infusion of 1-4 g/hr)

Magnesium sulfate has many effects; its mechanism in seizure

control is not clear.

Potential adverse effects:

Toxicity from overdose (respiratory depression,

cardiovascular collapse). bleeding. hypotension with hemorrhage. uterine contractility. Neonatal hypotonia and respiratory depression.

Renally excreted. Preeclamptics prone to renal failure. Magnesium levels must be monitored frequently either clinically (patellar reflexes) or by checking serum levels every 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 gluconate, Manage airway.

MgSO4 potentiate and prolong the action of both

depolarizing and non-depolarizing muscle relaxants.

o

At higher doses Mg2+ rapidly crosses the placental barrier, has been found to significantly FHR

variability.
o

Should be given cautiously with Ca2+ as may antagonize the anticonvulsant effect of MgSO4 . Also be cautious in patients with renal impairment. May the possibility of hypotension during regional block.

o o

Absence of headache, visual changes and

epigastric pain.

Sustained BP < 150/100 mmHg without

antiHT therapy

Spontaneous diuresis > 100 ml/hr for at

least 2 hrs.

Usually stopped 24 hrs after delivery.

Indications for urgent delivery:

Fetal distress. BP despite aggressive Rx (refractory hypertension for >24 hrs). Worsening end-organ function. Development or worsening of HELLP syndrome. Development of eclampsia. Worsening thrombocytopenia.

 To

establish & maintain hemodynamic stability (control hypertension & avoid hypotension). To provide excellent labour analgesia. To prevent complications of preeclampsia.

Intracerebral hemorrhage. Renal failure. Pulmonary edema. Eclampsia.

To

be able to rapidly provide anesthesia for C/S

 Superior

pain relief over parenteral

narcotics. Beneficial hemodynamic effects, with a small reduction in SVR & maintenance of CO. Epidural analgesia is a useful adjunct to antihypertensive therapy for blood pressure control . Improves renal and uteroplacental blood flow.

One of the most important advantages of labor epidural analgesia is that it provides a route for rapid initiation of anesthesia for emergency C/S. In the past there were concerns for: use of regional anesthesia for C/S in preeclamptics Possibility of severe hypotension secondary to sympathectomy in patient with volume contraction risk of pulmonary edema due to excessive fluid administration with regional block risk with use of pressor agents to treat hypotension

Platelets >1lakh/mm3 , coagulation profile not indicated Platelets <1 lakh/mm3 -clinical evidence of bleeding. -platelet trend-Every 6hourly if stable, every 1-3hrly if declining. -coagulation profile: PT/APTT/INR -quality of platelets.

Platelets <50,000: contraindication

Remove epidural catheter only when platelet count returns normal (at least 75000-80000/mm3).

Emergency imaging studies and neurologic evaluation if epidural hematoma suspected.

In various studies, it has been found that low dose aspirin doesnt significantly affect bleeding time, neuraxial analgesia can be given safely without any complication.

Advantages 1. Quicker and more reliable in on set. 2. Less potential trauma in the epidural space. 3. Risk of hypotension was almost six times less in patients of severe preeclampsia than the normal parturients. ( Aya et al) 4. Less ephedrine required as compared to epidural anaesthesia (Sharwood-smith et al) 4. Uteroplacental blood flow not altered. 5. Better neonatal outcome. 6. Shorter duration of hospital stay as compared to GA.

General anaesthesia:
Indications:
Severe fetal compromise.

Pulmonary oedema Coagulopathy Sustained fetal bradycardia with reassuring maternal airway Severe ongoing maternal hemorrhage Contraindications to neuraxial technique After Eclampsia, where altered neurological deficit persists.

General vs. spinal (CSE) vs. epidural

Prospective, randomized study. All these types of anesthesia were used safely BP on laryngoscopy avoided by controlling hypertension pre-op with hydralazine; IV NTG & lidocaine immediately preintubation

BP with regional avoided by 1000 ml Ringer Lactate pre-load & 5 mg boluses of ephedrine for SBP 100

 BP

20% lower in regional vs general groups at skin incision only; no difference in mean pressures. Regional pts received 800 ml more IV fluid

2200 ml vs. 1500 ml No associated pulmonary edema

Infant

outcomes were similar Cases were not urgent; none for non-reassuring FHR pattern

In an urgent situation there might not be time to adequately control hypertension pre-op prior to inducing general anesthesia

 Retrospective Lowest

study (Hood, et al., Anesthesiology

1999;90:1276-82).

intraoperative blood pressures not different. Total ephedrine use was small & not different. Spinal group received 400 ml more IV fluid No pulmonary edema attributable to intraop fluid Maternal & infant outcomes were similar

 Patients with severe pre-eclampsia experience

less frequent, less severe hypotension than healthy parturient. Spinal may cause greater degree of hypotension than epidural, however it is easily treated and short lived, no difference in outcome. Spinal anaesthesia is reasonable anaesthetic option in severe pre-eclampsia for CS where there is no indwelling catheter or contraindication to spinal anaesthesia. Hypotension- titrated vasopressor doses (greater vascular sensitivity to vasoconstrictor) (Anaesthesia and analgesia 2013; 117: 686-693)

 General

anesthesia is a well-known hazard in obstetric anesthesia: 16 times more likely to result in anesthetic-related maternal mortality Mostly due to airway/respiratory complications, which would only be exaggerated in pre-eclampsia. Intra cranial hemorrhage may occur due to hypertensive response to intubation.

Prior to placing regional block in a preeclamptic it is recommended to check the platelet count. Patients with platelet count >75,000 /cumm are considered eligible to receive spinal and epidural anaesthesia. Any clinical evidence of DIC would contraindicate regional anaesthesia Platelet transfusion are indicated in all patients whose platelet count is less than 20,000/cumm or in the presence of significant bleeding from punctured sites. Tests for platelet function include bleeding time test, thromboelastography (most reliable test), aggregometry, and flow cytometry.

 Immediate
Stabilise

hospitalisation

mother

antihypertensives
anti seizure prophylaxis

correct coagulation abnormalities

fetal condition- FHR, doppler

Assess

ultrasound, biophysical profile.

 Ultimate

goal: >34 wks gestation deliver <34wks expectant management if stable maternal and fetal conditions Platelet transfusion if: <40,000/mm3 before cesarean <20,000/mm3 before delivery. GA- anaesthetic technique of choice for C/S. Role of corticosteroids- corrects the lung maturity before 34 wks of gestation

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 cause severe increase in Blood pressure Labetolol & NTG are commonly used acutely Fentanyl (2.5 mcg/kg), alfentanil (10 mcg/kg), lidocaine may be given to blunt response.

 Magnesium

sulfate potentiates depolarizing & non-depolarizing muscle relaxants Initial dose of succinylcholine is not reduced. Neuromuscular blockade should be monitored & reversal confirmed. GA is preffered in cases of suspected placental abruption, coagulopathy, severe pulmonary edema, eclampsia, severe foetal distress, patient refusal.

Syntocinon is the drug of choice for uterine contraction in the setting of severe hypertension and should be carefully titrated to haemodynamic responses. The use of ergometrine has been associated with hypertensive crises and death in women with preeclampsia; therefore, ergometrine should not be used for uterine contraction.

Usually reserved for patients with complications Oliguria unresponsive to modest fluid challenge (500 ml RL 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

 Preeclampsia

is a serious multi-organ system disorder of pregnancy that continues to defy our complete understanding. is characterized by global endothelial cell dysfunction.
cause remains unknown.

It

The

There

is no effective prophylaxis.

 Delivery

is the only effective cure.

Magnesium

sulfate is now proven as the best medication to prevent and treat eclampsia. analgesia for labor pain management & regional anesthesia for C/S have many beneficial effects & are preferred.

Epidural