Pih

Dr.SREEJITH.H

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

Pregnancy Induced HypertensionPreeclampsiaEclampsiaChronic hypertensionChronic hypertension with

superimposed preeclampsia

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

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

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

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

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

DISEASE OF THEORIESEtiology is unknown.Many theories:

Abnormal Placentation Endothelial cell dysfunction Imbalance b/w TXA2 & PGI2 dietary deficiency (calcium, magnesium,

zinc)▪ supplementation has not proven effective

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)

Aspirin has been extensively studied as a targeted therapy to thromboxane production

CLASP study, 1994, multicenter, randomizedCLASP 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

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

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

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)

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

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

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.

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

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

LIKE A FLASH OF LIGHTENING Preeclampsia complicated by convulsion

/coma Most common in primi & multiple pregnancyCause of convulsion Hypertensive encephalopathy Vasospasm- ischemia Infarction Haemorrhage Oedema

Antepartum – 50%,intrapartum-30% postpartum-20%

3 stagesPremonitory stage- unconsciousness,

twitching of facial musclesTonic stage(30s) – tonic spasm,

opisthotonmClonic stage (1-4 min)– frank

convulsions

Differential Diagnosis Epilepsy,ICSOL,Meningitis,HysteriaManagement 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

MATERNAL Eclampsia, Renal Failure, Pulmonary edema, CVA, Blindness, PPH, Sepsis, Residual HTNFETAL IUGR, IUD, RDS, Prematurity, Intracranial HaemorrhageCAUSES OF MATERNAL DEATH Eclampsia, Intracranial haemorrhage, ARF, Pulmonary edema, DIC, HELLP

CS Fetal DistressWorsening of Biophysical Profile RAPID DELIVERYEclampsia Severe HTN not responding to treatmentRenal & Hepatic Dysfunctioncoagulopathy

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

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

Most commonly, for acute control: 1.)Hydralazine Arterial dilator, dose 5-10mg iv ,slow onset 20-30mtsDOA:

2-3 hrs 2) Labetolol10-20mg iv, Improves placental blood flow ,Rapid onset of

action 1-2mtsDOA-2-3hrsCI- Bronchial asthma,CCF Most common for chronic control: Alpha methyl dopa.Central alpha 2 agonistDose – 250 mg bdDOC for chronic treatment

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

Evidence is strong that magnesium sulfate is indicated for seizure treatment in eclamptics seizure prophylaxis in severe

preeclampticsRole of magnesium prophylaxis in

mild preeclamptics is less clear awaits large, prospective, randomized,

placebo-controlled trial

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

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

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.

Labor analgesia Anaesthesia for CS & Obstertic

complication Neonatal resuscitation To prevent complications of

preeclampsia intracerebral hemorrhage/convulsions renal failure pulmonary edema Eclampsia

To establish & maintain hemodynamic stability (control hypertension & avoid hypotension)

To provide excellent labor analgesiaTo prevent complications of

preeclampsiaTo be able to rapidly provide

anesthesia for C/STo avoid drug induced depression

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

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

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)

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

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

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 preeclampsiaHawkins, Anesthesiology 1997;86:273

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

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.

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

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.

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.