pregnancy induced hypertension

PIH & Anaesthesia

Speaker: Dr. Deepa Sinha

Moderator: Dr. Anil Kumar

INTRODUCTION

Hypertension is one of the most common complication during pregnancy

Increased maternal and perinatal morbidity and mortality.

It is a sign of an underlying pathology that may be pre-existing or appears for the first time during pregnancy that is why it is also called as TOXEMIA OF PREGNANCY.

INCIDENCE

6% to 8% of all the pregnancies

HISTORY:

Fits occurring during pregnancy were recognized as

early as in 4th century B.C. by Hippocrates

Eclampsia is a Greek word that means SHINE FORTH

implies sudden development

1903 Chesley- Preeclampsia word included in books

1976 Pritchard and Mc Donald- Hypertensive disorders

of pregnancy & Diagnostic criteria of preeclampsia:

hypertension, proteinuria, edema after 20 weeks

DEFINITION:

Hypertension is defined as systolic pressure of

at least 140 mm of Hg and diastolic pressure

of at least 90 mm of Hg.

Proteinuria is defined as more than 300 mg /24

hrs. Or two clean catch midstream or catheter

specimens of urine collected at least more

than four hours apart.

CLASSIFICATION OF PIH ACCORDING TO AMERICAN SOCIETY OF HYPERTENSION

1.Preeclampsia-eclampsia

2.Chronic hypertension of any cause

3.Preeclampsia superimposed on chronic

hypertension

4.Gestational hypertension

PREECLAMPSIA-ECLAMPSIA

It is a multi-system disorder of unknown etiology.

New onset of hypertension & proteinuria in a previously normotensive woman

After 20 weeks of gestation Returning to normal after 12 weeks of

pregnancy. Oedema not a part of diagnosis now. A retrospective diagnosis

Eclampsia : new onset of seizures or unexplained coma during pregnancy or postpartum period in patients with pre-existing preeclampsia and without pre-existing neurological disorder.

SEVERE ECLAMPSIA HAS FOLLOWING CRITERIA:

• Systolic BP of 160 mm of Hg or Diastolic BP of 110 mm of Hg

Or

Higher on two occasions at least 4 hours apart while the patient

is on bed unless antihypertensive therapy is initiated before this

time

• Thrombocytopenia i.e. platelet count less than 100,000/microliter

• Impaired liver functions indicated by abnormally elevated blood

concentrations of liver enzymes, severe persistent right upper

quadrant or epigastric pain unresponsive to medication and not

accounted for by alternative diagnoses, or both

Progressive renal insufficiency in serum creatinine level greater than 1.1 mg/dl or a doubling of serum creatinine concentration in the absence of other renal disease

• Pulmonary oedema• New onset of cerebral or visual disturbances

NOTE: In view of recent studies that indicate

minimal relationship between the quantity of

urinary protein and pregnancy outcome in

these patients, massive proteinuria i.e. greater

than 5 mg has been eliminated and also foetal

growth restriction as it is managed similarly in

pregnant women with or without preeclampsia.

RISK FACTORS:

Maternal factors Obesity Nulliparity Maternal age more than 40 yr. Previous preeclampsia Chronic hypertension Diabetes Renal disease Multiple gestation Genetic Thrombophilias- anti-phospholipid syndrome, protein c,s

deficiency, factor v Leiden

Placental factors Poor placentation i.e. decreased

trophoblast invasion Hyperplacentosis Placental ischemia Molar pregnancy

ETIOLOGY AND PATHOGENESIS

Exact cause is unknown that’s why it is called as “the disease of theories.”

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

Other causes are:a. Inflammatory mediators: imbalance between Prostaglandins and I2 and thromboxane causing Vasoconstriction, Platelet aggregation, increased Vasopressor response and increased uterine activity.b. Genetic: Family history of pre eclampsia: genetic originMutations in Complement Regulatory Protein geneGenes assoc.: MTHFR, F5 Leiden, AGT, HLA, NOS3, F2(prothrombin), ACE

c. Immunologic: Exposure to sperms of different partner long term exposure to paternal antigen in sperms of same partner- protective activated auto antibodies to angiotensin receptor-1 AA-AT1 that activates AT1 receptors causing increased sensitivity to angiotensins and finally leading to hypertension.

d. Antiangiogenic protein:

MARKERS OF PREECLAMPSIA:

↑ plasma Homocystiene ↑ serum sFlt1(soluble fms-like tyosine

kinase) ↓serum and urinary Platelet Growth

Factor ↓ Vascular Endothelial Growth Factor

A. Maternal:a) Cardiovasular System: -Reduction in total blood volume is proportional to severity of the disease-Decreased colloid oncotic pressure coupled with increase vascular permeability, loss of intra vascular fluids and proteins into the interstitial tissues that increases risk of pulmonary oedema.

• Increased peripheral vascular resistance and sympathetic over activity leads to elevated BP• Cardiac output is variable i.e. it could be either increased, decreased or unchanged• Pulomary capillary wedge pressure also vary with severity of systemic vascular resistance. If systemic vascular resistance is high then PAWP is low.• In the end it is a low volume, high pressure and high resistance state.

b)Respiratory System: it’s a state of generalised oedema involving face, neck upper airway specifically larynx, pharyngeal oedema that may hamper in visualisation of vocal cord making it a case of difficult intubation.

c) Central Nervous System: Signs of hyper-irritability such as headache, visual disturbances,hyperexcitability, hyperreflexia, coma,seizures all due to cerebral edema and hypoperfusion

d) Renal: Renal functions are grossly affected. Arteriolar spasm leads to proteinuria, decreased GFR, decreased urea clearance, elevated uric acid and creatinine level. Out of these hyperuricemia is an early sign of deteriorating renal function resulting in decreased urine output and may progress to anuria.

e) Hepatic: there is distention of liver capsule due to edema, periportal necrosis, fibrin deposition in hepatic sinusoids occurs leading to HELLP syndrome, Periportal haemorrhage , subcapsular bleeding,hepatic rupture: 32% maternal mortality

f) Coagulation abnormalities: Hemoconcentration (pts with anemia may appear to have normal hematocrit) Thombocytopaenia is most common. Despite of normal platelet count, platelet function is impaired. Platelet count correlates with disease severity and incidence of abruptio placenta. DIC due to activation of coagulation cascade causes overconsumption of coagulants and platelets leading to spontaneous haemorrhage.

B. Uteroplacental circulation: Uterine and intervillous blood flow is diminished by 50-70% due to hemoconcentration, increased blood viscosity and vasoconstriction leading to hypo perfusion causing foetal hypoxia and IUGR. Placental abruption is more common in patients with preeclampsia.

HELLP SYNDROME:

Consists of Haemolysis, elevated liver enzymes and low platelets. Incidence rate is 4-12% in preeclamptics and associated with high mortality and morbidity. Diagnostic criteria: Haemolysis defined as abnormal peripheral smear

and increased bilirubin >1.2 mg/dl Elevated liver enzymes i.e. increased serum

glutamic oxaloacetic transaminase >70IU and increased serum Lactate dehydrogenase >600 U/L

Low platelet count <1,00,000 mm3

MANAGEMENT OF HELLP SYNDROME:

• Immediate hospitalisation• Stabilise mother• Antihypertensive• Anti-seizure prophylaxis• Correct coagulation abnormalities• Assess foetal condition- FHR, Doppler ultrasound, biophysical profile

PREDICTION OF PREECLAMPSIA

No screening test is really helpful Various screening methods are:- Diastolic notch at 24weeks by Doppler ultrasonography- Absence or reversal of end diastolic flow- Average mean arterial pressure ≥ 90 mmHg in second trimester- Infusion test: angiotensin infusion required to raise the blood pressure >20 mm Hg from baseline

Roll over test: Rise in blood pressure >20 mmHg from baseline on turning supine at 28-32 weeks gestation is positive.

2. ECLAMPSIA

Is the new onset of seizures or unexplained coma during pregnancy or postpartum period in patients with pre-existing PE and without pre-existing neurological disorder.

Epidemiology: •0.1- 5.5 per 10,000 pregnancies •Decreasing incidence with time •Antepartum(50%): mostly in third trimester •Intrapartum (30%): •Postpartum(20%): usually within 48hours, fits beyond 7days generally rules out Eclampsia

RISK FACTORS:

• Maternal age less than 20 years• Multigravida• Molar pregnancy• Triploidy• Pre-existing hypertension or renal disease• Previous severe Preeclampsia or Eclampsia• Nonimmune hydrops fetalis• Systemic Lupus Erythematosus

CLINICAL FEATURES

Eclamptic convulsions are epileptiform and consist of four stages• Premonitory stage: twitching of muscles of face, tongue, limbs and eye. Eyeballs rolled or turned to one side• Tonic stage: opisthotonus, limbs flexed, hands clenched• Clonic stage: 1-4 min, frothing, tongue bite, stertorous breathing• Stage of coma: variable period.

Pathogenesis: Loss of normal cerebral auto regulatory mechanisms cerebral hyperperfusion leading to Edema & ↓cerebral blood flow.

DIAGNOSIS: Lab Investigations: •Complete Blood Count •Platelet count •LFT •RFT •Urine analysis •Serum electrolytes •Peripheral blood smear •Prothrombin time •Type and screen antibody if present •Angiotensin II test: a dose of 8mk/kg/body weight to increase Diastolic Blood pressure by 20 mm of Hg is taken as positive

Management: 1. Control Hypertension 2. Improve intravascular volume 3. Prevent convulsions 4. Prevent complications 5. Deliver viable fetus

1. Control Hypertension: Most commonly, for acute control: hydralazine, labetalol • 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 effect

ANTI-HYPERTENSIVE DRUGS:

2. Improve intravascular volume: Main aim is to increase CVP & PCWP range 4-6 cm H2O & 5-10 mm HG and to increase urine output to 1 ml/kg/hr. There is a controversy between colloid and

crytalloid as both complicates the condition causing low colloid oncotic pressure and leaky capillary predisposing them to risk of non-carcinogenic pulmonary oedema

Fluid recommendation: crystalloids to be administered at the rate of 1-2 ml/kg/hr. and alternating according to CVP, PCWP and Urine Output.

3. Seizure Prophylaxis & Treatment: Magnesium sulphate therapy. Magnesium sulfate has many effects; its mechanism in seizure control is not clear. It is an 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 haemorrhage • 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

Normal Level: 1.5-2 mg/dl Therapeutic level: 4-8 mg/dl ECG Changes (increased PQ interval, QRS

widening) 5-10 mg/dl Patellar reflexes lost: 8-10 meq/L Nausea, diplopia, slurred speech: 9-12 mg/dl 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 1 g 10% calcium gluconate slow - Administer Oxygen - Secure airway - Ventilation

Anaesthetic Implication: MgSo4 potentiate and prolongs both actions of depolarizing and non-depolarizing Muscle relaxants. Intubating dose of succinylcholine should not be decreased as onset and duration of action of single dose does not alter in preeclamptic patients. NDMR when used neuromuscular monitoring with peripheral nerve stimulation and dose titration should be done accordingly.

VARIOUS REGIME OF MAGNESIUM THERAPY

• Pritchard Regime: - Loading dos: 4g (20 ml of 20%) MgSo4 IV over 4 min. immediately followed by 10g (20 ml of 50%) IM i.e. 5 gm in each buttocks- If convulsion persists after 15 min 2 g IV over 2 min- Maintenance dose: 5g IM every 4 hours alternate side• Zuspan or Sibai regime:- Loading dose: 6 g IV over 20 min- Maintenance dose: 2-3 g/hr. IV every 6 hr

4. 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.

WHEN TO DELIVER??

Maternal Indication: - Recurrent Severe Hypertension - Recurrent symptoms of severe preeclampsia - Progressive renal insufficiency i.e. serum creatinine concentration greater than 1.1 mg/dL or a doubling of the serum creatinine concentration in the absence of other renal disease - Persistent thrombocytopenia or HELLP syndrome - Pulmonary oedema - Suspected abruption placenta - Progressive labour or rupture of membranes

Fetal Indication: - Gestational age of 34 0/7 weeks - Severe fetal growth restriction - Persistent Oligohydramnios - BPP of 4/10 or less on at least two occasions 6 hours apart - Reversed end-diastolic flow on umbilical artery Doppler studies - Recurrent variable or late deceleration during NTS

Fetal death

PAE:

What all to be evaluated before inducing?? - Condition of mother: stabilization is required before inducing - Severity of condition - Associated organ involvement - Airway assessment - BP - Fluid status - Evidence of coagulation - Medication - Fetal status

Investigation: - CBC - Renal function test - Coagulation profile - Recent platelet count

Monitoring: • Basic Parameters: - Non-invasive BP - Urine output - Pulse oximetry - Capnography - Fetal monitoring • Additional Parameters: - Intra-arterial BP - PCWP - CVP

Before Induction: - Patent 18 G iv cannula - Anti-hypertensive/Anti-convulsants - Aspiration prophylaxis

Type of Delivery and Anaesthesia

1. Normal Vaginal Delivery: Main aim is - To establish & maintain hemodynamic stability (control hypertension & avoid hypotension) - To provide excellent labor analgesia - To prevent complications of preeclampsia Intracerebral haemorrhage Renal failure Pulmonary Edema Eclampsia - To be able to rapidly provide anaesthesia for C/S

a) Controlled IV analgesia: Fentanyl - Loading dose: 1 mcg/kg - Maintenance dose: 25-50 mcg every 20 minb) Regional Anaesthesia: Epidural Block- Guidelines- - CBC and Coagulation profile - Baseline BP - Continue anticonvulsive therapy - Crytalloid and albumin to increase CVP - Segmental Epidural block with dilute increments

Advantage of Epidural Block: - Hypertensive response to pain is attenuated by epidural block - Decreased levels of catecholamine which facilitates BP control - May improve intervillous blood flow and stable cardiac output - Can also be used in Caesarean section

a) Regional Anaesthesia: Give aspiration prophylaxis Availability of blood and blood products Pre-hydration Oxygen administration: 6lt/min Epidural Block: 8-10 ml of 1.5-2% lignocaine or

0.5% Bupivacaine with 25-50 mcg of Fentanyl and the block should be raised to a minimum level of T4

Sub-arachnoid Block: 5-10mg of 0.5% bupivacaine with 20 mcg of Fentanyl

If hypotension occurs treat with Inj Ephedrine

Avoid ergot alkaloids once baby is extracted

Pot-op pain relief with epidural Fentanyl infusion of 10-25 mcg or Morphine 4 mg

Platelet count and regional anaesthesia: 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 anaesthesia in preeclampsia

Any clinical evidence of DIC would contraindicate regional anaesthesia.

Platelets <1 lakh/mm3-clinical evidence of bleeding-Platelet trend-Every 6hourly if

stable, every 1-3hrly if declining -coagulation profile: PT/PTTK/INR

-quality of platelets-risk vs benefit

Platelets <50,000: contraindication

Bleeding time has been discredited as an indicator of epidural bleeding risk and is not indicated.

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 doesn’t significantly affect bleeding time; neuraxial analgesia can be given safely without any complication

Low-dose aspirin is not a contraindication to regional anaesthesia in preeclampsia

b) General Anaesthesia: When to Induce???

- Coagulopathy - Fetal distress requiring emergency LSCS - Patient refusal

Hazards of GA: - Upper airway oedema: careful airway assessment is required. - Difficulty in cord visualisation - Worsening of mallampatti grading - Difficulty in laryngoscopy and intubation: Maternal BP should be stabilized and seizure prophylaxis should be given in view of response to laryngoscopy and intubation. Labetalol & NTG are commonly used acutely

- Fentanyl (2.5 mcg/kg), alfentanil (10 mcg/kg), lidocaine may be given to blunt response- MgSo4 therapy interfering with DMR and NDMR- Impaired hepatic/renal blood flow affecting drug metabolism and clearance- High risk of Aspiration

How to Induce??• Prior to induction aspiration prophylaxis is administered: 30 ml of 0.3 M of Sodium Citrate 30 min before induction• IV lines• Monitors• Failed intubation kit• Working suctions•All drugs- GA, anti-hypertensives, anti-convulsive

Pre-oxygenate the patient Pre-medicate Induction: Rapid sequence induction using

Thiopentone 4-5mg/kg and Succinylcholine 1-1.5 mg/kg

Intubation: sellicks manuever is maintained till the cuff of endotracheal tube is inflated. Small size cuffed endotracheal tube is used 6.0-6.5 ID

Maintained With: N2O:O2 (50:50) and a volatile agent preferably Isoflurane.

•If the patient is on MgSo4 therapy then neuromuscular blocked must be monitored with peripheral nerve stimulator and dose should be titrated accordingly•Avoid ergot alkaloids•Extubtion response to be pre-treated with lignocaine or beta blockers like esmolol•Continue anti-convulsive therapy in post op period.•Semiconscious patient with cerebral lesions should be ventilated electively.

Regional Vs General Anaesthesia: Epidural anaesthesia would probably be

preferred by many anaesthesiologists 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 anaesthesia with the potential for encountering a swollen, difficult airway and/or labile hypertension

General anaesthesia is a well-known hazard in obstetric anaesthesia:

16X more likely to result in aesthetic-related maternal mortality

Mostly due to airway/respiratory complications

Conclusion

Preeclampsia is a multisystem disorder. Management is supportive, delivery is

the only definitive. Preeclampsia patients: High risk for

difficult intubation. Hypertensive response to laryngoscopy

may lead to intracranial haemorrhage.

Spinal Anaesthesia not contraindicated in severe Preeclampsia.

Eclampsia can be prevented by prophylactic MgSO4 therapy.

Eclamptic patients should be monitored for at least 24 hrs. Post-partum.

Magnesium sulfate is now proven as the best medication to prevent and treat eclampsia.

Epidural analgesia for labour pain management & regional anaesthesia for C/S have many beneficial effects & are preferred.

REFERENCE:

Miller’s Anaesthesia 7th Edition Stoelting’s anaesthesia and co-existing

disease 5th edition Barash 6th editon Hypertesion in Pregnancy; the

american college of OBGNY

Thank you…