02/02/2017

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Hypertensive Disorders in

Pregnancy

By

Mr Yasir M Shaukat

ED SpR

Classification

1. PRE-EXISTING (CHRONIC) HYPERTENSION

1. PRE-ECLAMPSIA

3. ECLAMPSIA

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Pre-existing (chronic) hypertension:

–Hypertension is present before

pregnancy, detected in early pregnancy

and postpartum.

PRE-EXISTING (CHRONIC)

HYPERTENSION

Causes

• Essential hypertension: of unknown aetiology.

• Secondary to chronic renal disorder: e.g. – Glomerulonephritis.

– Hydronephrosis.

– Pyelonephritis.

– Renal artery stenosis.

• Secondary to cardiovascular disease: e.g. – Coarctation of the aorta.

– Polyartheritis nodosa.

– Systemic lupus erythematosus.

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PRE-EXISTING (CHRONIC)

HYPERTENSION

• Secondary to endocrine disorders: e.g.

– Primary aldosteronism.

– Phaeochromocytoma.

– Adrenocortical tumours.

– Diabetes mellitus.

Effect of Pregnancy on Chronic

Hypertension

• Blood pressure falls by the second trimester in

most of cases, but rises during the third

trimester to a level some what above that in

early pregnancy.

• Deterioration of the underlying disease.

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Effect of Chronic Hypertension on

Pregnancy

Maternal:

• superimposed pre-

eclampsia/ eclampsia in 15-

20% of cases

Foetal:

– Intra-uterine growth

retardation.

– Intra-uterine foetal death.

Treatment

• Rest

• Antihypertensives

• Observation

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Pregnancy-induced hypertension

(PIH):

– Transient hypertension:

• Late onset hypertension, without proteinuria or

pathologic oedema

– Pre-eclampsia:

• Hypertension with proteinuria and / or oedema after 20

weeks of pregnancy, but may be earlier

– Eclampsia:

• Pre-eclampsia + convulsions.

PRE-ECLAMPSIA

• Incidence: 5-10%.

• Multisystem disorder

• Develops after 20 weeks gestation

• Aetiology unknown

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Predisposing factors

• Primigravidae more than multigravidae.

• Pre-existing hypertension.

• Previous pre-eclampsia.

• Family history of pre-eclampsia.

• Obesity.

Signs

• Hypertension

• Proteinuria (albuminuria)

• Oedema

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Hypertension

• Blood pressure of 140/90 mmHg or more or an

increase of 30 mmHg in systolic and/or 15

mmHg in diastolic blood pressure over the pre-

or early pregnancy level.

Proteinuria (albuminuria)

• Urinary protein greater than 0.3gm/L in 24 hours collection or greater than 1gm/L in two random samples obtained at least 6 hours apart.

• Indicates glomerular damage and occurs after hypertension

• Proteinuria usually in range of 1-3 gm daily ,50-60% is albumin, in severe cases may exceed 15gm.

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Oedema

• Weight gain > 1 kg in any one week or 2.25 kg

in any one month.

• Clinical oedema in about two-thirds of patients

with PIH. However, two-thirds of pregnant

women with clinical oedema do not develop

hypertension.

Symptoms pre-eclampsia

• Headache: usually frontal, may be occipital. Due to cerebral oedema and hypertension.

• Visual disturbances: blurring of vision, flashes of light or blindness.

• Epigastric or right upper quadrant pain: due to enlargement or subcapsular haemorrhage of the liver.

• Nausea and vomiting: due to congestion of gastric mucosa and/ or cerebral oedema.

• Oliguria or anuria: due to kidney pathology.

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Investigations

• Complete urine examination: for proteinuria, pus cells, RBCs, casts, specific gravity, culture and sensitivity.

• Renal function tests: serum uric acid > 6 mg % is abnormal during pregnancy. It is more specific for pre-eclampsia than creatinine.

• FBC and Coagulation screen: Platelet count, fibrinogen and FDP as DIC may develop.

• Fundoscopy.

• Foetal well being: – ultrasound,

– daily foetal movement count,

– non-stress test,

– oxytocin challenge test (if needed).

• Imminent eclampsia: It is a state in which the patient is about to develop eclampsia. Usually there are:

– blood pressure much higher than 160 /110 mmHg,

– heavy proteinuria (+++or ++++),

– hyperreflexia,

– severe continuous headache,

– blurring of vision,

– epigastric pain.

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Why is Pre-eclampsia important?

• Foetal complications:– Prematurity

– IUGR

– IUD

– Acute foetal distress

• Maternal complications:– HTN

– Risk CVA

– Pulmonary oedema

– Renal failure

– Liver failure

– DIC

– Placenta abruptio

– Eclampsia

Management severe pre-eclampsia

• Treatment:– Control BP (anti-hypertensives)

– Prevent seizures (MgSO4)

– Fluid management

– Decide on mode and timing of delivery

• Observations:– Maternal

• Symptoms

• BP + HR

• Reflexes +/- clonus

• Urine protein

• Urine output

– Fetal• CTG

• USS or Doppler if indicated

• One-to-one midwife care

• Transfer to Labour ward when stable

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Anti-hypertensives

• Acute hypertensive crisis– Systolic BP >180

– Diastolic BP >110

– Mean arterial pressure >125

• Persistent hypertension– BP > 160/100

• Treatment– Acute: IV Labetalol/Hydralazine/GTN

– Persistent: Labetalol/Methyldopa/Nifedipine

Acute hypertensive crisis

• Aim BP 130-140/90-100

• Avoid too rapid fall in BP

• Continuous FHR monitoring

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Definition - Eclampsia

• Seizures in women with PIH/PE not due to

other causes

• Any seizure in pregnancy is usually treated as

eclampsia until proven otherwise

• Antenatally 38%, Intrapartum 18%,

Postpartum 44% (especially 1st 24h)

Management of seizure

• Seizures are usually self-limiting

• MgSO4 is anticonvulsant of choice– Both in controlling as well as preventing

– IV Diazepam is NOT the drug of choice, unless MgSO4 not available

• Avoid polypharmacy to treat seizures -> increase risk of respiratory arrest

• Protocol– Loading dose MgSO4 (4g over 10mins)

– Maintainance dose 1g/hr

– Usually continued for 24h after delivery or after the last convulsion

• Important: rapid injection of MgSO4 can cause cardiorespiratory arrest!

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Monitoring on MgSO4

• Hourly monitoring

• Patellar reflexes should be present• Absence earliest sign of toxicity

• RR: 12-16

• UOP: >30mL/hr

• O2 Sats

Management of MgSO4 toxicity

• UOP <100mL/4h:– Fluid challenge

– If no clinical signs toxicity � reduce rate to 0.5g/hr

• Absent patellar reflexes:– Stop MgSO4 infusion

– May resume if reflexes return

• Respiratory depression:– Stop infusion

– O2 and monitor closely

– HDU/ITU

• Respiratory/Cardiac arrest– Resuscitate

– Stop infusion

– IV Calcium Gluconate 10% 10mL IV over 3-5 mins

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Management of recurrent seizures

• 2nd bolus of MgSO4

• 2g if <70kg and 4g if >70kg

• Check deep tendon reflexes and RR before repeating dose

• If further seizures:– Diazepam

– Thiopentone

– Intubation

– Intermittent positive pressure ventilation and muscle relaxation

– CT Head to rule out bleed

Delivery

• In severe pre-eclampsia/eclampsia definitive Tx is delivery

• Delivery decision based on– Patient’s condition (Clinical/Biochemical)

– Gestational Age

• If delivery to be delayed and gestation less than 34 weeks– IM Dexamthasone 6mg BD for 48hours

– Close monitoring

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Post delivery care

• HDU Care for first 24-48h post delivery

• Fluid balance chart

• CAUTION - Majority eclamptic seizures occur AFTER delivery

• Reduce anti-hypertensives as indicated

• Repeat Investigations (FBC, Clotting, LFTs, U&E’s)

HELLP syndrome

• HELLP, a syndrome characterized by

Haemolysis, elevated liver enzyme levels

and a low platelet count, is an obstetric

complication that is frequently misdiagnosed

at initial presentation.

• Many investigators consider the syndrome to

be a variant of preeclampsia,

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HELLP syndrome

• In some cases , HELLP symptoms are the

first warning of pre-eclampsia

• Misdiagnosed as hepatitis, idiopathic

thrombocytopenic purpura, gallbladder

disease, or thrombotic thrombocytopenic

purpura

Epidemiology and Risk Factors

• HELLP syndrome 0.2 to 0.6 % of all pregnancies.

• Superimposed HELLP syndrome develops in 4 to 12 percent

of women with preeclampsia or eclampsia.

• Maternal mortality has been estimated to be as high as 2-24%

• Perinatal mortality is equally high, ranging from 9 –39 %.

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Clinical Presentation

• 90% of patients present with general malaise

• 65 % with epigastric pain

• 30 % with nausea and vomiting

• 31 percent with headache

• All are nonspecific symptoms

Clinical Presentation

• Early diagnosis of this syndrome is critical

• Any pregnant woman who presents with

malaise or a viral-type illness in the third

trimester should be evaluated with a complete

blood cell count and liver function tests

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Clinical Presentation

• The physical examination may be normal in patients with HELLP syndrome

• Right upper quadrant tenderness 90 %

• Oedema is not a useful marker

• Hypertension and proteinuria may be absent or mild.

Diagnosis

• Concurrence of hemolysis, elevated liver

enzymes, and low platelet count.

• However, there is obviously still a lack of

consensus on the laboratory parameters

and their cutoff values used to diagnose

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Laboratory Diagnostic Criteria for

HELLP syndrome

• Haemolysis Abnormal peripheral smear : spherocytes, schistocytes, triangular

cells and burr cellsTotal Bilirubin level > 1.2 mg/dLLactate dehydrogenase level > 600U/L

• Elevated liver function test resultSerum aspartate amino transferase level > 70U/L Lactate dehydrogenase level >600 U/L

• Low platelet countPlatelet count < 150 000/mm3

Platelet countappears to be the

most reliable

indicator of the

presence of HELLP

syndrome

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Management

• Delivery

• Corticosteroids

• Magnesium sulphate

• Antihypertensives

• Blood products

• Hypertension is controlled at less than 160/110

mm hg,

• Oliguria responds to fluid management .

• Elevated liver function values are not

associated with right upper quadrant or

epigastric pain.

• Class II –III .(platelet count).>50000

Eligibility to conservative

management

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Management

• Patients with HELLP syndrome should be treated prophylacticallywith magnesium sulfate to prevent seizures, whether hypertension is present or not.

• Antihypertensive therapy should be initiated if blood pressure is consistently greater than 160/110 mm hg despite the use of magnesium sulfate. The goal is to maintain diastolic blood pressure between 90 and 100 mm hg.

The most commonly used antihypertensive agent has been

� hydralazine

� Labetolol

� Nifedipine

Management

• Corticosteroid therapy should be instituted in

patients with HELLP syndrome who have a

platelet count of less than 100,000 per mm3

• Should be continued until liver function

abnormalities are resolving and the platelet

count is greater than 100,000 per mm3

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Management

• Between 38 -93 % of patients with

HELLP syndrome receive some form of

blood product.

• Patients with a platelet count greater than

40,000 per mm3 are unlikely to bleed.

• The mortality rate for women with HELLP syndrome is approximately 1.1 %

• From 1 to 25 % of affected women develop serious complications such as DIC, placental abruption, adult respiratory distress syndrome, hepatorenal failure, pulmonary edema, subcapsular hematoma and hepatic rupture.

• A significant percentage of patients receive blood products.

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• Infant morbidity and mortality rates range from 10 to 60 %, depending on the severity of maternal disease.

• Infants affected by HELLP syndrome are more likely to experience intrauterine growth retardation and respiratory distress syndrome.

• Patients with HELLP syndrome who complain of

severe right upper quadrant pain, neck pain or

shoulder pain should be considered for hepatic

imaging regardless of the severity of the

laboratory abnormalities, to assess for subcapsular

haematoma or rupture.

• by three to four days postpartum The laboratory

abnormalities in HELLP syndrome typically

worsen after delivery and then begin to resolve.

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Questions?