Hypertensive disease during px

Hypertensive Disorders of Pregnancy

Hypertension: High: blood pressure: elevation of the arterial BP above the normal range(>140/90)

• Is the second common cause of maternal death.

Note:

– Measure the BP in the sitting position with cuff at the level of the heart.

– Allow the mother to sit 5 – 10 minutes before measuring

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Classification:• There are more than 80 ways of classifying

hypertensive disorders of pregnancy. Let us the see one of them: 1. Chronic hypertension2. Pregnancy Aggravated hypertension(PAH)

– Preeclampsia superimposed on chronic hypertension

3. Pregnancy induced hypertension (PIH)– Pre eclampsia- eclampsia– Gestational hypertension

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Pregnant woman with BP > 140/90mmHg

Before 20 Weeks > 20 weeks

No proteinuria Proteinuria No proteinuria Proteinuria

Chronic HTN Pre eclampsia Gestational HTN PreeclampsiaSuperimposed on Chronic HTN

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1. Chronic hypertension: Elevated BP that predates the pregnancy, documented before 20 weeks of pregnancy, or present 6 weeks postpartum

• Diagnosis is made if BP is raised on two consecutive occasions with at least 4 hours interval.

A. Mild chronic HTN: BP <160/100 mmHg

B. Severe Chronic HTN: BP > 160/110mmHG

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2. Pre eclampsia- eclampsia: Elevated BP and proteinuriathat occurs after 20 weeks of gestation. Eclampsia is the severe form of preeclampsia, the new onset of seizure or coma in a woman with pre eclampsia.

3. Pre eclampsia superimposed on chronic HTN:

• An acute increase in the level of hypertension and new onset of protienuria, in a woman with chronic HTN

4. Gestational HTN: Elevated BP without protienuriadeveloped after 20 weeks of gestation in regresses postpartum

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1. Pre Eclampsia

Incidence: B/n 5 – 8 % of all pregnancies are complicated by hypertension and therefore those preeclampsia acoounts for 80%.

• Occurs more frequently in:

– Young primigravidae

– First pregnancies from new partner

– Mother over 35 years of age

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Pathophysiology of Pre eclampsia:

• It is important to distinguish preeclampsia from chronic or gestational HTN.

• Pre eclampsia is more than HTN; its systemic syndrome, and several of its ‘non hypertensive’ complications can be life threatening when BP elevations is quite mild.

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Etiology/Causes:

• The exact cause is unknown but it is taught to be due to abnormal placentation; the physiological changes in the uteroplacentalarteries do not extend beyond the deciduomymetrial junction leaving a constricting segment b/n radial arteries and decidual portion leading to HTN.

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Pathological Changes:

• In normal pregnancy CO, HR, and blood volume increase while peripheral resistance and responsiveness to angeotensin II decrease No hypertension.

• In pre eclampsia:

1. Endothelial cell damage affects capillary permeability. Plasma leaks from the damaged vessels producing edema with in the tissue.

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2. The reduced intravascular compartment causes hypovolemia and haemoconcentartion. In severe cases lung becomes congested with fluid and pulmonary edema develops. Oxygenation is Impaired and cyanosis occurs.

3. With vasoconstriction and damage to the endothelium the coagulation cascade is activated. Increased platelet consumption produces thrompocythopnia and Disseminated intravascular Coagulation (DIC) occurs.

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• Poor perfusion to the trophoblast release of one or more of the clotting factors which damage the endothelial cells producing vasoconstriction substances.

• As the process fibrin and platelets deposit occur. This will occlude blood flow to many organs, particularly the Kidneys, Liver, Brain and Placenta.

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4. In Kidneys: vasospasm of the afferent arterioles result in decreased renal blood flow damage to the endothelial cells of the glomrulus (Glumerulo endohetliosis) allow plasma protein to urine Proteinuria

5. In severe cases liver is affectedintracapsular hemorrhage necrosis and edema of the liver cells epigastric pain

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6. The brain becomes edematous and this in conjunction with hypertension and DIC can produce necrosis of the blood vessels and thrombosis resulting in head aches, visual disturbance and convulsion.

7. In the uterus vasoconstriction reduces the uterine blood flow and vascular lesions occur in the placental bed placental abruption.

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8. Reduced blood supply to the choriodecidualspaces reduced oxygenationintrauterine growth restriction (IUGR)

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Classification of Pre eclampsia:

1. Mild Pre eclampsia

– BP>140/90 but less than 160/110mmHg

– Protienuria ++ on dipsticks or 3gm/24hrs in absence of UTI

– Generalized edema

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2. Severe Pre eclampsia:

• Criteria to diagnose for severe pre eclampsia:– BP >160 systolic, 110 diastolic

– Protienuria > 5gm/24 hrs or +++ urine drip

– Oligouria: less than 400 ml/24 hrs

– CNS: Visual changes, head ache, mental status change

– Pulmonary edema

– Epigastric (RUQ) pain

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S/S of severe preeclampsia cont…

– Impaired liver function tests

– Thrompocythopnia<100,000

– IUGR

– Oligohydramnious

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Diagnosis of Pre eclampsia:

• The two essential feature of pre eclampsia are Hypertension & Protienuria.

A. Blood Pressure (BP):

A rise of 25mmHg above mother’s normal diastolic or 90 mmHg on two occasions at least 4 hrs apart.

NB: Taking BP in early pregnancy helps to know changes in BP later

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B. Protienuria:• In absence of UTI is indication of renal damage• Is the most serious manifestation• Usually the last manifestation of pre eclampsia• Is an index of severity of pre eclampsia. Protienuria Albux: + = 300mg/L +++ =3gm/L++= 1gm/L ++++ =10gm/LNB: The urine should be of midstream

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Other causes of proteienuira like:

• Contaminate urine

• Chronic nephritis

• Heart failure

• Pyelonephritis should be ruled out.

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3. OedemaIt is important to note:• Oedema is not included in the above

definition as oedema, whilst of concern to the woman, is probably of little clinical importance. It occurs equally in pregnant women with or without pre-eclampsia.

• However, the rapid development of generalised oedema may be abnormal and commonly seen in women with pre-eclampsia.

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Effects of pre eclampsia:A. On the mother:

– Eclampsia– Placental abruption– Damage to heart, kidneys, lungs and brain– Damage to the capillary in the fundus of the eye leading

to blindnessB. On the fetus:– LBW– Intrauterine hypoxia– IUFD– Pre term baby requiring resuscitation.

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The role of Midwife in detection of pre eclampsia:

• Pregnancy induced hypertension (pre eclampsia) is unlikely to be prevented, early detection and appropriate management ca minimize the severity of the condition ( ECLAMPSIA)

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A midwife is in a unique position to identify those woman with pre disposion to pre eclampsia:

• History taking at booking visit will include:– Adverse social circumstances or poverty

– Family tendency towards hypertension

– Mothers age and parity

– A new partnership

– A past history of pre-eclampsia

• Note: Checking of BP, Wt, Urine for protein are essential elements of ANC

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Management of Mild Pre eclampsia / PIH:

Aims of care:

• To provide rest and tranquil environment

• To monitor the condition and

• To prevent its worsening by giving appropriate care and treatment.

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Note: The ultimate aim is to prolong pregnancy until the fetus is sufficiently mature enough to survive, while safeguarding the mother’s life. Management then depends on:

1. Severity of the pre eclampsia

2. Duration of the pregnancy and

3. Respond to treatment

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General principles:

• Reduce vasospasm

• Prevent eclampsia

• Prevent renal and liver impairments

• Deliver a health baby

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Management:

• Rest

• Sedation

• Diet rich in protein, fiber, vitamins

• Taking BP every 4 hrs, urine for protein daily

• Abdominal palpation daily to rule out placental abruption

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• Fetal kick chart

• Anti hypertensive e.g. Methyldopa/Aldomet

• Anti conversant: e.g. Diazepam/Vallium

• Anti thrombin agents: e.g. Aspirin

• Investigation for maturity and placental dysfunction: Ultrasound, estimation of placental steroids, Shake test for surfactant, Lechtin/sphingomyellin ratio of liquor to indicate lung maturity.

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Ambulatory Care:

• Bed rest at home as much as possible, minimum ½ an hr after meal + 10 hours per day

• Sedation: e.g. Diazepam BID or TID

• Weekly follow up and if any risk factor occurs admit to hospital.

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Hospital Care: • Investigations• Bed rest• Sedation • Diet: Normal ward diet• Antihypertensive:

– Methyldopa– Hydralazine– Nifedipne– Propranol

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• Nursing care:

– Quite area

– Observation 4 hourly

– Laying on side

– Ally anxiety

Management of Labor:

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Indications of delivery in pre-eclampsia:

A. Maternal– GA > 38 weeks

– Platelet count <100,000 cells/mm3

– Progressive deterioration in liver and renal functions

– Suspected abruption placenta

– Persisting severe head aches, visual disturbance, nausea, epigastric pain or vomiting

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B. Fetal:

• Severe fetal growth restriction/ retardation

• None reassuring fetal heart rate patterns /NRFHRP/

• Oligohydramnious

NB: The “cure” for pre eclampsia is delivery.

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First Stage of labor:• The MW should remain with the mother• BP(Mean arterial pressure/MAP) ½ hourlyMAP = systolic+2Diastolic

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• MAP should be less than 105. • Fluid balance:

– Be careful of fluid overload– Oxytocin should be administered with caution b/s it

has anti diuretic effect.

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– Urinary catheter should be inserted and urine output should be measured hourly: >30ml/hr reflects adequate renal function.

• Plasma volume expanders• Pain relive• Fetal heart rate monitoringSecond stage of labor:

– Vacuum or forceps to shorten 2nd stage

• Third stage of labour• Do not use ergametrine/Use Oxytocine

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Following delivery: The maternal condition should be monitored at least 4 hourly for the first 24 hrs.

Management of severe pre eclampsia

• Should be managed as eclampsia!!!!

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S/S of impending or imminent eclampsia:

The following s/s should alert the MW to the onset of ECLAMPSIA:

• Sharp rise in BP

• Diminished urinary output

• Increase in proteinuria

• Severe persisisting frontal headache

• Confusion: Cerbral edema

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• Visual disturbance(Flushing light,- Retinal edema)

• Epigastric pain: Liver damage

• Nausea and vomiting

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Eclampsia…

Definition: Eclampsia is defined as the occurrence of one or more convulsions or coma in association with syndrome of pre-eclampsia.

Incidence: in developed countries: 1 in 200 deliveries.

in developing countries: 1 in 100 deliveries

Note: Eclampsia can be prevented by properly managing pre-eclampsia although it is difficult when it is fulminating pre – eclampsia.

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Stages of fit:

1. Premonitory stage: lasts about 10 -20 seconds. Patient is restless, twitching of facial muscles, eye roll, respiration becomes spasmodic.

2. Tonic stage: Lasting about 10 – 20 seconds, general muscle rigidity, and whole body goes in to tonic spasms, Backaches, features distorted by grimace, tongue may be bitten, breathing ceases and pt becomes cyanosed.

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3. Colonic stage: Lasting about 60 – 90 minutes. Convulsive movements frothy saliva fills the mouth, may be stained. The woman becomes unconscious.

4. Stage of coma: Snoring breathing continued and may be persistent for minutes or hours. Further convulsive movements sometimes recur with or without pt gaining from consciousnes.

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DDx: (other causes of convulsion):

• Epilepsy

• Cerebral malaria

• Brain damage

Prevention: Careful and frequent observations in the antenatal period by detecting and treating pre-eclampsia should almost prevent eclampsia.

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Aims of treatment:

• To prevent further convulsions

• Once convulsions are controlled, termination of pregnancy will result in improvement of the generalized vasospasm.

• Control the blood pressure.

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Emergency Care:

• Clear air way, do not leave the pt alone.

• Oxygen administration continuously to improve tissue oxygenation.

• Prevent pt from injury during fit:

– Place a padded spatula b/n her teeth to prevent from biting her tongue or the tongue can block air ways.???

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– Turn her one side

– Lower her head to drain secretions from mouth and throat.

– Do not attempt to control the convulsions as it seems to stimulate the fit.

• Suctions is continued to clear nose and pharynx of froth secretions.

• Sedation: Diazepam 10 mg IV & 10 mg IM is commonly used.

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Management:

1. Anti convulsing therapy:

A. Magnesium Sulphate:

• There has been world wide variation in clinical practice for the treatment and prevention of eclampsia

• MgSO4 was the most effective drug in reducing death and further fits

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• MgSO4 is a CNS depressant.

• It affects neuromuscular impulse transmission, which reduces the hyper- reflexia associated with severe pre-eclampsia.

• Vasodilitatory effect:– decrease BP

– reduces cerebral ischemia

– blocks some of the neuronal damage associated with ischemia

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MgSO4 Recommendations for use:

• Following a seizure to prevent the next seizure• For women with severe pre-eclampsia who

are hyper-reflexic and immediate birth is required, and

• For women with severe pre-eclampsia who are requiring transfer to another unit for birth.

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Dose of MgSO4:A. Loading Dose: • Give 4gm of MgSO4 IV over 5 minutes• Follow promptly with 10 g of 50% MgSO4

solution: Give 5 g in each buttock as deep IM injection with 1 ml of 2% lidocaine in the same syringe. Ensure aseptic technique whine giving the IM injection.

• Warn the woman that feeling of warmth will e felt MgSO4 is given.

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• If convulsion reoccur after 15 minutes, give 2 gm of 50% of MgSO4 solution over 5 minutes.

B. Maintainance Dose:

• Give 5g of MgSO4 solution with 1 ml of 2% lgnocaine in the same syringe by deep IM injection in to alternate buttocks every 4 hrs.

• Continue treatment for 24 hrs after delivery or the last convulsion whichever comes first.

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Closely Monitor the woman for the signs of the toxicity of MgSO4:

• Before repeating the administration ensure that:

– RR is at least less than 16/minute

– Patellar reflex are present(DTR)

– Urinary output is at least 30ml pr hr over 4 hrs

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Withhold MgSO4 if:

• RR falls below 16/mn

• Patellar reflexes are absent

• Urinary out put falls below 30ml/hr over the preceding 4 hrs

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Keep antidote ready:

• In case of respiratory arrest:

– Assist ventilation (mask and bag, anesthesia apparatus, intubation)

– Give Calcium guconate 1gm (10ml 0f 10% solution) IV slowly until calcium gluconante begins to antagonize the effects of MgSO4 and respiration begins.

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B. Diazepam:

Use Diazepam only if MgSO4 is not available.

A. Loading dose:

• Diazepam 10mg IV slowly over 2 minutes.

• If convulsions reoccur repeat the loading dose.

B. Maintain ace dose:

• Diazepam 40mg in 500 ml IV fluids (NS or RL)

• Do not give more than 100 mg/24hrs(risk of respiratory depression)

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2. Treatment of Hypertension:

• If the diastolic BP is 110 mmHg or more, give antihypertensives.

• The goal is to keep the diastolic BP b/n 90 and 100 mmHg to prevent cerebral hemorrhage.

• Hydralazine is the drug of choice.

Dose of Hydralazine:

• Give Hydralazin 5mg IV slowly every 5 minutes

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until BP is lowered(less than 110mmHg). Repeat hourly as needed or give Hydralazine 12.5 mg IM every two hrs as needed.

• If Hydralazine is not available, use labetolol or nifedipine: – Labetolol 10mgIV

Or

– Nifedipine 5mg under the tongue, if no response(Diastolic BP still> 110mmHg) after 10 minutes, give additional 5mg under the tongue.

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