On the Brink of Birth

A full term fetus, is shown in its mother’s womb in this Leonardo da vinci drawing. One of the first accurate renderings of a part of the human anatomy. The smaller sketches depict details of the uterus. Of all the triumphs of the body, its crowning glory is the power to reproduce its kind and pass some of its hereditary characteristics on to later generations.

Embryo to Fetus

fifteen days twenty-one days thirty days thirty-four days six wks eight wks

Life: One Seed + One Egg Life begins when an egg, previously released from one of the two ovaries, merges with just one of the hundreds of millions of sperm cells supplied through the vagina by the male reproductive system. The fertilized egg then descends to the wall of the uterus, where it implants itself to begin gestation.

Fetus

The average weight of the Indian baby at 40 weeks of

pregnancy is 2,750Gms at birth.

New Born

A healthy new born cries vigorously as soon as he is born, kicking his limbs actively, giving the greatest joy to the tired mother.

INTRODUCTION

Pregnancy causes physiologic changes in all maternal organ systems; most return to normal after delivery.

In general, the changes are more dramatic in multifetal than in single pregnancies.

Major adaptations in maternal anatomy, physiology, and metabolism.

BODY WATER METABOLISM

Condition of chronic water overload

Active Na and water retention

1. Changes in osmoregulation

2. Renin-angiotensin system

Body water increase 6.5L 8.5L

1. 1500 cc increase in blood vol

2. RBC increase ~400cc

OSMOREGULATION

Na retention increases 900 mEq but serum Na decreases 3-4 mmol/l

Plasma osmolarity decreases 10 mOsm/kg

Enhanced tubular reabsorption of Na secondary to aldosterone,estrogen and deoxycorticosterone.

CARDIOVASCULAR CHANGESHeart Displaced to the left and upward Apex is moved laterally Apparent cardiomegaly on chest x-ray Increase in left ventricular end-diastolic dimension Cardiac output (CO) increases

RESPIRATORY CHANGESUpper Respiratory Tract Hyperemia and edema induced by estrogen Nasal stuffiness and epistaxis

Mechanical changes

earlier than mechanical pressure of rising uterus Chest circumference expands 5-7 cm Subcostal angle increases from 68 to 103 degrees Transverse diameter increases 2cm Level of diaphragm rises 4cm but excursion is not

impeded Respiratory muscle function is not affected by

pregnancy

LUNG VOLUME AND PULMONARY FUNCTION

Elevation of the diaphragm decreases the volume of the lungs in the resting state, reducing Total Lung Capacity (TLC) by 5%

Functional Residual Capacity (FRC) by 20% FRC mainly decreased by Residual Volume (RV)

Vital capacity does not change Spirometry is not changed in pregnancy

Forced Expiratory Volume in 1 sec (FEV1) is unchanged

Peak flow is unchanged

HEMATOLOGIC CHANGES

40-50% increase in blood volume beginning at 6 weeks and plateaus at 30 weeks

Both plasma volume and cell mass increase

Physiologic anemia of pregnancy at 30 weeks

Increase in erythropoietin and reticulocyte count

IRON METABOLISM Iron (Fe) bound transferrin transported to

liver, spleen, muscle and bone marrow incorporated into hemoglobin and myoglobin

1000mg iron requirement, about 3.5 mg/dL of Fe

Requirements increase in third trimester

Fetus receives Fe through active transport

IRON SUPPLEMENTATION

Iron supplementation usually not needed before 20 weeks

30mg of elemental FE 325 mg ferrous gluconate

Fe supplements

Ferrous sulfate ( 65mg elemental Fe)

Ferrous gluconate (35mg of elemental Fe)

PLATELETS

Progressive decline in count from 1st-3rd tri

Increased platelet destruction

Gestational thrombocytopenia of pregnancy

OTHER HEMATOLOGIC CHANGES

Leukocytosis secondary to neutophils Estrogen induced Cortisol induced

Altered immune status Modulation away from cellular immunity

towards humoral immunity Paradoxical decline of immunoglobins A,G,M Only IgG crosses the placenta

URINARY SYSTEMAnatomic Changes Renal hypertrophy Dilation of renal pelvis/calyces

15mm on the right in 3rd trimester

5mm on the left

Predisposition to pyelonephritis in the presence of asymptomatic bacteriuria

Dilation of ureters to 2 cm Mechanical compression Progesterone-induced smooth muscle

relaxation

BLADDER CHANGES

Bladder trigone elevation occurs with increased vascular tortuousity throughout the bladder leading to microhematuira

Decrease bladder capacity

Increased frequency of micturition.

DIGESTIVE TRACT CHANGES

Addition of 300 kcal/day Gingivitis of pregnancy Stomach

Gastroesophageal refluxGastric compression due to enlarging

uterus

Decrease sphincter tone

Small bowel

Motility is reduced due to progesterone allowing for more efficient absorption

Large bowel

Decreased transit times allows for both water and sodium absorption

Liver Size and histology are unchanged Clinical and laboratory changes mimic disease

states Palmar erythema

SKELETAL AND POSTURAL CHANGES

Lordosis of pregnancy~ progressive increase in anterior convexity of the lumbar spine

Preserves center of gravity

Ligaments of the symphysis and sacroiliac joints loosen during pregnancy due to relaxin

ENDOCRINE CHANGES

Thyroid Physiology Euthyroid state Increase in thyroxine-binding globulin Slight thyromegaly T4 and T3 remain normal Fetal thyroid active by 12 weeks gestation

Adrenal function Increases in corticosteroid-binding globulin Increases in free cortisol Zona fasciculata is increased Marked increase in CRH from placental

sources Delayed plasma clearance of cortisol due to

renal changes Resetting of hypothalamic-pituitary sensitivity

to cortisol feedback on ACTH production

Pituitary gland Enlarges due to proliferation of prolactin-

secreting cells Enlargement makes it more susceptible to

alterations in blood flow, ie PPH Prolactin levels are increased (ten times higher

at term) to prepare breasts for lactation

Pancreas and Fuel Metabolism Physiologic glucose intolerance to ensure

continuous transport of nutrients from mother to fetus

Fasting hypoglycemia Postprandial hyperglycemia Hyperinsulinemia

Diabetogenic effects of pregnancy

Cortisol

Prolactin

Estrogen and progesterone

Fetal glucose levels are 20 mg/dl less than maternal values

INTEGUMENTAL CHANGES

Hyperpigmentation 90% of pregnancies

Localized to areas of increased melanocytes

Chloasma of pregnancy

Definition :

• Intra uterine growth restriction is said to be present in those babies whose birth weight is below the tenth percentile of the average for the gestational age.

• Growth restriction can occur in preterm, term or post-term babies.

Incidence :

• Dysmaturity comprises about one-third of low-birth weight babies.

• In developed countries, its overall incidence is about 2-8%.

• The incidence among the term babies is about 5% and that among the post-term babies is about 15%.

Nomenclature :

• SGA and IUGR are too often used synonymously although there is a degree of overlap.

• SGA fetus is not necessarily growth retarded.

• The baby may be constitutionally small.

• Similarly late onset of pathological cessation of growth may produce a baby with typical features of IUGR but may not be small for gestation (ie. Appropriate for gestational age).

• However, both attempt to identify fetuses or neonates that are small for reasons other than being preterm.

Normal fetal growth

• Is characterized by cellular hyperplasia followed by hyperplasia and hypertrophy and lastly by hypertrophy alone.

Types: Based on the clinical evaluation and ultrasound examination the small fetuses are divided into:

1.   Fetuses that are small and healthy. The birth weight is less than 10th percentile for their gestational age. They have normal ponderal index, normal subcutaneous fat and usually have uneventful neonatal course.

2. Fetuses where growth is restricted by pathological process (true IUGR). Depending upon the relative size of their head, abdomen and femur, the fetuses are subdivided into:

(a) Symmetrical or Type I (b) Asymmetrical or Type II.

Symmetrical (20%) –

• The fetus is affected from the noxious effect very early in the phase of cellular hyperpllasia.

• The total cell number is less. This form of growth retardation is most often caused by structural or chromosomal abnormalities or congenital infection (TORCH).

• The pathologic process is intrinsic to the fetus and involves all the organs including the head.

Asymmetrical (80%) – • The fetus is affected in later months during the

phase of cellular hypertrophy. • The total cell number remains the same but size

is smaller than normal. • The pathologic processes that too often result in

asymmetric growth retardation are maternal diseases extrinsic to the fetus.

• These diseases alter the fetal size by reducing utero-placental blood flow or by restricting the oxygen and nutrient transfer or by reducing the placental size.

Etiology: The causes of fetal growth retardation can be divided into four types.

Maternal – • Maternal nutrition before and during pregnancy –

Critical substrate requirement for the fetus such as glucose, aminoacids and oxygen are lacking during pregnancy.

• This is an important cause of small weight of the babies in the developing countries.

• As most of the fetal weight gain (two-third) occurs beyond 24th week of pregnancy, malnutrition, anaemia, hypertension, antiphospholipid syndrome in the second half of pregnancy play significant role in the reduction of the birth weight.

Fetal – There is enough substrate in the maternal blood and also crosses the placenta but is not utilized by the fetus. The failure of non utilization may be due to

(1) Congenital anomalies either cardio vascular, renal or others

(2) Chromosomal abnormality is associated with 8-12% of growth retarded infants. The common abnormalities are trisomy 21, trisomy 18 (Edward’s Syndrome), trisomy 16, trisomy 13 and Turner’s syndrome

(3) Accelerated fetal metabolism due to TORCH agents (toxoplasmosis, rubella, cytomegalovirus and herpes simplex) and parvo virus B19

(4) Multiple pregnancy – There is mechanical hindrance to growth and excessive fetal demand.

Placental – • The causes include cases of poor uterine blood flow to the

placental site for a long time. • This leads to chronic placental insufficiency with

inadequate substrate transfer. • This occurs in conditions such as preeclampsia, essential

hypertension, chronic nephritis, organic heart disease, placental and cord abnormalities such as chronic placental abruption, infarction, small placenta, circumvallate placenta, vellamentous insertion of cord etc.

Unknown – The cause remains unknown in about 40%

Diagnosis

• The ‘at risk’ mothers are teenaged in present pregnancy with reduced uteroplacental blood flow. This can be achieved as early as 12 weeks by a thorough and meticulous exam.

• Maternal weight gain remains stationary or at times falling (less than 2 kg/month during second half of pregnancy).

• If there is reduction of symphysis fundal height by 2 cm before 36 weeks or 3 cm thereafter or the measurement falls below the 10th percentile.

• Measurement of the abdominal girth showing stationary or falling values.

• Serial clinical examination by abdominal palpation to measure the relative growth of the uterus and its contents is the commonly used method. The diminishing amniotic fluid volume can also be assessed with fair degree of accuracy.

• Reduced or absent diastolic flow in umbilical artery as evidenced by Doppler blood flow velocimetry.

• Normally, the diastolic flow increases as pregnancy progresses.

• Presence of ‘notch’ in the early diastole waveform, especially in the uterine arteries, suggests incomplete invasion of trophoblasts of the spiral arteries.

• This ‘notch’ if confirmed at 24 weeks, predicts possible development of IUGR and pre-eclampsia.

Physical features at birth

• Weight deficit at birth is about 600 gm below the minimum in percentile standard.

• Length is unaffected.

• Head circumference is relatively larger than the body.

Physical features at birth

• Physical features show dry and wrinkled skin because of less subcutaneous fat, scaphoid abdomen, thin meconium stained vernix caseosa and thin umbilical cord. All these give the baby an ‘old man look’. Pinna of ear has cartilaginous ridges. Plantar creases are well defined.

• The baby is alert and having normal cry. Eyes are open.

• Reflexes are normal including Moro-reflex.

ComplicationsFetal: (A) Antenatal – Chronic fetal distress, fetal death, (B) Intranatal – Hypoxia and acidosis (C) After birth:Immediate: (1) Asphyxia (intrauterine and neonatal), (2) Hypoglycemia due to shortage of glycogen reserve in the

liver as a result of chronic hypoxia (3) Meconium aspiration pneumonia (4) Microcoagulation leading to DIC during first day of life. (5) Hypothermia (6) Pulmonary hemorrhage (7) Polycythaemia (8) Hyperviscosity syndrome (9) Necrotizing enterocolitis due to reduced intestinal blood flow.

Late: • Symmetrical growth retarded baby is likely to

grow slowly after birth. • Whereas the asymmetrical one is more likely to

grow faster after birth. • The fetuses have retardation of growth

evidenced before third trimester are likely to have retarded neurologic and intellectual development in infancy.

• The worst prognosis is for IUGR caused by congenital infection, congenital abnormalities and chromosomal defects.

Mortality

• The immediate neonatal mortality is about 6 times more than the normal newborn or even similar weight appropriate to the shorter gestational age.

• Most of the babies die within 24 hours.

• The morbidity rate rises to about 50%.

Management during pregnancy

1. Adequate bed rest specially in left lateral position (2 hours following lunch and 8 hours at night).

2. To correct malnutrition by adequately balanced diet, 300 extra calories per day are to be taken.

3. To institute appropriate therapy for the associated complicating factors likely to produce growth retardation.

4. Avoidance of smoking and alcohol.

5. Low dose aspirin (50 mg daily) may be helpful.

6. Detect fetal anomalies.

Yoga practices have helped to prevent IUGR

Hypertension is one of the common complications.

Increased maternal and perinatal morbidity and mortality.

Underlying pathology Pre-existing or During pregnancy

PreeclampsiaEclampsiaGestational hypertension

Hypertension (BP ≥ 140/90 mm Hg) during pregnancy can be classified as chronic or gestational.

Chronic hypertension is BP that is high before pregnancy or before 20 wk gestation. It is seen about 1 to 5% of all pregnancies.

Gestational hypertension develops after 20 wk gestation (typically after 37 wk) and remits by 6 wk postpartum; it occurs in about 5 to 10% of pregnancies, more commonly in multifetal pregnancy.

PREECLAMPSIA

Preeclampsia is a common problem during pregnancy, affecting up to one in seven pregnant women around the world.

This condition is defined by high blood pressure and excess protein in the urine after 20 weeks of pregnancy.

It can lead to serious, even deadly complications for mother and the unborn baby.

Globally, preeclampsia and other high blood pressure disorders during pregnancy are a leading cause of maternal and infant illness and death.

The only cure for preeclampsia is delivery of the baby. After baby is born, blood pressure usually returns to normal within a few days.

So delivery is the obvious solution when preeclampsia is found near the end of the pregnancy, which is typically the case.

Preeclampsia is a multisystem disorder which is peculiar to the pregnant state.

It usually manifests for the first time beyond the 20th week and is characterised by the appearance of hypertension to the extent of 140/90 mmHg or more with proteinuria or edema or both.

The cause remains obscure but there is intense vasospastic condition affecting almost all the vessels specially those of the uterus and the kidneys.

Pathophysiological changes are more evident on the uteroplacental bed, liver and kidneys.

The change are mostly related to a combination of vasospastic state and Disseminated Intravascular Coagulopathy (DIC).

HELLP syndrome (Hemolysis; Elevated Liver Enzymes; Low Platelet Count) is observed in 10-15% of those with preeclampsia – eclampsia.

Incidence varies from 5-15%, more in primigravidae. The onset is usually insidious. It is principally a syndrome of signs, such as rapid

gain in weight, edema of legs, raised BP and proteinuria.

Maternal hazards include eclampsia, abruptio placentae, oliguria or anuria, dimness of vision or blindness, increased operative interference, postpartum shock and puerperal sepsis.

Fetal risk are due to intrauterine death, dysmaturity, asphyxia or prematurity.

Prevention includes regular antenatal check-up to detect at the earliest the evidences of preeclampsia features so that prompt therapy can be instituted.

Treatment modalities, a case of severe preeclampsia should have prophylactic anticonvulsant therapy and urgent termination of pregnancy.

Predisposing factors: Elderly and young primigravidae Family history of pre-eclampsia, eclampsia or

hypertension Poor and under-privileged sector – more due to

neglect in antenatal care rather than nutritional cause

Pregnancy complications such as hydatidiform mole, multiple pregnancy, polyhydramnios, Rh-incompatibility

Medical disorders – hypertension, nephritis, diabetes

Hereditary – though to be single recessive gene disorder.

Basic pathology is intense vasospasm affecting almost all the vessels - uterus, kidney and brain.

Responsible agent for vasospasm - humoral in origin.

Edema Excessive accumulation of fluids in the

extracellular tissue spaces is not clear. Excessive retention of sodium in the edematous

state is probably due to increase aldosterone out of activation of corticosterone by angiotensin.

Proteinuria: Spasm of the afferent glomerular arterioles -->

anoxin damage to the endothelium of the glomerular tuff --> increased capillary permeability --> increased leakage of proteins.

Tubular reabsorption is simultaneously depressed. Albumin constitutes 50-60% and alpha globulin

constitutes 10-15% of the total proteins excreted in the urine.

Clinical types

Proteinuria is more significant than blood pressure to predict fetal outcome.

Mild Severe

Mild: this includes cases of sustained rise of blood pressure of more than 140/90 mmHg but less than 160 systolic or 110 diastolic without significant proteinuria.

A persistent diastolic pressure of > 110 mmHg. Persistent severe epigastric pain Cerebral or visual disturbances Oliguria Protein excretion of >5 gm/day Platelet count <1,00,000/µL Elevated liver enzymes Retinal hemorrhages, exudates or papilledema Intrauterine growth restriction of the fetus Pulmonary edema.

Severe: is diagnosed when one or more of the following manifestations exist.

Clinical features

Pre-eclampsia frequently occurs in primigravidae (70%). It is more often associated with obstetrical medical complications such as multiple pregnancy, polyhydramnios, pre-existing hypertension, diabetes etc.

The clinical manifestations appear usually after the 20th week. Onset: Usually insidious and the syndrome runs a slow course.

On rare occasion, the onset becomes acute and follows a rapid course.

Symptoms: Pre-eclampsia is principally a syndrome of signs and when symptoms appear, it is usually late.

Mild symptoms: Slight swelling over the ankles which persists on rising from the bed in the morning or tightness of the ring on the finger is the early manifestation of pre-eclampsia edema. Gradually, the swelling may extend to the face, abdominal wall, vulva and even the whole body.

SIGNS AND SYMPTOMS The signs of preeclampsia are elevated blood

pressure (hypertension) and the presence of excess protein in urine (proteinuria) after 20 weeks of pregnancy.

Other signs and symptoms are not always noticeable:

Severe headaches Changes in vision, including temporary loss

of vision, blurred vision or light sensitivity Upper abdominal pain, usually under the ribs

on the right side Unexplained anxiety

Nausea or vomiting

Dizziness

Decreased urine output

Swelling (edema), particularly in the face and hands.

Abnormal weight gain: rapid weight gain more than 2.3 kg a month or more than 0.46 kg a week.

Rise in blood pressure: > 140/90 mmHg. Edema: Visible edema over the ankles on rising

from the bed in the morning is pathological. May spread to other parts of the body in uncared cases. Sudden and generalized edema may indicate imminent eclampsia.

No manifestation of chronic cardiovascular or renal pathology.

Abdominal examination reveals chronic placental insufficiency such as scanty weight --> visible edema and/or hypertension --> proteinuria.

Alarming symptoms - associated with acute onset of the syndrome

Headache – either located over the occipital or frontal region.

Disturbed sleep Decreased urinary output – less than 500 mL in 24 hours

is very ominous. Epigastric pain – acute pain associated with vomiting, at

times coffee color, is due to hemorrhagic gastritis or due to subcapsular hemorrhage in the liver.

Eye symptoms – blurring or dimness of vision or at times complete blindness. Vision is usually regained within 4-6 weeks following delivery. The eye symptoms are due to spasm of retinal vessels, edema and retinal detachment. Reattachment of the retina occurs following subsidence of edema and normalization of blood pressure after delivery.

Investigations Urine: Proteinuria is the last feature of pre-

eclampsia to appear. It may be trace or at timescopious so that urine becomes solid on boiling (10-15 gm/liter). There may be few hyaline casts, epithelial cells, or even few red cells. 24 hours urine collection for protein measurement is done.

Ophthalmoscopic examination: Retinal edema, constriction of the arterioles, alteration of normal ratio of vein: arteriole diameter from 3:2 to 3:1 and nicking of the veins where crossed by the arterioles.

Blood values: Blood changes are not specific and often inconsistent. Serum uric acid level (biochemical marker of pre-eclampsia) of more than 4.5 mg% indicates the presence of pre-eclampsia. Blood urea level remains normal or slightly raised. Serum creatinine level may be more than 1 mg/dL. There may be thrombocytopenia of varying degrees. Hepatic enzyme levels may be increased.

Antenatal fetal monitoring – Antenatal fetal well being assessment is done by clinical examination, daily fetal kick count, ultrasonography for fetal growth and liquor pockets, cardiotocography, umbilical artery flow velocimetry and biophysical profile.

Course of the disease: Pre-eclampsia is usually insidious in onset and runs a slow course. Rarely, the onset may be acute and follows rapid course of events.

If detected early: With prompt and effective treatment the pre-eclamptic features may subside completely.

If left untreated and uncared for: Pre-eclamptic features remain stationary at varying

degrees till delivery. Aggravation of the pre-eclamptic features with

appearance of symptoms of acute fulminating pre-eclampsia as mentioned earlier. This happens mostly in cases with acute onset.

Eclampsia – It may occur following acute fulminating pre-eclampsia or bypassing it. In fact, eclampsia can occur even with a blood pressure of 140/90 mmHg

Spontaneous remission of the pre-eclampsia features – a rare and fortunate event.

COMPLICATIONS OF PREECLAMPSIA

HELLP syndrome Eclampsia – within 48 hours Liver necrosis Brain – cerebral edema Heart failure Salt retention

PATHOPHYSIOLOGY Brain: Apart from cerebral edema, capillary thrombosis,

patches of hemorrhages and necrosis may occur. Cerebral function is not impaired although there is increased irritability as evidenced in the electro-encephalogram (EEG). This explains exaggerated reflexes on examination.

Heart: Sub-endothelial hemorrhages may occur. Focal necrosis and hemorrhage in the myocardium may affect the conducting system leading to heart failure.

Lungs: There is evidence of edema or hemorrhagic bronchopneumonia.

Other organs: Adrenal glands show hemorrhage and necrosis. Stomach shows feature of hemorrhagic gastritis.

The warning signs and symptoms of ECLAMPSIA :

Pain in the upper right side of abdomen Severe headache Vision problems, seeing flashing lights Change in mental status, decreased alertness Abnormal weight gain 0.46 kg per week or 2.3

kg per month.

Problems for the fetus Preeclampsia affects the arteries carrying

blood to placenta. Less oxygen and nutrients. Slow growth or low birth weight. Preterm birth. Preeclampsia increases the risk of placental

abruption — in which the placenta separates from the inner wall of the uterus before delivery.

Severe abruption causes heavy bleeding, resulting in shock.

GESTATIONAL HYPERTENSION

A sustained rise of blood pressure to 140/90 mmHg or more on at least two occasions 4 or more hours apart beyond the 20th week of pregnancy or during the first 24 hours after delivery in a previously normotensive woman is called gestational hypertension.

It is associated with a much higher incidence of essential hypertension in later life than pre-eclampsia.

Both are thus seem to be two phases of the same disorder.

It should fulfill 3 criteria Absence of any evidences for the underlying

cause of hypertension Unassociated with other evidences of

preeclampsia (edema or proteinuria). The blood pressure should come down to normal

within 10 days following delivery.

The hypertensive effect may be a stress response. Perinatal mortality remains unaffected. These patients are more likely to develop

hypertension with the use of oral contraceptives or in subsequent pregnancies.

Gestational edema is excessive accumulation of fluid with demonstrable pitting edema over the ankles greater than 1+ after 12 hours in bed or gain in weight of 2 kg or more in a week due to influence of pregnancy.

Gestational proteinuria is the presence of protein of more than 0.3 gm in the 24 hours urine during or under the influence of pregnancy in the absence of hypertension, edema or renal infection. It may be orthostatic proteinuria.

Effects of pregnancy on the disease There may be a midpregnancy fall of blood

pressure in about 50%, the BP tends to rise in the last trimester which may or may not reach its previous level.

In 50%, the BP tends to rise progressively as pregnancy advances.

In about 20%, it is superimposed by pre-eclampsia evidenced by rise of BP to the extent of 30 mm systolic and 15 mmHg diastolic associated with edema and/or proteinuria.

Rarely, malignant hypertension supervenes. In 30%, there is permanent deterioration of the

hypertension following delivery.

Effects of the disease on pregnancy

Maternal risk: In the milder form, the maternal risk remains unaltered but in the severe form or when superimposed by pre-eclampsia, the maternal risk is much increased.

Fetal risk: Due to chronic placental insufficiency, the babies are likely to be growth retarded. In the milder form, with the BP less than 160/100 mmHg, the perinatal loss is about 10%. When the BP exceeds 160/100 mmHg, the perinatal loss doubles and when complicated by pre-eclampsia, it trebles.

PRINCIPLES OF TREATMENT

To stabilise the BP to below 160/100 mmHg

To prevent superimposition of preeclampsia

To monitor the maternal and fetal well being

To terminate the pregnancy at the optimal time.

General Management

In mild cases with BP less than 160/100 mmHg, adequate rest (physical and mental), low salt and a sedative (phenobarbitone) are all that are needed.

The check up should be more frequent 1-2 weeks interval up to 28 weeks and thereafter weekly.

Depends upon the severity of disease.

Obstetric Management

Antihypertensive Drugs

Routine use of antihypertensive drug is controversial.

It may lower the BP and thereby benefit the mother but the diminished pressure may reduce the placental perfusion which may be detrimental to the fetus.

Antihypertensive drugs should be used only when the pressure is raised beyond 160/100 mmHg.

In cases, where the drugs have been used before pregnancy, care should be taken to adjust the dose during pregnancy, specially, during the midpregnancy when the BP tends to fall.

MANAGEMENT

• Rest

• Diet

• Laxative

• Diuretics

• Antihypertensives

• Doxazosin Mesylate• Irbesartan• Candesartan• Valsartan• Fosinopril Sodium• Lercanidine HCl• Nebivolol HCl• Quinapril• S-Atenolol• Telmisartan• Trandolapril• Imidapril

Group Practice

Breathing Exercises

Ankle Stretch Hands In & Out

Breathing Exercises

Tiger Stretch Side Stretch

Loosening Exercise

Anguli

Sitting Postures

Vajrasana Ardha Matsyendrasana

ASANAS

Sitting Postures

Baddhakonasana

ASANAS

Sitting Postures

Squatting

ASANAS

Sitting Postures

Prasaritha

ASANAS

Sitting Postures

Uphavista Konasana

ASANAS

Sasankasana

ASANAS

Supine Postures

Viparita Karani

Both leg raising

ASANAS

Viparita Karani both leg raising

with wall Support

Supine Postures

Matsyasana

ASANAS

Supine Postures

Pavanamuktasana

ASANAS

Prone Postures

Ardha Shalabhasana

ASANAS

1. Mastery over Prana

– Slowing of breath

– Awareness of breathing

– Balance between the two nostrils.

2. There is intimate connection between mind and Prana.

Pranayama

Relaxation Technique

Meditation

Omkar Meditation

Mudra

Aswini Mudra

Effects of Yoga in High Risk Pregnancy

Results of the research study showed Significant increase in birth weight Beneficial trend in

PIH IUGR Preterm delivery Cesarean section