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. Chronic hypertension complicates 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.
A sustained rise of blood pressure to 140/90 mmHg or more on at least two occasions 4 or more hours apart beyond the 20 th 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 is 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.
CHRONIC HYPERTENSION IN PREGNANCY
The presence of hypertension of any cause antedating or before the 20 th week of pregnancy.
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.
The principles of management are
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.
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.
Routine use of antihypertensive drug is controversial.
It may low 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.
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 may also be called toxemia or pregnancy-induced hypertension.
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.
However, if she diagnosed earlier, treatment is trickier.
Preeclampsia is a multisystem disorder which is peculiar to the pregnant state.
It usually manifests for the first time beyond the 20 th 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 DIC.
HELLP syndrome is observed in 10-15% of those with preeclampsia – eclampsia.
The 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 or 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.
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 aren't always noticeable, but may experience:
Changes in vision, including temporary loss of vision, blurred vision or light sensitivity
Upper abdominal pain, usually under the ribs on the right side
Nausea or vomiting
Decreased urine output
Swelling (edema), particularly in the face and hands.
Preeclampsia superimposed on chronic hypertension.
Other high blood pressure disorders during pregnancy
Preeclampsia used to be called toxemia because it was thought to be caused by a toxin in a pregnant woman's bloodstream.
Insufficient blood flow to the uterus
Injury to blood vessels
Damage to the lining of blood vessels
A disruption in the hormones maintaining blood vessels
Immune system lowering
Lack of magnesium or calcium
The biggest risk factor for preeclampsia is simply being pregnant.
Additional risk factors include:
History of preeclampsia.
Age – younger than 20 or older than 35.
In a 2006 study, pregnant women who had high levels of two specific proteins in their blood were found to be more likely to develop preeclampsia than were other women.
These proteins interfere with the growth and function of blood vessels.
Research to confirm the findings is needed — but the discovery suggests that a blood test may one day serve as an effective screening tool for preeclampsia.
SCREENING & DIAGNOSIS
Preeclampsia usually shows up unexpectedly during a routine prenatal blood pressure check and urine test.
It's important to seek regular prenatal care throughout the pregnancy.
Normal blood pressure readings for pregnant women are below 130/85 mmHg.
A blood pressure reading of 140/90 mmHg or higher is considered above the normal range.
A biophysical profile combines an ultrasound with a nonstress test to provide more information about baby's breathing, tone, movement and the volume of amniotic fluid in uterus.
COMPLICATIONS OF PREECLAMPSIA
HELLP syndrome – is one of two serious complications of preeclampsia. HELLP stands for: H emolysis — the destruction of red blood cells; E levated L iver Enzymes; L ow P latelet Count
The warning signs and symptoms of ECLAMPSIA :
Pain in the upper right side of abdomen
Vision problems, seeing flashing lights
Change in mental status, decreased alertness
Problems for the fetus
Preeclampsia affects the arteries carrying blood to placenta.
Less oxygen and nutrients.
Slow growth or low birth weight.
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.
INTRAUTERINE GROWTH RETARDATION [IUGR]
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.
Intrauterine growth retardation (IUGR) means the unborn baby is not growing properly.
The baby's weight is lower than it should be for its stage of the pregnancy.
The baby's growth and weight are important.
Small babies are more likely to have problems near the time of birth and after delivery.
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%.
How does it occur?
Alcohol during pregnancy
With history of small babies in previous pregnancies
Some of the conditions that can cause IUGR :
a placenta that is unable to provide proper nourishment to the baby
birth defects or inherited problems, such as heart, kidney, or chromosome problems in the baby
high blood pressure
physical defects in the uterus
too little or too much amniotic fluid
exposure to radiation or chemicals
chronic illness in the mother, such as heart, kidney, or lung disease, or lupus.
Developed & Developing Countries
SIGNS AND SYMPTOMS
Poor weight gain.
Fetal weight abnormal for gestational age.
Confounding variables such as maternal height, weight, race, fetal sex and birth weights of previous babies may be corrected for by computer, using algorithms to derive specific customized growth charts.
Wilcox et al 1993, bearing in mind that up to 40% of the variation in birth weight is related to genetic contributions from both the mother and the fetus.
When patients are referred with suspected IUGR, the ultrasound diagnosis of true IUGR should be based on a number of features apart from a reduced size (e.g. estimated fetal weight <10 th centile).
Biometric assessment should consist of measurement of the abdominal circumference, head circumference, femur length and cerebellar diameter.
The latter is a particularly stable measurement even in profound IUGR (Reece et al 1987).
This will give an indication of the relative fetal size and the body proportionality with the classic categorization into symmetrical (type II-80%) IUGR associated with restriction of fetal nutrients and oxygen.
However, this has limited clinical potential as both patterns overlap in individual cases and the two types probably reflect the timing and duration, rather than the cause of poor growth (Lin & Evans 1984; Lin 1985).
A repeat ultrasound examination may be necessary 2 weeks later in order to assess the growth velocity and to avoid the erroneous diagnosis os true IUGR in a fetus which is only constitutionally small but otherwise healthy.
Typically a fall of >1.5SD in the AC measurement over this period would be regarded as being indicative of true IUGR (Chang et al 1993).
Assessment of liquor volume is equally important with most centers now recognizing the value of the Amniotic Fluid Index measurements as a repeatable and reliable technique.
Fetal AC <5the centile
Fetal growth velocity <1.5SD in 2 weeks
Amniotic Fluid Index <5 th centile
Abnormal umbilical artery Doppler studies.
Having made the diagnosis it is then important to identify the etiology.
This involves taking details of obstetric and medical history to identify important risk factors such as advanced maternal age, smoking, alcohol consumption, drug abuse and maternal medical disorders such as hypertension, diabetes.
Enquiry should also be made about possible viral infections (rash and flu-like symptoms) and any history of previous babies with IUGR or structural or chromosomal abnormalities.
The maternal blood pressure should be checked and urinalysis should be performed.
Measurement of the symphysis-fundal height, while useful for screening and monitoring is largely superseded by ultrasound when investigating true IUGR but should be recorded to allow subsequent clinical monitoring of growth (especially to aid the continuation of management in the community) to complement other techniques.
Relationship of socio-environment to IUGR
Medical and obstetrical history
Blood pressure and urinalysis
Infection screen (TORCH and Parvovirus)
IUGR and Smoking
IUGR and Alcohol
Ultrasound and Doppler studies in IUGR
Biometry (HC, AC, HC:AC, FL, cerebellar diameter)
Markers for abnormal karyotype
Features of infection
Biophysical profile score
Doppler (umbilical artery and uteroplacental arteries)
Liquor (amniotic fluid index)
Assessing fetal hypoxia
Fetal hypoxia may also be indirectly assessed using the BPS or more recently by pulsed Doppler cerebral blood-flow studies.
It is through that increased end diastolic flow velocities in the middle cerebral and carotid arteries correlate with increased cerebral blood flow and shunting away from non-essential fetal vasculature such as the renal and mesenteric arterial systems (Vyas et al 1990).
Thus, absolute and sequential changes in the cerebral vessel waveforms and comparison with other vascular beds may prove a useful surrogate measure for fetal adaptation to hypoxia (Di Renzo et al 1992): supplementary testing includes traditional cardiotocography (CTG) which may be refined by computerized analysis such as the system 8000, which provides an objective assessment of heart-rate variability (Dawes et al 1992).
It is doubtful whether other methods such as contraction stress testing and vibro-acoustic stimulation have much to offer when compared with the BPS and CTG.
Middle Cerebral Artery Doppler
Treatment of IUGR
Treatment for IUGR is usually delivery of the fetus by the most appropriate route.
Some modalities such as bed rest, oxygen therapy and the administration of nutrients have been criticized, through the treatment of maternal medical disorders such as hypertension and sickle cell disease may be beneficial.
The administration of aspirin has received interest of late despite the Cochrane Database of Systematic Reviews of antiplateler agents for IUGR and pre-eclampsia which failed to show any benefit from therapy.
The recent Collaborative Low-dose Aspirin Study in Pregnancy (CLASP 1994) also failed to show any convincing benefits in a hetrogenous group of 9364 at-risk women, although the work by McParland and his colleagues (1990), who showed improvement in Doppler blood studies following administration of low-dose aspirin (75 mg daily) to women with abnormal uteroplacental Doppler studies, suggests that careful selection of patients for aspirin therapy may yield some benefits.
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:
Fetuses that are small and healthy. The birth weight is less than 10 th percentile for their gestational age. They have normal ponderal index, normal subcutaneous fat and usually have uneventful neonatal course.
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 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 24 th week of pregnancy, malnutrition, anaemia, hypertension, antiphospholipid syndrome in the second half of pregnancy play significant role in the reduction of the birth weight.
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
Congenital anomalies either cardio vascular, renal or others
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.
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.
The cause remains unknown in about 40%
Problems for the baby :
Problems at the time of delivery
Death, in extreme cases.
GESTATIONAL DIABETES MELLITUS [GDM]
Gestational diabetes is a type of diabetes that occurs only during pregnancy.
Like other forms of diabetes, gestational diabetes affects the way the body uses blood sugar (glucose).
As a result, blood sugar level is too high.
If untreated or uncontrolled, gestational diabetes can result in a variety of health problems for the pregnant woman and the fetus.
GLYCOSURIA IN PREGNANCY
Significant disturbances in carbohydrates metabolism occur in about 1% of pregnancies and the incidence of overt diabetes is about 1 in 300 pregnancies.
Renal glucosuria – renal threshold is diminished due to the combined effect of increased glomerular filtration and impaired tubular reabsorption of glucose.
It is present in mid pregnancy.
If glucose tolerance test is done, glucose leaks out in the urine even though the blood sugar is well below 180 mg per 100 mL (normal renal threshold).
No treatment is required and the condition disappear after delivery.
2. Impaired glucose tolerance during pregnancy – During pregnancy there is – Accelerated absorption of glucose from the alimentary tract resulting in alimentary glycosuria.
Complex endocrinal changes resulting in delayed utilization of glucose to form liver glycogen due to anti-insulin activity.
These indicate that the pregnancy has got a diabetogenic effect which results in glycosuria in small but distinct group of cases specially in later months.
3. Clinical diabetes – either preexisting or detected for the first time during pregnancy.
4. Lactosuria – Glucose is converted into lactose during later months of pregnancy and throughout lactation.
The lactose so formed, is excreted in urine.
It reduces Benedict’s solution but remains unaffected in Diastix test.
Fasting glucosuria if present, is ominous even though glucose tolerance test is apparently normal.
Glycosuria on one occasion before 20 th week and on two or more occasions, thereafter, is an indication for glucose tolerance test.
Glycosuria occurring any time during pregnancy with a positive family history of diabetes or past history of having a baby weighting 4 kg or more.
Investigations in a case of glycosuria
STEP-I Confirmation is to be done by testing a second fasting morning specimen of urine. Urine tested for acetone – if positive diabetes is confirmed.
STEP-II Blood glucose estimations – fasting sugar exceeds 90mg/100mL or after 2 hours is over 120mg/100mL proceed to Step-III.
STEP-III A glucose tolerance test with 100 gm (WHO-75 gm) glucose is to be performed.
Indications of glucose tolerance test
Fasting glucose on 1 occasion before 20 th week and on 2 or more occasions thereafter
Following a positive ‘screening test’ – (Vide – Gestational diabetes)
If fasting blood sugar exceeds 90 mg/100mL or if that after 2 hours of ingestion of 75gm glucose is over 120mf/100mL.
Nomenclature : The term includes cases with abnormal carbohydrate tolerance with onset or first detected during the present pregnancy.
The entity does not present until late in the second or during third trimester.
Previously, the definition stipulated that the GTT should come down to normal following delivery.
This requires the knowledge of normal tests both before and after pregnancy.
A substitute nomenclature ‘Pregnancy induced glucose intolerance’ seems appropriate.
The potential candidates:
Positive family history of diabetes.
Having a previous birth of an overweight baby of 4 kg or more
Previous stillbirth with pancreatic islet hyperplasia revealed on autopsy
Unexplained perinatal loss
Presence of polyhydramnios or recurrent vaginal candidiasis in present pregnancy
Age over 30
The method employed is by using 50 g oral glucose tolerance test without regard to time of day or last meal, between 24-28 weeks of pregnancy.
A plasma glucose value of 140 mg per cent or that of whole blood of 130 mg per cent at 1 hour is considered as cut off point for consideration of a 100 g (WHO – 75 g) glucose tolerance test.
Criteria for diagnosis of GDM with 100 g oral glucose tolerance test GTT Time Whole blood (mg%) Plasma (mg%) Fasting 90 105 1 hour 165 190 2 hours 145 165 3 hours 125 145 If any 2 or more values are elevated, the glucose tolerance test result must be considered abnormal.
Criteria for diagnosis of impaired glucose tolerance and diabetes with 75 g (WHO) oral glucose Plasma (mg%) Time Normal Impaired glucose tolerance Diabetes Fasting <105 105 to <140 >/=140 2 hours post glucose <160 160 to <200 >/=200
Venous whole blood values are 15% less than the plasma.
m mol/L = mg% x 0.0555
Increase perinatal loss is associated with fasting hyperglycemia. Fetal anomalies not increased. Expected in view of absence of metabolic disturbance found during organogenesis.
Increase incidence of macrosomia
Tendency to develop overt diabetes (10-15%) later in pregnancy
Patient needs more frequent antenatal supervision with periodic check up of fasting blood glucose level which should be less than 90mg per cent.
The control of high blood glucose may be done by restriction of diet or by insulin.
The abnormal weight gain is to be checked and early hospitalization may be justified to formulate obstetric management.
Human insulin should be started if fasting plasma glucose level exceeds 105mg/dL and 2 hours postprandial value is greater than 130mg/dL even on diet control.
If otherwise uncomplicated and controlled by diet only, one may wait for spontaneous onset of labor.
The pregnancy should not be allowed to pass beyond the expected date.
In the presence of complicating factors or cases controlled by insulin, termination beyond 38 weeks may be justified for fetal interest.
Classification of pregnant diabetics
Fetal and maternal outcome of diabetic pregnancy depends on severity of the disease and its duration.
Priscilla White’s classification was originally used to assess the perinatal outcome and to formulate the obstetric management.
But it is now mainly used for statical correlation of different types of pregnant diabetes.
Currently vasculopathy is given more importance to predict the outcome.
Priscilla White’s classification of pregnant diabetes Class – A Class – B Class – C Class – D Class – E Class – F Class – R Gestational diabetes Overt diabetes – onset > age 20, duration <10 yrs Overt diabetes – onset < age 20, “ ” <10-19 yrs Overt diabetes – onset < age 10, “ ” 20 yrs. Benign retinopathy Calcified pelvic vessels Diabetic nephropathy with proteinuria Malignant diabetic retinopathy
Current classification of pregnant diabetics Group – A Group – B Group – C Gestational diabetes Overt diabetes without vasculopathy Diabetes with vasculopathy (retinopathy and/or nephropathy)
EFFECTS OF PREGNANCY ON DIABETES
Difficult to stabilise the blood glucose during pregnancy due to altered carbohydrate metabolism and an impaired insulin action.
The insulin antagonism is probably due to the combined effect of human placental lactogen, estrogen, progesterone, free cortisol and degradation of the insulin by the placenta.
Insulin requirement during pregnancy increases as pregnancy advanced.
As more glucose leaks out in the urine due to renal glycosuria, control of insulin dose cannot be made by urine test and repeated blood glucose estimation becomes mandatory.
With the ‘accelerate starvation’ concept, there is more rapid activation of lipolysis with short period of fasting.
Ketoacidosis can be precipitated during hyperemesis in early pregnancy, infection and fasting of labor.
It can be iatrogenically induced by beta sympathomimetics and corticosteroids used in the management of preterm labor.
Insulin requirement falls significantly in puerperium.
Vascular change, specially retinopathy, nephropathy, coronary artery disease, and neuropathy may be worsened during pregnancy.
Some women worry that having gestational diabetes will cause birth defects.
Fortunately, this usually isn't the case. In general, birth defects originate during the first three months of pregnancy, while gestational diabetes generally doesn't develop until the second or third trimester.
This means blood sugar levels are normal during the first critical months.
Most women with gestational diabetes go on to deliver healthy babies.
Untreated or uncontrolled blood sugar levels can cause problems for patient and the fetus.
Complications in mother
Gestational diabetes in another pregnancy.
Type 2 diabetes.
Complications the fetus
Consistently keeping blood sugar levels within a normal range can reduce these possible complications:
Respiratory distress syndrome.
Stillbirth or death.
Maternal: During pregnancy
Abortion is unrelated to controlled diabetes but recurrent spontaneous abortion may be associated with uncontrolled diabetes.
Prenatal labor (17%) may be due to infection or polyhydramnios.
Infection occurs more often, specially urinary tract infection.
Increased incidence of preeclampsia (25%) is associated even in the absence of vascular lesion.
Polyhydramnios (25-50%) is a common association. Large baby, large placenta, fetal hyperglycemia leading to polyuria, increased glucose concentration of liquor irritating the amniotic epithelium or increased osmosis are some of the probabilities.
Maternal distress may be due to the combined effects of an oversized fetus and polyhydramnios.
During labor : There is increased incidence of prolongation of labor due to big baby, shoulder dystocia, perineal injuries, postpartum hemorrhage, operative interference.
Puerperium : Puerperal sepsis, failing lactation.
Fetal macrosomia (30-40%) probably results from :
Maternal hyperglycemia hypertrophy and hyperplasia of the fetal islets of Langerhans increased secretion of fetal insulin stimulates carbohydrate utilization and accumulation of fat. Insulin growth factor (IGF-I&II) involved in fetal growth and adiposity. With good diabetic control, incidence of macrosomia is markedly reduced.
Elevation of maternal free fatty acid (FFA) in diabetes leads to its increase transfer to the fetus acceleration of triglyceride synthesis adiposity.
Congenital malformation (6-8%) is probably related to the severity of diabetes affecting organogenesis in the first trimester.
Congenital malformation, commonly include cardiac abnormalities (ventricular or atrial septal defects), neural tube defects (anencephaly, spinabifida, microcephaly) and caudal regression syndrome (sacral agenesis).
Good control of diabetes both preconceptionally and in first trimester reduces the incidence of congenital malformations.
Early detection of fetal anomalies
Estimation of glycosylates hemoglobin A (HbA1c) – before 14 weeks of gestation can predict affection of the fetus. Mother with HbA1c value less or equal to 8.5% have got least chance of severe malformation of the fetus. Chance of major congenital malformation is more if the values rise to 9.5% or more.
Maternal serum alpha fetoprotein level at 16 weeks and a detailed high resolution ultrasonographic exam of the fetus including assessment of fetal cardiac structure at 20 weeks are advocated.
Birth injuries are associated with prolonged labor and shoulder dystocia, due to an oversized (macrosomic) baby.
Unexplained fetal death has got multifactorial pathogenesis but the final event being hypoxia and acidosis. It may be due to the combined affect of impaired uterine blood flow, reduced episodes of fetal hypoglycemia and fetal blood hyperviscosity and thrombosis.
Perinatal mortality : The overall perinatal mortality is increased 2-3 times than the non-diabetics. The neonatal deaths are principally due to hypoglycemia, respiratory distress syndrome, polycythaemica and jaundice.