Gestational Diabetes Mellitus

Gestational diabetes (GDM) is a condition in which women without previously diagnosed diabetes exhibit high blood glucose levels during pregnancy.

 

Gestational diabetes generally has few symptoms and it is most commonly diagnosed by screening during pregnancy. Diagnostic tests detect inappropriately high levels of glucose in blood samples. Gestational diabetes affects 3-10% of pregnancies. No specific cause has been identified, but it is believed that the hormones produced during pregnancy increase a woman's resistance to insulin, resulting in impaired glucose tolerance.

 

Babies born to mothers with gestational diabetes are at increased risk of problems typically such as being large for gestastional age (which may lead to delivery complications), low blood sugar, and jaundice. Gestational diabetes is a treatable condition and women who have adequate control of glucose levels can effectively decrease these risks.

 

Women with gestational diabetes are at increased risk of developing type 2 diabetes mellitus after pregnancy, while their offspring are prone to developing childhood obesity, with type 2 diabetes later in life. Most patients are treated only with diet modification and moderate exercise but some take anti-diabetic drugs, including insulin.

RISK FACTORS

 

§  Previous diagnosis of gestational diabetes or prediabetes, impaired glucose tolerance, or impaired fasting glycaemia

§  Family history revealing a first degree relative with type-2 diabetes

§  Maternal age - a woman's risk factor increases as she gets older (especially for women over 35 years of age)

§  Ethnic background (those with higher risk factors include African-Americans, Afro-Caribbeans, Native Americans, Hispanics, Pacific Islanders, and people originating from the Indian subcontinent)

§  Being overweight, obese or severely obese increases the

§  A previous pregnancy which resulted in a child with a high birth weight (>90th centile, or >4000g

§  Previous poor obstetric history

 

PATHOPHYSIOLOGY

§  The precise mechanisms underlying gestational diabetes remain unknown. The main cause of GDM is increased insulin resistance.

§  Pregnancy hormones and other factors are thought to interfere with the action of insulin as it binds to the insulin receptor. The interference probably occurs at the level of the cell signaling pathway behind the insulin receptor.

§  Since insulin promotes the entry of glucose into most cells, insulin resistance prevents glucose from entering the cells properly. As a result, glucose remains in the bloodstream, where glucose levels rise.

§  More insulin is needed to overcome this resistance; about 1.5-2.5 times more insulin is produced than in a normal pregnancy.

§  Insulin resistance is a normal phenomenon emerging in the second trimester of pregnancy, which progresses thereafter. It is thought to secure glucose supply to the growing fetus.

§  Placental hormones, and to a lesser extent increased fat deposits during pregnancy, seem to mediate insulin resistance during pregnancy. Cortisol and progesterone are the main culprits, but human placental lactogen, prolactin and estradiol contribute too.

§  Because glucose travels across the placenta, the fetus is exposed to higher glucose levels. This leads to increased fetal levels of insulin (Hyperinsulinemia).

§  The growth-stimulating effects of insulin can lead to excessive growth and a large body (macrosomia).

§  After birth, the high glucose environment disappears, leaving these newborns with ongoing high insulin production and susceptibility to low blood glucose levels (hypoglycemia)

 

DIAGNOSIS

 

§  Blood glucose testing : A fasting plasma glucose level >125mg/dL or a casual plasma glucose >200 mg/dL meets the threshold for the diagnosis of diabetes.

 

Fasting and 2 hours postprandial venous plasma sugar during pregnancy.

Fasting	2h Postprandial	Result
<100 mg/dl	< 145mg/ dl	Not diabetic
>125 mg/ dl	>200 mg/ dl	Diabetic
100-125 mg/dl	125-200 mg/dl	Border line indicates glucose tolerance test.

 

Oral Glucose Challenge Test:

§  Also called the O'Sullivan test.

§  It is performed between 24–28 weeks, and can be seen as a simplified version of the oral glucose tolerance test (OGTT).

§  It involves drinking a solution containing 50 grams of glucose, and measuring blood levels 1 hour later.

§  A plasma value above 130-140mg/dl one hour after is commonly used as a threshold for performing a 3-hour OGTT.

 

Oral Glucose Tolerance Test (OGTT)

Prerequisites:   - Normal diet for 3 days before the test.

- No diuretics 10 days before.

- At least 10 hours fast.

- Test is done in the morning at rest.

 

Procedure: Giving 75 gm (100 gm by other authors) glucose in 250 ml water orally

 

Criteria for glucose tolerance test: The following are the values which the American Diabetes Association considers to be abnormal during the 100 g of glucose OGTT:

• Fasting blood glucose level ≥95 mg/dl
• 1 hour blood glucose level ≥180 mg/dl
• 2 hour blood glucose level ≥155 mg/dl
• 3 hour blood glucose level ≥140 mg/dl

If any 2 or more of these values are elevated, the patient is considered to have an impaired glucose tolerance test.

 

Glycosylated haemoglobin (Hb A1(

§  It is normally accounts for 5-6% of the total haemoglobin mass. A value over 10% indicates poor diabetes control in the previous 4-8 weeks.

 

§  If this is detected early in pregnancy, there is a high risk of congenital anomalies .

 

§  If this is detected in late pregnancy it indicates increased incidence of macrosomia and neonatal morbidity and mortality.

 

§  The mean glucose represented by the hemoglobin A1c level can be calculated using the "rule of 8's." A value of 8 percent equals 180 mg/dl, and each 1 percent increase or decrease represents ± 30 mg/dl.

 

§  Assessment for asymmetric fetal growth by ultrasonography, particularly in early third trimester, may aid in identifying fetuses that can benefit from maternal insulin therapy

 

§  Maternal surveillance should include blood pressure and urine protein monitoring to detect hypertensive disorders.

 

MANAGEMENT

 

Medical nutrition therapy should include the provision of adequate calories and nutrients to meet the needs of pregnancy and should be consistent with the maternal blood glucose goals that have been established. Noncaloric sweeteners may be used in moderation.

 

Diet therapy is critical to successful regulation of maternal diabetes. A program consisting of three meals and several snacks is used for most patients. Dietary composition should be :

ü50 -60%  carbohydrate,

ü20% protein,

ü25-30% fat with less than 10% saturated fats, up to 10% polyunsaturated fatty acids, and the remainder derived from monosaturated sources

 

Insulin Therapy

Insulin therapy is recommended when medical nutrition therapy fails to maintain self-monitored glucose at the following levels:

• Fasting plasma glucose <105 mg/dL
• 1-hour postprandial plasma glucose <155 mg/dL
• 2-hour postprandial plasma glucose <135 mg/dL

Goal of Insulin Therapy

Self-blood glucose monitoring combined with aggressive insulin therapy has made the maintenance of maternal normoglycemia (fasting and premeal glucose between 50-80mg/dl and 1 hour postprandial glucose <140mg/dl)

Twice daily ( before breakfast and before dinner) injections of a combination of short and intermediate acting insulins are usually sufficient to control most patients otherwise a subcutaneous insulin pump is used.

 

The total first dose of insulin is calculated according to the patient’s weight as follow:

In the first trimester ..........   weight x 0.7

In the second trimester........  weight x 0.8

In the third trimester........... weight x 0.9

 

If the total dose of insulin is less than 50 units/ day, it is given in a single morning dose with the ratio: Short acting (regular or Actrapid)/Intermediate (NPH or Monotard) = 1 : 2

 

In higher doses, As a general rule, the amount of intermediate-acting insulin will exceed the short-acting component by a 2:1 ratio. Patients usually receive two thirds their total dose with breakfast and the remaining third in the evening as a combined dose with dinner

 

Insulin Dose adjustment

§  Home glucose monitoring with a reflectance meter by measuring fasting and preprandial glucose values 4 times a day (30-40 min)before each meal.

§  All values are recorded in a daily log.

§  In patients who are not well controlled, a brief period of hospitalization is often necessary for the initiation of therapy. Individual adjustments to the regimens implemented can then be made.

 

KETOACIDOSIS

§  As pregnancy is a state of relative insulin resistance marked by enhanced lipolysis and ketogenesis, diabetic ketoacidosis may develop in a pregnant woman with glucose levels barely exceeding 200 mg/dl .

 

§  Thus, DKA may be diagnosed during pregnancy with minimal hyperglycemia accompanied by a fall in plasma bicarbonate and a pH value less than 7.30.

 

§  Clinical signs of volume depletion follow the symptoms of hyperglycemia, which include

o   Polydipsia and polyuria.

o   Malaise.

o   Headache.

o   Nausea/ Vomiting.

§  Occasionally, diabetic ketoacidosis may present in an undiagnosed diabetic woman receiving β-mimetic agents to arrest preterm labor.

 

§  Because of the risk of hyperglycemia and diabetic ketoacidosis in diabetic women . Terbutaline and magnesium sulfate has become the preferred tocolytic for cases of preterm labor in these cases.

 

§  Sometimes Administration of antenatal corticosteroids to accelerate fetal lung maturation can cause significant maternal hyperglycemia and precipitate DKA. In diabetic patients.

 

§  An intravenous insulin infusion will usually be required and is adjusted on the basis of frequent capillary glucose measurements.

 

§  Meticulous correction of metabolic and fluid abnormalities.

 

§  Every effort should therefore be made to correct maternal condition before intervening and delivering a preterm infant.

 

ANTEPARTUM FETAL EVALUATION

 

Antepartum fetal monitoring tests are now used primarily to avoid unnecessary premature intervention allowing the fetus to benefit from further maturation in utero.

Ultrasound

• Ultrasound is a valuable tool in evaluating fetal growth, estimating fetal weight, and detecting hydramnios and malformations.
• Maternal serum α-fetoprotein (MSAFP) at 16 weeks' gestation is often used in association with a detailed ultrasound study during the second trimester in an attempt to detect neural tube defects and other anomalies. Normal values of MSAFP for diabetic women are lower than in the nondiabetic population .
• Ultrasound examinations should be repeated at 4- to 6-week intervals to assess fetal growth. The detection of fetal macrosomia, the leading risk factor for shoulder dystocia, is important in the selection of patients who are best delivered by cesarean section.

Maternal assessment of fetal activity

• Maternal hypoglycemia, while generally believed to be associated with decreased fetal movement, may actually stimulate fetal activity.

The Non Stress Test (NST(

• Done weekly at 28 weeks and Twice weekly at 34 weeks
• Remains the preferred method to assess antepartum fetal well-being in the patient with diabetes mellitus
• If the NST is nonreactive, a biophysical profile (BPP) or contraction stress test is then performed .

Doppler Umbilical Artery Velocimetry

• Doppler umbilical artery velocimetry has been proposed as a clinical tool for antepartum fetal surveillance in pregnancies at risk for placental vascular disease.
• It is found that Doppler studies of the umbilical artery may be predictive of fetal outcome in diabetic pregnancies complicated by vascular disease.
• Elevated placental resistance as evidenced by an increased systolic/diastolic ratio is associated with fetal growth restriction and preeclampsia in these high-risk patients.

 

TIMING AND MODE OF DELIVERY

 

• There is very little evidence to support either elective delivery or expectant management at term in pregnant women with insulin-requiring diabetes.

• When antepartum testing suggests fetal compromise, delivery must be considered.

• Delivery by cesarean section usually is favored when fetal distress has been suggested by antepartum heart rate monitoring.

• If a patient reaches 38 weeks' gestation with a mature fetal lung profile and is at significant risk for intrauterine demise because of poor control or a history of a prior stillbirth, an elective delivery is planned.

• During labor, continuous fetal heart rate monitoring is mandatory. Labor is allowed to progress as long as normal rates of cervical dilatation and descent are documented.
• Arrest of dilatation or descent despite adequate labor should alert the physician to the possibility of cephalopelvic disproportion.

 

INSULIN MANAGEMENT DURING LABOUR AND DELIVERY

• Usual dose of intermediate-acting insulin is given at bedtime.
• Morning dose of insulin is withheld.
• Intravenous infusion of normal saline is begun.
• Once active labor begins or glucose levels fall below 70 mg/dl, the infusion is changed from saline to 5% dextrose and delivered at a rate of 2.5 mg/kg/min.
• Glucose levels are checked hourly using a portable meter allowing for adjustment in the infusion rate.
• Regular (short-acting) insulin in administered by intravenous infusion if glucose levels exceed 140 mg/dl.

Pre eclampsia

CLASSIFICATION OF HYPERTENSION IN PREGNANCY

HTN is the most common medical disorder in pregnancy – occurs in up to 22% of all pregnancies

A. Gestational hypertension: Without proteinuria or pathological edema

B. Preeclampsia: Hypertension and protenuria with or without pathological edema

C. Eclampsia : Pre eclampsia complicated with convulsions or coma

D. Chronic hypertension

§  Essential Hypertension

§  Chronic Renal Disease

§  Coarctation of Aorta

§  Pheochromocytoma

§  Thyrotoxicosis

§  Connective tissue disease-systemic lupic erthematous

E. Pre eclampsia or eclampsia superimposed on chronic hypertension

 

PREECLAMPSIA

Definition

Preeclampsia is a multisysytem disorder of unknown etiology characterized by development of hypertension to the extent of 140/90mm Hg or more with protenuria after the 20^th week in a previously normotensive and non-protenuric patient.

Etiology

Cause unknown: theories suggest vasospasm and ischemia, or abnormal immune system response. Arteriolar vasospasm causes endothelial cell damage, increases capillary permeability, and leads to edema

Risk Factors

•Low socioeconomic class

•Multiple foetuses, or hydatid

•Maternal age <20 or >35yrs

•Primipara

•Gestational or pre-gestational DM

•Renal disease

•Family history- four times the risk

Pathophysiology

• The normal endovascular invasion of cytotrophoblast into the spiral arteries fails to occur beyond deciduas-myometrial junction
• The musculo elastic media in the myometrial segment remains responsive to vasoconstrictor stimuli resulting in decreased blood flow
• Areas of ischaemia in tertiary villi of placenta
• Microvilli from trophoblasts are shed into maternal vascular system
• Damaged endothelial cells release vasoconstrictive agents
• Vasoconstrictve agents like Thromboxane, Endothelin  are released, and vasospasm results – i.e. hypertension occurs

 

Signs and Symptoms

 

Mild preeclampsia

• SBP >140, DBP >90 taken 2 separate times 4-6 hrs apart
• Proteinuria: >1+ protein with urine dipstick or >300 mg protein in 24-hr urine sample
• Slight

Severe preeclampsia

• SBP >160 or DBP >110 on 2 different occasions at least 4-6 hrs apart on bedrest
• Proteinuria: >2+ on urine dipstick or >2g in 24 hr urine sample. Swollen glomerular capillaries result in stretched out capillary walls
• albumin/protein escapes into urine
• Oliguria: urine output <500 mL in 24 hrs
• Other symptoms: cerebral/visual disturbances, hyperreflexia, N&V, pulmonary edema, epigastric pain, thrombocytopenia

 

HELLP Syndrome

 

Complication of severe preeclampsia that involves hepatic dysfunction.

HELLP stands for:

H         : Hemolysis of RBCs

EL       : Elevated liver enzymes

LP       : Low platelets (<1,00,000/mm3)

 

Similar to pre-eclampsia with

–RUQ/ epigastric pain

–N/V

–Jaundice

–Deranged LFT

Diagnosis of pre-eclampsia

• Investigate all organ systems – CVS, CNS, Resp.
• Haematological – Platelets, haematocrit
• Renal – proteinuria, creatinnine, (uric acid)
• Hepatic – AST
• Placenta – Doppler U/S umbilical artery, fetal growth

 

MANAGEMENT

Rest: Admission in hospital and rest is helpful for  continued evaluation and treatment of the patient. While in bed patient should be in left lateral position as much as possible, to lessen the effects of venacaval compression. Rest – (1) increases the renal blood flow (2) increases the uterine blood flow improves the placental perfusion and (3) reduces the blood pressure.

 

Diet: The diet should contain adequate of protein (about 100 gm). Usual salt intake is not restricted. Fluids need not be restricted. Total calorie approximate 1600 cal / day.

 

Sedative: To cut down emotional factor, mild sedative may be given orally as phenobarbitone 60 mg or diazepam 5 mg at bed time.

 

Diuretics: The diuretics should not be used injudiciously as they cause harm to the baby by diminishing placental perfusion and by electrolyte imbalance. The compelling reasons for its use are – (1) cardiac failure (2) Pulmonary oedema (3) along with selective antihypertensive drug therapy (diazoxide group) where blood pressure reduction is associated with fluid retention. (4) Massive oedema, not relieved by rest and producing discomfort to the patient. The most potent diuretic commonly used is frusemide (Lasix) 40 mg – given orally after breakfast for 5 days in a week. In acute condition, IV route is preferred.

 

Antihypertensives:  Antihypertensive drugs have limited value in controlling blood pressure due to pre- eclampsia. The compelling indications of its use are: (1) Persistent rise of blood pressure specially where the diastolic pressure is over 110 mm Hg. The use is more urgent if associated with proteinuria. (2) In severe pre-eclampsia to bring down the blood pressure during continued pregnancy and during the period of induction of labour. The common oral drugs used are

 

Drug	Mode of action	Dose
·       Methyl dopa ·       Labetalol ·       Nifedipine ·       Hydralazine	Central and peripheral and adrenergic action Adrenoceptor antagonist (α and β blocker) Calcium channel blocker Vascular smooth muscle relaxant	250 – 500 mg tid or qid 250 mg tid or qid 10 – 20 mg bid 10 – 25 mg bid

 

In hypertensive crisis: Any of the drugs is helpful by intravenous infusion till the diastolic pressure comes down to <110 mm Hg.

(1) Labetalol (200 mg of normal saline) at the rate of 20 mg/hr t be doubled every 30 minutes. (2) Hydralazine 5 mg I.V. bolus to be followed by infusion 25 mg in 200 ml normal saline, the rate being 2.5 mg / hour to be doubled every 30 minutes.

(3) Nitroglycerin 5 μg/mins. I.V. or Sodium nitroprusside 0.25 – 5 μg/min I.V.      

Progress chart: The effect of treatment should be evaluated by maintaining a chart which records the following:

(1) Blood Pressure – at least four times a day.

(2)  State of oedema and daily weight.

(3) Fluid intake and urinary output.

(4) Urine examination on admission and to be repeated, if necessary.

(7) Fetal well being assessment

 

DURATION OF TREATMENT: The definitive treatment of pre-eclampsia is termination of pregnancy. The aim of the treatment is to continue the pregnancy, until the fetus becomes mature enough to survive in extra-uterine environment. Thus, the duration of treatment depends on – (1) severity of pre-eclampsia, (2) duration of pregnancy and (3) response to treatment.

 

Group – A : If the duration of pregnancy is remote from term, the patient may be discharged with advice to attend the antenatal clinic after one week. If the patient is near term, she should be kept foe a few days till completion of 37^th week. Thereafter, decision is to be taken either to terminate pregnancy or to wait for spontaneous onset of labour by the due date. It is not wise to allow the pregnancy to continue beyond the expected date.

Group – B: If the pregnancy is beyond 37 completed weeks, termination is to be considered without delay. If less than 37 weeks, expectant treatment may be extended judiciously at least up to 34 weeks. Careful maternal and fetal well being are to be monitored during the period with the available parameters.

Group – C: The couple is counseled. Termination of pregnancy is considered irrespective of duration of gestation. Seizure prophylaxis (magnesium sulphate) should be started. Steroid therapy is considered if the duration of pregnancy is <34 weeks. It prevents neonatal RDS, IVH and maternal thrombocytopenia.

 

METHODS OF TERMINATION:         

 

·       Induction of labour

Indications:

(1) Aggravation of the pre-eclamptic features in spite of medical treatment and / or appearance of newer symptoms such as epigastric pain.

(2) Hypertension persists in spite of medical treatment with pregnancy reaching 37 weeks or more.

(3) Acute fulminating pre-eclampsia irrespective of the period of gestation.

(4) Tendency of pregnancy to overrun the expected date.

           

Methods: If the cervix is ripe, surgical induction by low rupture of the membrane is the method of choice. Oxytocin infusion may be added to accelerate the process in selected cases. Raised blood pressure alone is not a contraindication to oxytoin infusion, if the cervix is unripe and the termination is not an urgent one, prostaglandin (PGE₂₎ gel 500 μg intercervical or 1-2 mg in the posterior fornix is inserted to make the cervix ripe when low rapture of the membranes can be performed.

·       Caesarean section

Indications:

(1)When an urgent termination is indicated but the cervix is unfavorable (unripe and closed) for surgical induction.

(2)Severe pre-eclampsia with a tendency to prolong the induction – delivery interval.

(3)Associated complicating factors such as elderly primigravide, contracted pelvis, malpresentation etc.

 

MANAGEMENT DURING LABOUR:

• Blood pressure tends to rise during labour and convulsions may occur (intra-partum eclampsia). The patient should be in bed.
• Liberal sedatives should be given in the form of pethidine 75-100 mg intramuscularly and to be repeated at intervals. Antihypertensive drugs may be given if the blood pressure becomes high.
• Blood pressure and urinary output are to be noted regularly so as to detect imminent eclampsia. Careful monitoring of the fetal well being is mandatory.
• Labour duration is curtailed by low rupture of the membranes in the first stage; and forceps or ventouse in second stage.
• Intravenous ergometrine following the delivery of the anterior shoulder is withheld as it may cause further rise of blood pressure.
• The patient should be sedated immediately following the delivery of the baby with intramuscular morphine 15 mg to prevent postpartum eclampsia and to keep the patient under close observation for several hours.

 

PUERPERIUM: The patient is to be watched closely for at least 48 hours, the period during which convulsions usually occur. Tab phenobarbitone 60mg in repeated doses can produce effective sedation. The patient is to be kept in the hospital, till the blood pressure is brought down to a safe level and proteinuria disappears.

 

Nursing Management

• Nursing management focuses on prompt diagnosis, prevention of complications, and delivery of an uncompromised fetus
• Monitor BP, proteinuria, and edema: edema in face, hands, abdominal area vs. dependent edema which is normal during pregnancy
• Observe for these symptoms: HA, visual disturbances, epigastric pain, RUQ pain, hyperreflexia, clonus
• Auscultate lungs for crackles or diminished lung sounds that might indicate pulmonary edema
• Signs of impending seizure (eclampsia): hyperreflexia, severe epigastric pain, , vomiting.
• Protecting the patient is key – side rails up and padded, suction accessible, O2 available
• Fetal surveillance
• Lab studies: CBC, clotting studies, liver enzymes
• type & screen or crossmatch