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Medical Complications in Pregnancy:


metabolic disorder of multiple aetiology that affects the normal metabolism of carbohydrates, fats and protein characterized by chronic hyperglycemia as a result of defective in insulin secretion, insulin action or both diagnosis Fasting plasma concentration: >7.8 mmol/L 2 hour plasma concentration(OGTT): >11.1 mmol/L If two hours level are between 7.8 and 11.1,most likely pt. have impaired glucose tolerance test.(pre diabetes)

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Type 1(IDDM) Type 2(NIDDM) Gestational diabetes Others -genetic defects in insulin processing or action
-endocrinopathies -drugs -exocrine pancreatic defects -genetic syndromes associated with dm


as glucose intolerance of variable severity with onset or first identified during the present pregnancy. Constitutes 90 percent of diabetes in pregnancy Generally occurs in the latter half of pregnancy. Therefore it has no effect on organogenesis and does not cause congenital defects Disappear after delivery


type 1(iddm) or type 2(niddm) Type 1 occurs in younger age group and end organ complications is likely to be more. Hence they to have increased maternal and obs risks Type 2 usually occurs in obese patients and have less maternal and obs compared to type 1

Pregnancy alters carbohydrate in such away more glucose is made available to the fetus

What cause the diabetogenic state?

Elevated placental hormones such as estrogens, progesterone, prolactin, human placental lactogen. Plasma cortisol also rises during pregnancy. Cause contrainsulin effect and state of insulin resistance Further aggravated by increase body weight and increase caloric intake during pregnancy Gestational diabetes develops when the pancreas ,despite the production of insulin cannot overcome the effect of these counter regulatory hormones. In contrast pregestational diabetes becomes worse during pregnancy


Historical factors
Age>30 years Previous gdm Family history of dm Bad obs history History of macrosomia Prev. fetal anomalies History of recurrent abortions or unexplained stillbirth Drug history-steroids, tocolytic drug


Clinical factor in the present pregnancy

Congenital fetal anomalies Pre-eclampsia Obesity>90 kg Recurrent uti, vaginal candidiasis Presence of glycosuria on more than 2 occasions

Gdm is asymptomatic ,hence we need screening test to detect gdm

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Universal screening(all pregnant women)

Selective screening(presence of risk factors for gdm)

for universal screening do the glucose challenge test

No special preparation is needed for this test 50 grams of oral glucose is given between 24 to 28 weeks pog Blood glucose is determined 1 hours later. A plasma glucose level of > 7.8 is considered significant to perform confirmation diagnostic test.

Selective screening-oral glucose tolerance test

75 grams of oral glucose is given Only 2 reading are taken-fasting glucose level and 2 hour post glucose The diagnosis of dm is made when fasting glucose level are 7.8 and or 2 hour level of >11.1 If the 2 hours levels are between 7.8 and 11.1,the patient is said to have impaired glucose tolerance test and should be treated as gdm.

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Pre-eclampsia Recurrent infection-vaginal candidiasis,uti Retinopathy Nephropathy Neuropathy Micro/macroangiopathy Polyhydramniospprom, cord prolapse, ketoacidosis Increased instrumental and CS rates Study shows that after gdm,40-60% of women develop type 2 dm within 10 years

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Miscarriage Congenital anomalies(4 fold)-sacral agenesis,ntd,cardiac and renal anomalies Macrosomia Respiratory distress syndrome Hypoglycemia-result of hyperplasia of beta cell SIUD Prematurity Malpresentation Shoulder dystocia. Polycythemic -jaundice


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Blood sugar level-weekly assessment is required. Useful in deciding whether to start insulin or adjusting insulin dosage Urine microscopy and culture-to exclude uti(bacteriuria) HbA1c-done in first trimester. It gives retrospective assessment 12 weeks ago. High HbA1c at the end of first trimester indicates sugar control was poor during organogenesis period. Maternal serum AFP-done between 16 to 20 weeks pog


Diagnostic imaging-gestational age, fetal abnormities, fetal growth, liquor volume. Doppler of umbilical artery-done in cases of diabetic vasculopathy

Antenatal management Plasma glucose level should be maintained between 4-6 mmol/L Early dating and scan to exclude fetal abnormalities Diet control should be attempted first. If failure insulin should be started. Admission-poor blood sugar control, PIH, polyhydramnios. BSP should be monitored Timing for delivery-if on insulin,38 weeks, if on diet control, can prolonged to term Mode of delivery-lscs if macrosomia baby,malpresentation,evidence of fetal compromise Check BP Fetal growth chart Monitor closely with continuous ctg

Oral hypoglycemic drug are generally not recommended as it can cause teratogenic effect towards fetus and can cross placenta causing hypoglycemia



Total calories advised is 24-30 kcal/kg of the present body weight.In obese diabetic pt. 24kcal/kg is advised The calories should be distributed between 3 meals and 3 snacks Dietary control decrease postprandial glucose level and it also improve insulin action. Blood glucose level and weight gain can be used to formulate a meal plan


Light exercise help by lowering fatty acid Contracting muscle help stimulate glucose transport hence decrease blood sugar Better done after meals Exercise involving the muscle of upper part of the body is sufficient to lower down glucose level.



15% required insulin therapy Insulin is indicated in all pregestational diabetes and poorly controlled gdm The popular regimes use a mixture of short acting and medium acting insulin

Pre-pregnancy counselling

play an important roles for pregestational diabetes in order to prevent early pregnancy loss and congenital anomalies. Complete assessment of diabetic status should be done to find out whether she is fit to go through pregnancy. HbA1c can be done to evaluate blood glucose control 12 weeks ago. Those with oral hypoglycemic should be switched to insulin therapy.


of pt. with positive gct will have gdm 15% percent of GDM will required insulin 15% of GDM will have macrosomia 15% of GDM will have impaired gtt after delivery