Maternal Diabetes: Clinical Presentation

Maternal Diabetes

• Diabetes Mellitus is genetically and clinically diverse, sharing carbohydrate intolerance.
• Accurate classification during pregnancy is vital due to complex metabolic changes complicating diabetic control and endangering the fetus.
• Diabetes mellitus complications affect 1–2% of pregnancies.
• Fetal mortality rates are 2-3 times higher in pregnancies complicated by diabetes.

Clinical Presentation of Diabetic Mothers

• Mothers with certain diabetes classes commonly have large for gestational age (LGA) infants.
• Macrosomia, enlarged placenta, and increased amniotic fluid are typical.
• Severely affected fetuses may develop fetal soft tissue thickening or even edema, especially scalp edema.
• Fetal enlargement can be symmetrical, but it predominantly happens in the abdomen.
• Shoulder dystocia is common due to increased fat stores, causing delivery difficulties.
• Scalp edema in fetuses of diabetic mothers is a poor prognostic sign, often leading to poor outcomes or death at birth.
• Scalp edema can occur due to fetal death, erythroblastosis fetalis, non-immune fetal hydrops, and sickle cell anemia.
• Scalp edema is less severe in fetuses of diabetic mothers compared to those in fetal death.
• Stillbirths or fetal deaths later in pregnancy are more common in insulin-dependent diabetic patients.
• There is also increased frequency of congenital heart, skeletal, CNS, renal, and GI abnormalities.
• Single umbilical artery (SUA) occurs in 6–7% of infants of diabetic mothers, prompting a search for other fetal anomalies
• Major congenital anomalies are the primary cause of perinatal mortality in infants of diabetic mothers.

Importance of Blood Glucose Control and Ultrasound Surveillance

• Outcomes for infants of diabetic mothers (IDM) depend on preconception and first-trimester blood glucose control.
• Fetal growth relies on glucose as its primary fuel
• Problems are avoided with normal, controlled glucose levels.
• Fetal problems arise when the mother has significantly high and uncontrolled glucose levels, in the case of poorly controlled diabetes due to insulin insufficiency.
• Ultrasound surveillance in IDM aims to reduce perinatal morbidity and can assess:
  • Gestational age
  • Growth abnormalities - Intrauterine growth restriction and macrosomia parameters like estimated fetal weight and abdominal circumference
  • Dynamic fetal status - Biophysical profile and Doppler assessment of arterial resistive indices
  • Congenital anomalies

Ultrasound Findings and Management of Diabetes during Pregnancy

• Ultrasound reveals indirect info on blood glucose control:
  • Polyhydramnios and large fetuses with increased adipose tissue are linked to poor glucose control.
  • Hypertensive states of pregnancy are more common in pregnancies complicated by diabetes.
• Macrosomia is associated with some cases of diabetes.
• Some diabetic classes are linked to small fetuses.
• Intrauterine growth restriction is associated with vascular disease as a result of the long term effects of diabetes.

Gestational Diabetes Mellitus (GDM)

• GDM is carbohydrate intolerance with onset or first recognition during pregnancy and it should be screened for due to associated risks.
• GDM affects 1-3% of pregnancies, varies by population and it a metabolic stress test for diabetes
• Women developing GDM may be obese, hyperinsulinemic, and insulin-resistant, or thin and insulin-deficient.
• Fetal anomalies and other manifestations of diabetic mothers (macrosomia, polyhydramnios, thick placentas)
• Congenital organ malformations are less common with gestational diabetes because of its later onset

Maternal Hypertension & Associated Risks

• Maternal hypertension endangers both mother and fetus.
• Maternal hypertension is associated with small placentas that decrease uteroplacental blood flow and compromise placental function.
• Compromised placental function results in intrauterine growth restriction
• Maternal hypertension may be chronic or pregnancy-associated.
• Pregnancy-induced hypertension is linked to prostaglandin abnormalities, previously grouped as "toxemia" caused by hypothetical toxins.
• Pregnancy-induced hypertension includes preeclampsia (edema, rapid weight gain, high blood pressure, proteinuria) and eclampsia (convulsions, coma).
• Pregnancy-induced hypertension typically starts after the 24th week and resolves after delivery.
• Chronic hypertension is suspected if found before 20 weeks and confirmed if persistent afterwards.

Complications of Maternal Hypertension

• Maternal hypertension is associated with increased risk of abruptio placenta and placental infarcts .
• Abdominal pain in hypertensive patients raises suspicion for abruptio placenta.
• Maternal hypertension accelerates placental maturity and increases prematurity.
• Intrauterine growth restriction results from restricted blood supply due to poorly developed placenta.

Doppler Waveform Patterns

• Abnormal Doppler waveform patterns in the umbilical or uterine artery indicate impaired placental blood supply and fetal growth.
• Pregnancy-induced hypertension impairs normal arterial changes.
• Normal pregnancies show decreasing impedance (increased diastolic flow) in these arteries up to the second trimester, stabilizing thereafter.
• Treatment includes antihypertensive medications, rest, and early delivery if needed.

Erythroblastosis Fetalis (Immune Hydrops Fetalis)

• Immune hydrops fetalis is characterized by fluid accumulation in fetal body cavities and soft tissues (pleural, pericardial, peritoneal)
• Immune hydrops happens when maternal antibodies destroy fetal red blood cells, resulting in increased fetal erythropoiesis, hypoproteinemia, and heart failure
• Rh incompatibility is now uncommon due to rhesus immunoglobulin prophylaxis.
• Nonimmune hydrops fetalis (NIHF) is more common from various causes, with an incidence of approximately 1 in 1500 to 4000
• Erythroblastosis fetalis is when the immune response destroys fetal erythrocytes as specific antibodies produced in maternal blood cross placenta and reach fetus.
• Rh incompatibility is the most common cause(ABO or any irregular blood group antigen).
• Rh incompatibility initially accounted for 98% of sensitized pregnancies, but with prophylaxis, now it accounts for 55%; sensitivity to atypical red blood cell antigens accounts for the other cases.

Rh Factor and Immunization

• Human red blood cells contain complex group of inherited qualities containing antigen-antibody reactions.
• The Rh factor is one of the more important antigens
• 85% of individuals have the Rh factor ("Rh positive")
• 15% lack it ("Rh negative").
• Introduction of Rh positive blood into Rh negative mother leads to anti-Rh agglutinin formation, destroying Rh positive blood cells.
• Anti-Rh agglutins in circulation of a Rh negative mother destroys the red cells of Rh positive fetus
• This is likely to develop hemolytic disease.

Development of Anti-Rh Agglutinins

• Immunization with the formation of anti-Rh agglutinins results from mother-child blood mixture.
• Anti-Rh agglutins form if trans-placental transmission follows first delivery, following abortion (therapeutic or spontaneous), after placental abruption, placental intravillis hemorrhaging, or any cause of fetal-maternal hemorrhage
• Hemolytic disease becomes common in subsequent pregnancies because the immunization degree increases with succeeding pregnancies.
• Antigens are small enough to pass through small leaks in placental barrier or antibodies are small enough to cross placenta and reach the fetus.

Prevention of Rh Sensitization

• Prevention includes Rh negative mother given immunization (RhoGAM) within 72 hours of Rh positive infant delivery or after exposure to sensitizing events.(It is a passive immunizing agent)
• Rh immunoglobulin removes Rh antigen-positive red blood cells before they are detected by the woman's system and prevents sensitization.
• Not all Rh isoimmunization have effective prophylaxis against Rh antigen. It’s essential to determine all mothers' blood type, errors, and proper dosage administration.

Immune Hydrops Fetalis Characteristics

• It occurs because antibodies in maternal serum are screened, identified, and quantified during pregnancy
• Features of immune hydrops fetalis are hemolytic anemia, jaundice, and hydrops.
• Destruction of fetal red blood cells from mother's anti-Rh agglutinins results in fetal anemia.
• Jaundice develops because red cells are destroyed, delivering hemoglobin for transformation.
• Hepatomegaly with fetal ascites (fluid accumulating in the serous cavities and body tissues)
• Edema present in scalp and other tissues.
• Hydrothorax and pericardial effusion may present - often as an early sign of immune hydrops fetalis.
• Placenta enlarged and with lost architecture (loss of cotyledon definition)

Advanced Management of Severe Hydrops

• Transfusion: Ultrasound assists during transfusions, or bilirubin samples via amniocentesis measure disease severity (Liley Curve placing fetus at either low, mid, or high risk)
• Cordocentesis - Blood is directly sampled from umbilical vein, or transfuse/collect blood when hydrops fetalis

Syphilis in Pregnancy

• Syphilis results from transmission placenta from mother.
• Congenital syphilis incidence decreased in 1992 due to prenatal care serologic screening, penicillin therapy, etc
• Fetal retardation/death is can still occur from mother to fetus with large placenta. Ultrasonically, fetal ascites present with severe cases. Hepatomegaly, hyperbilirubinemia, and lymphadenopathy may be present.

Incompetent Cervix (Overview)

• Incompetent cervix (IC) presents after month 4 of pregnancy (second trimester) as painless abortion with minimal warning.
• Previous IC is from birth trauma/ D+C, along with congenital emotional factor/DES exposure.
• Ultrasound exam lowers uterine, or endocervical canal
• Patients need 2-3 Previous 2nd labor abortions in 2nd trimester/echogenic linear muscle along with linear lumen.

Diagnostic Ultrasound for Incompetent Cervix

• Sonolucency = amniotic fluid in endocervical canal along entire length
• Umbilical cord may be in bulging membrane
• Cervix - Less than 3cm (Normal = 2.5 - 4.5cm)
• Opening Os+ Lower Length (2.5cm to lower)
• Transabdominal ultrasound - Bladder present - Over distance = lower collapse
• Bladder void + scanned - Lower distention
• Translabial + Transvaginal- More Helps, or over TA -TV usually less than 2m length

Limitations and Time frame for Ultrasound Diagnosis of Incompetent Cervix

• Before 14+15 weeks, volume too low for uterus distention. After 17-18 weeks fluid + lower cervix may be present
• Ultrasound every 2/3 weeks through week 24/unlikely incompetent.
• 85% Patients with Cerclage = Term. Surgical suture reflects bright echoes/closure.

Other Maternal Complications

• Many obstetric events, abortion, ectopic pregnancy, placental defects/ anemia, hyperemesis gravidarum, thrombophlebitis, renal+ UTI, thyroid disease, SLE, liver, malignant/benign, cardiomyopathy, gallbladder, Premature labor, membrane rupture, and many infections can affect the fetus.
• Infections from drugs + caffeine can affect the fetus.