Table 10-3. Classification of Diabetes Mellitus by Pathophysiology
| Gestational | Pregnancy onset | Insulin resistance |
| Type 1 | Juvenile onset | Ketosis prone |
| Type 2 | Adult onset | Insulin resistance |
Table 10-4. White Classification of Diabetes in Pregnancy
Class A1 GDM with normal FBS not requiring insulin
Class A2 GDM with elevated FBS requiring insulin
Class B Overt DM onset after age 20 years and duration <10 years
Class C Overt DM onset age 10–19 years or duration 10–19 years
Class D Overt DM onset before age 10 years or duration ≥20 years
Class E Overt DM with calcified pelvic vessels
Class F Overt DM with nephropathy
Class R Overt DM with proliferative retinopathy
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Table 10-5. Gestational Diabetes
| Questions | Criteria/Problems | Diag/Mgmt |
| 1-hr 50g OGTT | <140 mg/dL | GDM ruled out |
| Screening test | ||
| 3-hr 100g OGTT | >2 values ↑ | GDM diagnosed |
| Definitive diagnosis | ||
| Home glucose monitoring | Mean glucose values FBS | Start insulin |
| >90; 1 hr pp >140 | ||
| Fetal demise risk factors | 1-Needs insulin | Starting 32 wk |
| 2-HTN | NST & AFI 2/wk | |
| 3-Previous demise | ||
| L&D problems | Arrest stage 1 or 2 | CS if estimated fetal weight |
| Shoulder dystocia | >4500 g | |
| Post partum management | Prevent postpartum | FBS >126 mg/dL |
| hemorrhage | 2 hr 75 gm OGTT | |
Antepartum Overt Diabetes Management
• Hemoglobin A 1C . Obtain a level on the first visit to ascertain degree of glycemic controlduring the previous 60–120 days. Repeat levels each trimester.
• Renal status. Obtain an early pregnancy baseline 24-h urine collection for total proteinand creatinine clearance.
• Retinal status. Obtain an early pregnancy ophthalmologic funduscopic evaluation forproliferative retinopathy.
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• Home blood glucose monitoring. Patient checks her own blood glucose values atleast 4 times a day with target values of FBS 60–90 mg/dL and 1 h after a meal of <140 mg/dL.
Preconception Anomaly Prevention
• Anomaly risk. Women with overt diabetes are at increased risk of fetal anomalies.This risk can be minimized by lifestyle modification.
• Euglycemia. Maintaining glucose values at normal levels reduces anomaly risk closeto that of nondiabetes; start 3 months prior to discontinuing contraception.
• Folate supplementation. Folic acid, 4 mg a day, should be started 3 months prior toconception to prevent both fetal neural tube defects, as well as congenital heart defects.
Antepartum Fetal Assessment
• Anomaly screening. Anomalies are mediated through hyperglycemia and are high-est with poor glycemic control during embryogenesis. Anomalies are not increased in GDM because hyperglycemia is not present in the first half of pregnancy. Mostcommon fetal anomalies with overt DM are NTD and congenital heart disease. An uncommon anomaly, but one highly specific for overt DM, is caudal regression syn-drome. Obtain a quadruple-marker screen at 16–18 weeks to assess for NTD as wellas a targeted ultrasound at 18–20 weeks to look for structural anomalies. If the glyco-sylated hemoglobin is elevated, order a fetal echocardiogram at 22–24 weeks to assess for congenital heart disease.
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• Fetal growth. Monthly sonograms will assess fetal macrosomia (most commonlyseen) or IUGR (seen with longstanding DM and vascular disease).
• Fetal surveillance. Start weekly NSTs and amniotic fluid index (AFIs) at 32 weeks iftaking insulin, macrosomia, previous stillbirth, or hypertension. Start NSTs and AFIs at 26 weeks if small vessel disease is present or there is poor glycemic control. Biophysicalprofiles can be performed at the time of monthly sonograms.
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Intrapartum Management
• Timing of delivery. Fetal maturity is often delayed in fetuses of diabetic mothers, yetprolonging the pregnancy may increase the risk of stillbirth; delivery planning is a result of balancing these factors. The target delivery gestational age is 40 weeks, but may be necessary earlier in the presence of fetal jeopardy and poor maternal glycemic control. An amniotic fluid lecithin to sphingomyelin (L/S) ratio of 2.5 in the presence of phosphatidyl glycerol assures fetal lung maturity.
• Mode of delivery. The cesarean section rate in diabetic pregnancies approaches 50%because of fetal macrosomia, arrest of labor, and concern regarding shoulder dystocia.
• Glycemic control. Maintain maternal blood glucose levels between 80 and 100 mg/dLusing 5% dextrose in water and an insulin drip.
Postpartum Management
• Postpartum hemorrhage. Watch for uterine atony related to an overdistended uterus.
• Hypoglycemia. Turn off any insulin infusion because insulin resistance decreases withrapidly falling levels of hPL after delivery of the placenta. Maintain blood glucose lev-els with a sliding scale.
Neonatal Problems
• Hypoglycemia caused by persistent hyperinsulinemia from excessive prenatal trans-placental glucose.
• Hypocalcemia caused by failure to increase parathyroid hormone synthesis after birth.
• Polycythemia caused by elevated erythropoietin from relative intrauterine hypoxia.
• Hyperbilirubinemia caused by liver immaturity and breakdown of excessive neonatalred blood cells (RBCs).
• Respiratory distress syndrome caused by delayed pulmonary surfactant production.
ANEMIA
An 18-year-old woman G3 P2 had prenatal laboratory tests drawn when she was seen for her first prenatal visit at 18 weeks’ gestation. The complete blood count showed the following: hemoglobin 9.5 g/dL, hematocrit 28%, MCV 75, and RDW 17.0. Her first child was delivered 2 years ago, with her second child born 1 year ago.
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Definition. A hemoglobin concentration of <10 g/dL during pregnancy or the puerperium.
This is less than the 12 g/dL, which is the lower limits of normal in the nonpregnant woman.
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OB Triad Iron Deficiency Anemia
Iron Deficiency Anemia
• Hemoglobin <10 g
• MCV <80 mm3
• RDW >15%
OB Triad
This is a nutritional anemia resulting in decreased heme production. It is the most common ane-mia in women because of menstrual and pregnancy needs.
Diagnosis. RBCs are microcytic and hypochromic. Hemoglobin <10 g/dL, MCV <80, RDW >15.
Pathophysiology. Falling hemoglobin values do not occur until complete depletion of ironstores in the liver, spleen, and bone marrow, which is followed by a decrease in serum iron with increase in total iron binding capacity (TIBC).
Pregnancy Requirements. A pregnant woman needs 800 mg of elemental iron, of which 500mg goes to expand the RBC mass and 300 mg goes to the fetal-placental unit.
Risk Factors. Chronic bleeding, poor nutrition, and frequent pregnancies.
Symptoms. Findings may vary from none to general malaise, palpitations, and ankle edema.
Fetal Effects. Increased IUGR and Preterm birth.
Treatment. FeSO4325 mg po tid.
Prevention. Elemental iron 30 mg per day.
Folate Deficiency Anemia
Folate Deficiency Anemia
• Hemoglobin <10 g
• MCV >100 mm3
• RDW >15%
This is a nutritional anemia resulting in decreased hemoglobin production.
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Diagnosis. RBCs are macrocytic. Hemoglobin≤10 g/dL, MCV >100, RDW >15. RBC folatelevels are low. Peripheral smear may show hypersegmented neutrophils.
Pathophysiology. Folate stores in the body are usually enough for 90 days. Falling hemoglobinvalues do not occur until complete depletion of folate stores.
Risk Factors. Chronic hemolytic anemias (e.g., sickle cell disease), anticonvulsant use (phe-nytoin, phenobarbital), and frequent pregnancies.
Symptoms. Findings may vary from none to general malaise, palpitations, and ankle edema.
Fetal Effects. Increased IUGR ,Preterm birth and NTD.
Treatment. Folate 1 mg po daily.
Prevention. Folate 0.4 mg po daily for all women; 4 mg po daily for those at high risk for NTDs.
Sickle Cell Anemia
This is an inherited autosomal recessive disease resulting in normal production of abnormal globin chains.
Screening Test. These are peripheral blood tests used to detect the presence or absence ofhemoglobin S. They do not differentiate between disease and trait.
Diagnostic Test. A hemoglobin electrophoresis will differentiate between SA trait (<40%hemoglobin S) or SS disease (>40% hemoglobin S).
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Risk Factors. African and Mediterranean descent is the only significant risk factor for sicklecell anemia.
Effects on Pregnancy.
• With SA, the patient may have increased urinary tract infections (UTIs) but pregnancyoutcome is not changed.
• With SS, the pregnancy may be complicated by increased spontaneous abortions,IUGR, fetal deaths, and preterm delivery.
Treatment. Avoid hypoxia, take folate supplements, and monitor fetal growth and well-being.
LIVER DISEASE
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