Presentation on theme: "JEAN KALIBUSHI B.,MD Resident in GO at Butare teaching hospital."— Presentation transcript:
JEAN KALIBUSHI B.,MD Resident in GO at Butare teaching hospital
ANAMNESIS A known diabetic patient,34years old MC: transfert from outpatient for better menagement of Cervical incompetence on 16 weeks+ 5days of amenorrhea ATCDs:G3POEVOA2 LMP:15/09/2007 MEDICAL: Diabetic since 28/dec/2007,on 20UI/day of long acting insulin SURG: myomectomy on 2004
NEXT Tobacco:never taken Alcohol: stopped since 2years 1/2
CLINICAL EXAM Vital signs: NAD Thorax: NAD Abdomen: HF: 16cm Gyneco.Ex: not done on admission CCL: Cervical incompetence(BCI) on diabetic history whith pregnancy of 16weeks+5days of amenorrhea
MANAGEMENT Admission: programmation of cerclage Pre-op test: Normal range On 10/01/08: cerclage done
FOLLOW UP OF BLOOD SUGAR On 10/01/08,On 20UI/day of long acting insulin: -204mg/dl :M -280mg/dl:EVEN On 11/01/08: -245mg/dl:M -187mg/dl:EVEN
NEXT On 12/01/08: -112mg/dl:M On 13/01/08: -185mg/dl:M -164mg/dl:S On 14/01/08: -118mg/dl:M
NEXT On 15/01/08: -172mg/dl:M On 19/01/08: 206mg/dl:M On 21/01/08: 138mg/dl:M On 23/01/08: 141mg/dl:M On 24/01/08: 176mg/dl, change of dose at 26UI of long acting Insulin in the morning and discharged the same day
READMISSION On 23/feb/08 for pre-term labor of 23weeks of amenorrhea Management: READMISSION Blood sugar on empty stomach:157mg/dl on 26UI of rapid insulin and buscopan On 24/01/08: Discharged again
DEFINITION Diabetes is a metabolic disease of CH due to relative or absolute deficiency in insulin. Gestational diabetes: Carbohydrate intolerance with onset or recognition during pregnancy. WHO Classification: TypeI;TypeII and Gestational diabetes I &II: Chronic conditions Gest Diab.: typically resolves with delivery of the child
EPIDEMIOLOGY Most common medical complications of pregnancy. 2% of all pregnancies affected by Diabetes 1% are GDM USA: 3-5 % among them: *10% pregestational(Type 1 &2) *90% Gestational
PATHOPHYSIOLOGY GD is similar to type 2 DM with a relative deficiency in insulin and insulin resistance. Type1: early in life, destruction of Langerhans cells. GD: Placenta produces hormones (hPL,P4,Cortisol,PGH,…) that antagonize insulin and reach max levels at 24 to 28 weeks. Early in pregnancy as a result of higher levels of estrogen, insulin sensibility will increase making diabetes patient more prone to hypoglycemia. In last 1/3 of gestation 40% of pregnant women become relatively insulin resistant and must secrete 3-4 X more insulin to maintain normal blood glucose level.
RISK FACTORS Age>25 years Strong familly ATCD of DM Prior atcd of new born weigth>4000g. Obesity (BMI≥ 30) Repeated spontaneous abortion Unexplained stillbirth or congenital abnormaly. Persitant glucosuria Polycystic ovarian sd.
Maternal affects 2x risk of UTI 2x risk of Pregnancy induced hypertension 2x risk Preeclampsia DKA (Peripartum mortality) Retinopathy Nephropathy Postpartum hemorrhage
SCREENING Fasting >125, 1hr PP >200 2 hr GTT: 1 hour 50g glucose challenge: > hour 100g glucose tolerance test: Fasting >95, 1hr >180, 2hr>155, 3 hr >140 2 or more abnormal values makes the diagnosis
WHITE Classification A1GDM: diet controlled A2GDM: requiring medical therapy B: Onset after age 20, duration <10yr, No vascular C: Onset between 10-19, duration 10-19yrs, no vascular disease D: Onset 20yrs, retinal or leg involvement F: Vascular nephropathy R: Retinopathy H: Coronary artery diseases.
REFERENCES 1.Lauren N. et al.Current diagnosis and treatment in GO.10th edition Gabbe SG, Graves CR. Management of diabetes mellitus complicating pregnancy.Obstet Gynecol 2003;102: ACOG.Pregestational diabetes mellitus.Obstet Gynecol 2005;105: Gary F.Williams obstetrics.22nd edition Kakudji.Cours de GO.Université de Lubumbashi.2003.