Overt

Diabetes
Mellitus
GRAND ROUNDS
General Data
M.J.I.
• 40 y.o.
• G2P0 (0010)
• Single
• Filipino
• Roman Catholic
• Liloan, Cebu
 • Elective cesarean delivery at 38 weeks

Chief
Complaint
 1 day PTA
History of • Irregular uterine contractions

Present Illness • No bloody or watery vaginal

discharge
• Good fetal movement
Past Medical History
• At 10 y.o., chickenpox
• 2003 - - Bronchial Asthma
￭ last attack: June 2022
￭ Salbutamol Ventolin Inhaler (2 puffs)
• 2016 - - Periodontal Infection
• 2018 - - Pneumonia
Past Medical History
• 2019 - - Diabetes Mellitus Type 2
- Sitagliptin Phosphate + Metformin HCl (Janumet) 50/500 mg tab TID
- Levemir 40 units OD
- Novorapid 20 units TID
- HBS: 300 mg/dL
- UBS: 91-98 mg/dL
• Allergic to seafood
• Non hypertensive
• No surgery or psychiatric history
Personal Social History
• Non-smoker
• Non-alcoholic beverage drinker
• No known food and drug allergies
Family History
Paternal Maternal
(+) Hypertension (+) Breast Cancer
(+) Diabetes Mellitus (+) Gestational Diabetes
(+) Stroke (+) Twinning
(+) Twinning
(+) Miscarriage
(+) Cleft palate
Menstrual History Sexual History
M - 12 y.o C - 37 y.o
I - regular
D - 5 days P - 2 partners
A - 3 moderately-soaked pads per day C - none
S - (+) increased appetite and P - none
irritability S - none
LMP: June 20, 2022
PMP: May 21, 2022
Obstetric History
G2P0(0010)

Year Type Place Outcome Complications Remarks

Complete
G1 2020
Abortion

2 Present
Prenatal History
First Prenatal - 8 weeks AOG

Medications: Laboratories:
Folic Acid • CBC
Caltrate Plus • Urinalysis
Aspirin
Prenatal History
17 weeks AOG

Laboratories:
• CBC
• Urinalysis
Medications: • Blood typing
• Hemarate • Pap smear
• Syphillis
• HbsAg
• HIV
Prenatal History
• 19 weeks AOG
⚬ Acute Complicated Cystitis - - - Cefuroxime 500 mg BID for 7 days
• 21 weeks AOG
⚬ (+) Quickening
⚬ Tetanus toxoid vaccine (1st dose)
• 25 weeks AOG
⚬ CAS: No fetal anomaly detected
• 27 wks AOG
⚬ TDAP vaccine
Prenatal History
30 weeks AOG
Biophysical profile:

30 wks AOG - 2200 g

35 wks AOG - 3900 g
31 wks AOG - 2500 g
36 wks AOG - 3600 g
32 wks AOG - 3100 g
37 wks AOG - 4000 g
34 wks AOG - 3800 g
Prenatal History
34 weeks AOG
Appraised for cesarean delivery
Weight gain: 9 kgs/19 lbs.

Prepregnancy weight: 105 kg Pregnancy weight: 114 kg

Height: 156 cm Height: 156 cm
BMI: 43.1 Obese Type 2 BMI: 46.8 Obese Type 2
Prenatal History

Prepregnancy BP:
120/80 mmHg

Pregnancy BP
120-130/80 mmHg
Review of Systems
General: no loss of appetite. no malaise. no fever. no chills. no weight loss.
Skin: no jaundice, no rashes, or edema
HEENT:
● Head: no headache
● Eyes: no visual loss and double vision. anicteric sclerae.
● Ears: no hearing loss, tinnitus, and ear discharge
● Nose: no nasal discharge, sneezing, and runny nose
● Throat: no dysphagia and sore throat
Review of Systems
Neck: no lumps, pain, and swollen glands
Respiratory: no cough, hemoptysis, and shortness of breath
Cardiovascular: no chest pain, chest discomfort, and palpitations
GIT: no nausea, anorexia, abdominal pain, vomiting, diarrhea, and bloody stool
GUT: no vaginal bleeding, no dysuria, polyuria, nocturia and hematuria
Musculoskeletal: no myalgia, arthralgia, and stiffness
Psychiatric: no depression or history of psychiatric consultations
Neurologic: no headache, dizziness, paralysis, and syncope
Hematology: no bruising. no bleeding
Review of Systems
Lymphatics: no enlarged lymph nodes and history of splenectomy
Endocrine: no excessive sweating, no known thyroid disorders or heat or cold intolerance
Allergies: no asthma, hives, and rhinitis, no known allergies
Physical Examination
General Survey: awake, alert, responsive, and not in respiratory distress with the following vital
signs:

BP: 130/90 mmHg Ht: 156c

HR: 94 bpm Wt: 114kg
RR: 21 cpm BMI: 46.8kg/m2 (obese III)
Temp: 36.2 C
Physical Examination

Skin: Warm to touch, good skin turgor and mobility, no lesions

HEENT: Normocephalic, anicteric sclera, pink palpebral conjunctiva, moist oral mucosa.
Neck: Supple, no neck vein distention, no lymphadenopathy.
C/L: Equal chest expansion, clear breath sounds, resonant on both lung fields.
Physical Examination
CVS: Adynamic precordium, distinct heart sounds, no murmurs.
Abdomen: gravid, linea nigra, FH 40cm, EFW 4185g, FHT 150s,
• L1 - breech, L2 - FB maternal R, FSP maternal L, L3 - cephalic not engaged, L4 - cephalic
prominence maternal L
GUT: IE: closed cervix
Musculoskeletal: good range of motion, MMT 5/5 all throughout
Physical Examination
Neurologic Examination:
Mental Status Exam: awake,coherent, cooperative, oriented to time place and person
Cranial Nerves:
I: Able to identify the smell through each nostrils
II: no visual field defects
II, III: (+) direct and consensual Pupillary Light Reflex
III, IV, VI: Full range of EOM
V: Good temporalis and masseter muscle tone
Physical Examination
VII: able to wrinkle the forehead, close eyelids with resistance, puff out cheeks,
smile, wrinkle skin of neck with resistance, symmetric; no nasolabial fold
flattening
VIII: able to hear and respond to whispered voice at 2ft distance
IX, X: Intact articulation of words
XI: Able to shrug shoulders and turn neck with resistance
XII: Tongue midline upon protrusion, no atrophy, no fasciculations
Laboratories and Ancillaries
 COMPLETE BLOOD COUNT (Nov. 15, 2022)
WBC 16.52 x 10^9/L 4.5-11.0
DIFFERENTIAL CT.
SEGMENTERS 72% 45-65
LYMPHOCYTES 16% 20-40
MONOCYTES 5% 2.0-9.0
EOSINOPHILS 6% 0.0-6.0
BASOPHILS 1% 0.0-2.0
RBC 4.5 x 10^12/L 3.7-5.1
HEMOGLOBIN 13.2 g/dL 12.0-15.0
HEMATOCRIT 38.7% 38.0-48.0
 COMPLETE BLOOD COUNT (Nov. 15, 2022)

MCV 86.2 fL 70.0-90.0

MCH 29.4 pg 23.0-31.0

MCHC 34.1 g/dL 30.0-35.0

RDW-CV 13.4% 11.0-16.0

PLATELET COUNT 275 x 10^9/L 150-450

 COMPLETE BLOOD COUNT (Jan. 30, 2023)
WBC 11.83 x 10^9/L 4.5-11.0
DIFFERENTIAL CT.
SEGMENTERS 75% 45-65
LYMPHOCYTES 16% 20-40
MONOCYTES 5% 2.0-9.0
EOSINOPHILS 4% 0.0-6.0
BASOPHILS 1% 0.0-2.0
RBC 4.7 x 10^12/L 3.7-5.1
HEMOGLOBIN 13.3 g/dL 12.0-15.0
HEMATOCRIT 40.4% 38.0-48.0
 COMPLETE BLOOD COUNT (Jan. 30, 2023)

MCV 40.4 fL 70.0-90.0

MCH 86.0 pg 23.0-31.0

MCHC 32.9 g/dL 30.0-35.0

RDW-CV 13.4% 11.0-16.0

PLATELET COUNT 250 x 10^9/L 150-450

 CLINICAL CHEMISTRY

LDH 187 u/L 120-246

URIC ACID 4.70 mg/dL 2.50-6.20

CREATININE 0.50 mg/dL 0.70-1.20

SGOT (AST) 19.00 u/L <31

SGPT (ALT) 13.00 uL <35

FBS 144.00 mg/dL 74.00-100.00

HbA1c 7.40 % 4.3-6.4

 CLINICAL MICROSCOPY URINALYSIS (Oct. 19, 2022)
Color yellow
Appearance cloudy
ph 5.5
Specific gravity 1.020
Protein Trace
Glucose Trace
Ketones Trace
Blood Negative
Urobilinogen Normal RBC 0-2
Nitrite Negative WBC 2-5
Leukocyte esterase Negative Epithelial cells Few
Bilirubin Negative Mucous
Admitting Impression
• G2P0(0010), Pregnancy Uterine, 37 6/7 Weeks AOG,
cephalic, not in labor
• Overt Diabetes Mellitus, insulin-requiring, uncontrolled
• Gestational Hypertension
• Obese Class III
• Advanced Maternal Age
• Bronchial Asthma, not in Acute Exacerbation
Differential Diagnoses

CHRONIC HYPERTENSION GESTATIONAL DM METABOLIC SYNDROME

• Filipino
• BP: 140/90 mmHg at 19
• Family history of DM
weeks AOG
RULE • BMI 43.1 • Obese
• BMI: 43.1 (Obese II)
IN • 40 years old • DM type 2
• Family hx of hypertension
• Presence of uterine
(paternal)
contractions

• Patient’s BP lowered to • Not a known

RULE 130/80 mmHg • Diagnosed with DM hypertensive
OUT • Pre pregnancy BP is at Type 2 on 2019 • To further rule out, a
120/80 mmHg lipid panel must be done
Laboratories and Ancillaries

SARS-COV2 Rapid Antigen Test

Specimen: Nasopharyngeal swab

Result: Negative
 3/12/23 Reference Range

WBC 10.57 4.5-11.0 g/L

Neutrophils 69 45-65

Lymphocytes 22 20-40

Monocytes 6 2-9

Eosinophils 3 0-6
Complete Blood
Basophils 0 0-2
Count
RBC 4.8 3.7-5.1 x 10*12/L

Hemoglobin 13.2 12.0-15.0 g/L

Hematocrit 40.9 38-48%

MCV 85.6 70-90 fL

MCH 27.6 23-31 pg

MCHC 32.3 11-16%

Platelet Count 234 150-450 x 10*9/L

 3/13/23 REFERENCE RANGE

PROTHROMBIN TIME

Control 11.8

Patient 11.5 10.0-14.0 secs

% activity 85.40 70.0-130.0%

INR 0.96 0.80-1.20

Clinical Chemistry

3/12/23 REFERENCE RANGE

LDH 187 120-246 u/L

URIC ACID 4.70 2.50-6.20 mg/dL

CREATININE 0.50 0.70-1.20 mg/dL

SGPT (AST) 19.00 <31 u/L

SGPT (ALT) 13.00 <35 u/L

Urinalysis (3/12/23) Blood Negative

Urobilinogen Normal

Color Yellow Nitrite Negative

Leukocyte
Negative
Appearance Clear Esterase
RBC 2-5
pH 6.0
WBC 0-2

Specific Gravity 1.020 Epithelial cells 2-5

Mucus threads Rare

Protein Trace
Bacteria Many
Glucose +2 Casts PENDING

Ketones Negative
Resting ECG
(3/13/23)
Primary Low Segment Transverse Cesarean
Section under Continuous Lumbar Epidural
Anesthesia

Procedure
 Intraoperative Findings:

Uterus was enlarged to gestation. Baby in right occiput transverse position. Placenta
anterofundal, complete with cotyledons. Moderate amount of clear amniotic fluid. Both
tubes and ovaries were grossly normal. EBL 700 cc..
Postoperative Diagnosis:

1. G2P1 (1011) Pregnancy Uterine, delivered a live female neonate, term, cephalic,
BW 5,110 grams (11 lbs 3 oz) LGA, AS 8,9,
BS 40 weeks; Fetal Macrosomia; via primary low segment transverse cesarean
section (Pfannenstiel) under Combined Spinal
Epidural Anesthesia
2. Overt diabetes mellitus – on insulin
3. Gestational hypertension
4. Obese Class III
5. Bronchial Asthma on remission
6. Advanced maternal age
COURSE IN THE WARDS (MOTHER)
complaints
complaints

BP: 100-150/7-80
mmHg
BP: 100-140/60-90
HR: 95-105 bpm
mmHg BP: 110/70 BP: 130/80 mmHg BP: 130/70 mmHg
HR: 90-100 bpm Temp: 36.5- 37.5 C Temp: 36.2C HR: 100 bpm
RR: 19-20 cpm
RR: 19-23 cpm HR: 80-90 bpm HR: 90bpm RR: 20 cpm
Temp: 36.2-36.5 C
Temp: 36.1-36.3 C RR: 18-20 cpm RR: 20cpm Temp: 36.4C
SpO2: 95-98% room
SpO2: 95-98% room air SpO2: 94-98% @ RA SPO2: 96% @RA O2sat: 98% at RA
air
UO: 35.92cc/hr, clear, UO: 20-23 cc/hr, clear
UO: 20-23cc/hr, clear,
concentrated urine and concentrated urine
concentrated urine Clean dry dressing Well-coapted wound, Well contracted uterus, Minimal
Clean and dry dressing Clean and dry dressing
Clean and dry Contracted uterus lochia
Well contracted uterus Soft abdomen
dressing Minimal lochia Voids freely
Normoactive bowel Well contracted uterus
Well contracted uterus
sounds
Normoactive bowel
sounds

Post-op Day 0 Post-op Day 1 Post-op Day 2 Post-op Day 3 Post-op Day 4
Patient is stable Patient is stable Patient is stable Patient is stable Patient is stable

Increase oral fluid Encourage to increase Dressing done today Continue current MGH today
intake oral fluid intake and to Continue BP and CBG medications Home meds as prescribed
Turn to sides sit up on bed monitoring Continue BP Follow up OB OPD on March 24, 2023 @ 8AM
FBC flushing May remove FBC, refer MGH tomorrow AM monitoring Continue BP monitoring at home at least 2-3x/day
Refer succeeding if unable to void MGH Follow up with IM/Endo as advised
urine output May release blood Repeat 75 grams OGTT 4-6 weeks postpartum
Continue BP and CBG Continue BP and CBG (April 14, 2023)
monitoring monitoring Advised on self-perineal care BID
Low salt, low fat, diabetic diet
Refer persistent SBP
Advised to come back anytime if with elevated BP,
elevations >140
headache, blurring of vision, profuse vaginal
mmHg bleeding or any unusualities
COURSE IN THE WARDS (BABY GIRL)
Date of Birth: 3/14/23 10:18 am

Type of Delivery: CS

APGAR score: 8,9

Ballad score: 40 weeks

Birthweight: 5110 g (11 lbs. 3 oz)

Head Circumference: 36 cm
Abdominal Circumference: 38 cm
Chest Circumference: 40 cm
Birth Length: 53 cm
Date 03/14/23 03/15/23 3/16/23 3/15/23
S - 5mL OGT aspirate with blood 15 mL OGT drain of clean saliva WBC 15.93
streak
Neutrophils 82
O Temp: 36.5- 37.5 C Temp: 36.7-37.1 C Temp:36.6-37.1 C
HR: 127-158 bpm HR: 115-151 bpm HR: 126-154 bpm 11
RR: 41-60 cpm
Lymphocytes
SpO2: 94-100% @ 2 LPM RR: 43-58 cpm RR: 47-58 cpm
5
(+) alar flaring SpO2: 97-100% @ 2 LPM SpO2: 93-100% @ 2 LPM Monocytes
2
CXR: streaky opacities in both
inner lung zones Eosinophils 0
CBC: iCa: 1.14 (1.05-1.32) (-) retractions
WBC:22.30 (13-38) Lympho:14 Na: 138.0 (137-145) Basophils 4.2
(20-55) K: 4.70 (3.5-5.1)
Hgb:20.9 (14-24) Hct:62.4 (44- Mg: 1.60 (1.60-2.30) 11.9
RBC
64)
35.7
Plt:272 (150-450)
pH: 7.375, pCo2: 36.4, p02: Hemoglobin
84.2
206.0
Hematocrit 28.1
A -Retained fetal lung fluid -Retained fetal lung fluid -Retained fetal lung fluid
-Compensated metabolic -Compensated metabolic 33.3
MCV
acidosis acidosis
221
P OGT EBM feeding (30 mL) via OGT Resume feeding via OGT MCH
For CBC at 6 hrs old, include Once tolerated 2 feedings Trial room air on 3/17/23
serum Na, K, iCa, Mg, ABG at discontinue IVF and shift to Continue antibiotics (Day 3) MCHC
6pm (3/14/23), 2D- echo, CXR heplock
APL, blood culture and Continue antibiotics (Day 2) Platelet Count
sensitivity
Meds (Day 1)
• Ampicillin 300 mg IVTT
Q12 hrs
• Amikacin 70 mg IVTT
Q24 hrs
Date 03/17/23 03/18/23

S - -

Temp:36.6- 37.1 C
HR:123-154 bpm
RR: 50-59 cpm Temp: 36.5- 37.3 C
SpO2: 93-100% @ RA then 0.5 LPM HR: 120- 158 bpm
O
RR: 42- 60 cpm
SpO2: 93-100% @ 0.25 LPM
Pink lips and extremities
(-) grunting, alar flaring, retractions
-Retained fetal lung fluid -Retained fetal lung fluid
A
-Compensated metabolic acidosis -Compensated metabolic acidosis

Revise 02 to 0.25 LPM via nasal cannula

Trial room air
P PRN for desat <95% and RR >60 cpm
Continue antibiotics (Day 4)
Continue antibiotics (Day 5)
DISCUSSIO
N
 ASTHMA IN PREGNANCY
• Exacerbations are common especially in the third trimester
• Mechanical or hormonal changes
• Cessations or reduction of asthma medications due to concerns by the
mother and/or the healthcare provider
• Increased susceptibility to viral respiratory infection
• ICS, B2 agonists, montelukast, theophylline - not associated with increased
incidence of fetal abnormalities

Global Initiative for Asthma 2022

 ASTHMA IN PREGNANCY

LABOR AND DELIVERY

• Salbutamol 2.5mg/nebule, 1 nebule via nebulization preoperatively
• High doses of beta agonists → Neonatal hypoglycemia
⚬ Monitor blood glucose levels for the first 24 hours

Global Initiative for ASthma 2022

 LABOR AND DELIVERY
⚬ Fentanyl > Meperidine for epidural analgesia
⚬ Surgical delivery: Conduction analgesia > tracheal intubation
⚬ Prostaglandin F2a contraindicated of postpartum hemorrhage → bronchoconstriction
PREGESTATIONAL/ OVERT
DIABETES
• Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL,
Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter
60: Diabetes Mellitus

• Phillipine Obstetrical and Gynelogical Society Inc. (2018). Clinical Practice

Guidelines on Diabetes Mellitus in Pregnancy. 3rd edition
 PREGESTATIONAL/OVERT DIABETES
• Defined as:
⚬ random plasma glucose level > 200 mg/dL + classic s/sx: polydipsia, polyuria, and unexplained weight loss OR
⚬ fasting glucose level > 125 mg/dL

• For women with only minimal metabolic derangement, the IADPSG

Consensus Panel (2010) recommends the following threshold values:

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus
 PREGESTATIONAL/OVERT DIABETES
• The diagnosis of overt diabetes during pregnancy
should be confirmed 6 weeks postpartum.
• Risk factors:
⚬ strong familial history of diabetes,
⚬ prior delivery of a large newborn
⚬ persistent glucosuria, or
⚬ unexplained fetal losses.

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus
HARM IN PREGNANCY

FETAL EFFECTS NEONATAL EFFECTS

MATERNAL EFFECTS
HARM IN PREGNANCY

FETAL EFFECTS NEONATAL EFFECTS

• SPONTANEOUS ABORTION • RESPIRATORY DISTRESS

• PRETERM DELIVERY SYNDROME
• MALFORMATIONS • HYPOGLYCEMIA &
• ALTERED FETAL GROWTH HYPOCALCEMIA
• UNEXPLAINED FETAL • HYPERBILRUBINEMIA &
DEMISE POLYCYTHEMIA
• HYDRAMNIOS • CARDIOMYOPATHY
• LONG-TERM COGNITIVE
DEVELOPMENT
• INHERITANCE
HARM IN PREGNANCY

FETAL EFFECTS

• SPONTANEOUS ABORTION Up to 25 % have an early miscarriage, and poor glycemic control

is an associated factor.
• PRETERM DELIVERY
• MALFORMATIONS • Galindo, 2006: those with HbA1c >12 % or whose pre-prandial
• ALTERED FETAL GROWTH glucose concentrations persisted > 120 mg/dL had an elevated
miscarriage risk.
• UNEXPLAINED FETAL
• Wei, 2019: those with a history of DM had an increased risk of
DEMISE miscarriage, and the risk rose to 8 % for each 20-mg/dL
• HYDRAMNIOS incremental rise in fasting glucose.
• Bacon, 2015: In 89 pregnancies in women with the monogenic
form of MODY, only women with the causative glucose kinase
(GCK) mutation were more likely to miscarry.
HARM IN PREGNANCY

FETAL EFFECTS

• SPONTANEOUS ABORTION
• PRETERM DELIVERY Overt DM is an undisputed risk factor.
• Berger, 2020: almost 20 % of women with DM were delivered
• MALFORMATIONS
preterm vs. 5.6 % of women without DM, obesity, or
• ALTERED FETAL GROWTH hypertension.
⚬ >60% were indicated preterm births
• UNEXPLAINED FETAL
⚬ >37% of women with diabetes and chronic hypertension
DEMISE delivered preterm.
• HYDRAMNIOS • Yanit, 2012: 19% of women with pregestational DM delivered <
37 weeks’ gestation vs. 9 % of controls.
• Murphy, 2021: in UK, the preterm delivery rate was 42 % for
8690 DM type 1, and 3 % for DM type 2.
HARM IN PREGNANCY

FETAL EFFECTS

• MALFORMATIONS • Jovanovič, 2015: incidence of major malformations in fetuses

• ALTERED FETAL GROWTH born to type 1 DM mothers ~11 % and is at least double the
• UNEXPLAINED FETAL rate in fetuses of non-DM mothers.
• Congenital anomalies constitute almost half of perinatal deaths
DEMISE
in diabetic pregnancies.
• HYDRAMNIOS
HARM IN PREGNANCY

FETAL EFFECTS

• MALFORMATIONS
• ALTERED FETAL GROWTH
• UNEXPLAINED FETAL
DEMISE
• HYDRAMNIOS
HARM IN PREGNANCY

FETAL EFFECTS
Diminished fetal growth may result from congenital
• ALTERED FETAL GROWTH
malformations or from substrate deprivation due to advanced
• UNEXPLAINED FETAL maternal vascular disease.
DEMISE • Fetal overgrowth is typical of pregestational DM.
• HYDRAMNIOS • Newborns are described as anthropometrically different from
other LGA neonates (Catalano, 2003; Durnwald, 2004).
⚬ Excessive fat deposition in the shoulders & trunk.
• The incidence of macrosomia rises significantly when mean
maternal CBS chronically exceed 130 mg/dL (Hay, 2012).
HARM IN PREGNANCY

FETAL EFFECTS

• UNEXPLAINED FETAL 3-4x higher in DM type 1 and are usually

associated with poor glycemic control
DEMISE
• HYDRAMNIOS • These are “unexplained” because common factors such
as obvious placental insufficiency, placental abruption,
fetal-growth restriction, or oligohydramnios are not
identified.
• Fetuses of diabetic mothers also often have elevated
lactic acid levels.
• Maternal ketoacidosis also can cause fetal death (Bryant,
2017)
HARM IN PREGNANCY

FETAL EFFECTS

• HYDRAMNIOS fetal hyperglycemia causes polyuria

• Dashe and coworkers (2000) at Parkland Hospital:
AFI parallels the amnionic fluid glucose level
among women with diabetes.
HARM IN PREGNANCY

NEONATAL EFFECTS

• RESPIRATORY DISTRESS Gestational age rather than overt diabetes is likely the most
significant factor associated with respiratory distress
SYNDROME
syndrome.
• HYPOGLYCEMIA &
⚬ Bental, 2011: rates of RDS in newborns of DM
HYPOCALCEMIA
mothers were not higher vs. neonates of non-DM
• HYPERBILRUBINEMIA & mothers.
POLYCYTHEMIA • Battarbee, 2020a: Diabetes does not appear to alter the
• CARDIOMYOPATHY beneficial effects of antenatal corticosteroids to hasten
• LONG-TERM COGNITIVE lung maturity
DEVELOPMENT
• INHERITANCE OF DM
HARM IN PREGNANCY

NEONATAL EFFECTS

• HYPOGLYCEMIA & • Hypoglycemia (< 45 mg/dL ): Newborns experience a

rapid drop in plasma glucose concentration after
HYPOCALCEMIA
delivery due to hyperplasia of the fetal β-islet cells
• HYPERBILRUBINEMIA &
induced by chronic maternal hyperglycemia.
POLYCYTHEMIA
• Hypocalcemia (total serum calcium concentration < 8
• CARDIOMYOPATHY
mg/dL): cause is unclear.
• LONG-TERM COGNITIVE
⚬ Theories include aberrations in magnesium–
DEVELOPMENT calcium economy, asphyxia, and preterm birth.
• INHERITANCE OF DM
HARM IN PREGNANCY

NEONATAL EFFECTS

• HYPERBILRUBINEMIA & • The pathogenesis of hyperbilirubinemia in neonates of DM mothers is

uncertain.
POLYCYTHEMIA
• Polycythemia is thought to be a fetal response to relative hypoxia
• CARDIOMYOPATHY polycythemia can lead to hyperbilirubinemia
• LONG-TERM COGNITIVE ⚬ sources of this fetal hypoxia are hyperglycemia-mediated increases
DEVELOPMENT in maternal affinity for oxygen and fetal oxygen consumption. 
• INHERITANCE OF DM ⚬ Hypoxia leads to increased fetal erythropoietin levels and red cell
production.
HARM IN PREGNANCY

NEONATAL EFFECTS

• CARDIOMYOPATHY Infants of diabetic pregnancies may have hypertrophic

• LONG-TERM COGNITIVE cardiomyopathy that primarily affects the interventricular septum
• this may lead to obstructive cardiac failure.
DEVELOPMENT
• INHERITANCE OF DM
HARM IN PREGNANCY

NEONATAL EFFECTS

• LONG-TERM COGNITIVE some studies found an association between maternal DM

DEVELOPMENT and decreased IQ and autism/developmental delay in their
• INHERITANCE OF DM offspring.
HARM IN PREGNANCY

NEONATAL EFFECTS

• INHERITANCE OF DIABETES • The risk of developing DM type 1 if either parent is

affected is 3 to 4 %.
• DM type 2 has a much stronger genetic component.
• If both parents have DM type 2, the risk approaches 40 %.
 HARM IN PREGNANCY

ATERNAL EFFECTS

• PRE-ECLAMPSIA Develops 3-4x more often among diabetic women:

• risk factors include any vascular complication and preexisting
• DIABETIC NEPHROPATHY
proteinuria, with or without chronic hypertension.
• DIABETIC RETINOPATHY
• DIABETIC NEUROPATHY
• DIABETIC KETOACIDOSIS
• INFECTIONS
 HARM IN PREGNANCY

ATERNAL EFFECTS

• PRE-ECLAMPSIA
• DIABETIC NEPHROPATHY Diabetes is one of the leading causes of end-stage renal disease
• Clinically detectable nephropathy begins with microalbuminur
• DIABETIC RETINOPATHY
— 30-300 mg/24 hours
• DIABETIC NEUROPATHY • Macroalbuminuria— >300 mg/24 hours—develops in patients
• DIABETIC KETOACIDOSIS destined to have end-stage renal disease.
• In general, pregnancy does not appear to worsen diabetic
• INFECTIONS
nephropathy.
 HARM IN PREGNANCY

ATERNAL EFFECTS

Benign or background or non-proliferative retinopathy:

• DIABETIC RETINOPATHY
• the first and most common visible lesions are small microaneurysms followed
• DIABETIC NEUROPATHY by blot hemorrhages that form when erythrocytes escape from the aneurysms
⚬ leak serous fluid that create hard exudates.
• DIABETIC KETOACIDOSISPreproliferative retinopathy:
• INFECTIONS • abnormal vessels of background eye disease become occluded - retinal
ischemia and infarctions (“cotton wool exudates”).
• Ischemia à neovascularization on the retinal surface and out into the vitreous
cavity.
• Vision is obscured when there is hemorrhage.
• Laser photocoagulation before hemorrhage reduces the rate of visual loss
progression and blindness by half.
 HARM IN PREGNANCY

ATERNAL EFFECTS

• DIABETIC NEUROPATHY Peripheral, symmetrical sensorimotor diabetic neuropathy is

uncommon in pregnant women.
• DIABETIC KETOACIDOSIS
• Diabetic gastropathy causes nausea and vomiting, nutritional
• INFECTIONS problems, and difficulty with glucose control.
• Women with gastroparesis should be advised that this
complication is associated with a high risk of morbidity and poo
perinatal outcome
• Treatment with metoclopramide and H2 – receptor antagonist
 HARM IN PREGNANCY

ATERNAL EFFECTS

• DIABETIC KETOACIDOSIS may develop with hyperemesis gravidarum, β-mimetic drugs given
for tocolysis, infection, and corticosteroids given to induce fetal lung
• INFECTIONS
maturation.
• DKA results from an insulin deficiency combined with an excess
in counter-regulatory hormones such as glucagon ---
gluconeogenesis and ketone body formation.
• maternal mortality rate with DKA is <1 %, but perinatal mortality
rates associated with a single episode of DKA may reach 35 %
(Bryant, 2017; Guntupalli, 2015).
 HARM IN PREGNANCY

ATERNAL EFFECTS

• DIABETIC KETOACIDOSIS
 HARM IN PREGNANCY

ATERNAL EFFECTS

• INFECTIONS Common infections include Candida vulvovaginitis,

urinary and respiratory tract infections, and puerperal
pelvic sepsis.
• Risk of asymptomatic bacteriuria in women with diabetes was
increased two-fold (Sheiner, 2009).
• Hill, 2005 : at Parkland Hospital, 5 % with DM developed
pyelonephritis vs. with 1.3 % without DM.
• Johnston and colleagues, 2017: 16.5 % of women with
pregestational DM had postoperative wound complications after
cesarean delivery
 Management: OVERT DIABETES MELLITUS

Preconceptional Care 05
• Optimal glycemic control Puerperium
• evaluation and treatment for No requirement of insulin for the
diabetic complications s]y. first 24 hours postpartum.
• Folate, 400 μg/day orally Restart oral agents.
01 04 Birth control.

Third Trimester Care

32-36 weeks AOG: fetal movement
First Trimester Care counting, periodic fetal heart rate
24-hour urine protein excretion and monitoring, intermittent biophysical
serum creatinine, retinal 02 03 profile evaluation, contraction
examination and echocardiogram; stress testing

screening for aneuploidy:

Second Trimester Care
Fetal echocardiography.
measurement of maternal serum
Normoglycemia with self
pregnancy-associated plasma
monitoring
protein A (PAPP-A), β-human
chorionic gonadotropin (hCG), and
ultrasound measurement of fetal
nuchal translucency
 MANAGEMENT OF DIABETES IN PREGNANCY: PRECONCEPTIONAL
CARE

• Optimal pre-conceptional glucose control using insulin (ADA):

⚬ preprandial glucose levels 70 to 100 mg/dL
⚬ peak postprandial values of 100 to 129 mg/dL
⚬ daily glucose concentrations < 110 mg/ dL

• HbA1C reflects an average of circulating glucose for the past 4-8 weeks,
￭ useful to assess early metabolic control : optimal value is < 6.9 % (ADA)
￭ 4-fold increased risk for malformations at levels HbA1C > 10 percent.

• If indicated, evaluation and treatment for diabetic complications such as retinopathy or nephropathy should
also be instituted before pregnancy.
• Folate, 400 μg/day orally is given periconceptionally and during early pregnancy to decrease the risk of
neural-tube defects.

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus
 MANAGEMENT OF DIABETES IN PREGNANCY: FIRST
TRIMESTER
• At Parkland: routine hospitalization during early
pregnancy to initiate an individualized glucose control
program and provide education
⚬ initial evaluations : assessment of 24-hour urine
protein excretion and serum creatinine level,
retinal examination, and echocardiogram if
chronic hypertension is comorbid.

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus
 MANAGEMENT OF DIABETES IN PREGNANCY: FIRST
TRIMESTER
Insulin Treatment
• overtly diabetic pregnant woman is best treated with
insulin.
• Maternal glycemic control can usually be achieved
with multiple daily insulin injections and adjustment of
dietary intake.
• Subcutaneous insulin infusion by a calibrated pump
may be used during pregnancy.

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus
 • Monitoring:

⚬Self-monitoring of capillary glucose levels

using a glucometer is recommended because
this involves the woman in her own care.
⚬Glucose goals recommended during
pregnancy are shown in the table.

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus
 MANAGEMENT OF DIABETES IN PREGNANCY: FIRST
TRIMESTER
• Diet.
⚬ Nutritional planning includes appropriate weight gain
through carbohydrate and caloric modifications based on
height, weight, and degree of glucose intolerance
⚬ the mix of carbohydrate, protein, and fat is adjusted to meet
the metabolic goals and individual patient preferences, but a
175-g minimum of carbohydrate
per day should be provided.
⚬ Carbohydrate should be distributed throughout the day in three
small- to moderate-sized meals and two to four snacks.

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus
 MANAGEMENT OF DIABETES IN PREGNANCY: FIRST
TRIMESTER

• Diet.
⚬Weight loss is not recommended, but modest
caloric restriction may be appropriate for
overweight or obese women.

⚬An ideal dietary composition is 55 percent

carbohydrate, 20 percent protein, and 25 percent fat,
of which < 10 percent is saturated fat.

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus
MANAGEMENT OF DIABETES IN PREGNANCY: 2ND
TRIMESTER

• Maternal serum alpha-fetoprotein determination

⚬ at 16-20 weeks’ gestation is used in association with
targeted sonographic examination at 18-20 weeks to detect
neural-tube defects and other anomalies
• Maternal alpha-fetoprotein levels
⚬ may be lower in diabetic pregnancies, and interpretation is
altered accordingly.
• Fetal echocardiography is an important part of second-trimester
sonographic evaluation
• Euglycemia with self-monitoring continues to be the goal in
management.
 MANAGEMENT OF DIABETES IN PREGNANCY: 3RD
TRIMESTER

• American College of Obstetricians and Gynecologists (2012) suggests initiating fetal

surveillance testing starting at 32 to 34 weeks’ gestation: fetal movement counting,
periodic fetal heart rate monitoring, intermittent biophysical profile evaluation, and
contraction stress testing.
• patients are routinely instructed to perform fetal kick counts beginning early
in the third trimester.
• At 34 weeks, admission is offered to all insulin-treated women.
⚬ While in the hospital, they continue daily fetal movement counts and
undergo FHR monitoring three times a week. Delivery is planned for
38 weeks.

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus
 MANAGEMENT OF DIABETES IN PREGNANCY: DELIVERY

• With no other complications, delivery at Parkland is typically planned for 38 weeks.

• For vaginal delivery, labor induction may be attempted when the fetus is not excessively
large and the cervix is considered favorable.
• Cesarean delivery at or near term has frequently been used to avoid the traumatic birth of
a large fetus in a woman with diabetes.

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus
 MANAGEMENT OF DIABETES IN PREGNANCY: DELIVERY

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus
 MANAGEMENT OF DIABETES IN PREGNANCY: DELIVERY

• ACOG (2020): ceasarean delivery should

be considered in women with gestational
diabetes whose fetuses have a
sonographically estimated weight ≥ 4500 g.

• POGS (2018) : sonographically estimated

weight ≥ 4000 g.

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus

Phillipine Obstetrical and Gynelogical Society Inc. (2018). Clinical Practice Guidelines on Diabetes Mellitus in Pregnancy. 3rd edition
 MANAGEMENT OF DIABETES IN PREGNANCY: PUERPERIUM

• Many diabetic women may require no insulin for the first ≥ 24 hours postpartum.
• Infection must be promptly detected and treated.
• For DM type 2 women who will be transitioned to oral agents, this can be done on
postoperative day 1.

Cunningham FG, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (eds).William’s Obstetrics 26ᵗʰ edition; 2022; chapter 60 Diabetes Mellitus
MANAGEMENT OF DIABETES IN PREGNANCY: PUERPERIUM

PROGESTERONE-ONLY INTRAUTERINE
CONTRACEPTIVES DEVICES
CONDITION BARRIER COC
POP DMPA/ ETG/ LNG CU-IUD LNG-IUD
NET-EN IMPLANT

History of GDM 1 1 1 1 1 1 1

DM 1 1 2 2 2 1 2
without vascular disease

DM
with nephropathy,
retinopathy, neuropathy , or 1 3 or 4 2 3 2 1 2
other vascular disease, or
DM
≥ 20 years

Phillipine Obstetrical and Gynelogical Society Inc. (2018). Clinical Practice Guidelines on Diabetes Mellitus in Pregnancy. 3rd edition
FOR YOUR KIND ATTENTION,

T ha nk yo u!