Diabetes in Pregnancy - Detailed Notes

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PART 1

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1. Carbohydrate Metabolism in Pregnancy

• HPL (Human Placental Lactogen) - main culprit
• Estrogen, Progesterone, Prolactin (PRL), Cortisol
• hCG - does NOT cause insulin resistance

• Fetus is entirely dependent on mother for glucose.
• Glycosuria is normal in pregnancy.

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2. Pregnancy Complications of Diabetes

Fetal complications:

• Maternal glucose crosses placenta → fetus absorbs it → fetal hyperglycemia
• Fasting hypoglycemia (advice: avoid fasting)
• Post-prandial hypoglycemia (due to IR)
• Fasting/vomiting/diarrhea → Hypoglycemia → Acetone bodies → Ketosis

High-risk pregnancy mechanism:

Hyperglycemia → feto-toxic → ↑↑ Free radicals → cross placenta → Congenital malformations of fetus

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3. Classification of Diabetes in Pregnancy

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4. Priscilla White Classification

              Priscilla White Classification
                         |
          --------------------------------
         |                              |
       Type A                        Non-Type A
  Gestational Diabetes           Pregestational Diabetes
         |
    -----------
   A1           A2
GDM on diet    GDM on Rx
             (Insulin / Metformin)

• Usually at 24-28 weeks
• Can be seen earlier (<20 wks) → usually pre-GDM
• Confirmed: Repeat sugar level at 6 weeks postpartum

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5. Investigations for GDM

• TIFFA (Targeted Imaging for Fetal Anomalies): Done in all GDM + Pre-GDM at 18-20 weeks

• 2hr PP blood sugar ≥ 200 mg/dL → Always give Insulin (irrespective of GDM or Pre-GDM)

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PART 2: Pregestational Diabetes

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6. Criteria for Pregestational Diabetes

• DIPSI Test: Recommended by Govt. of India at 1st ANC visit

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7. HbA1c - Risk Assessment for Congenital Anomalies

• Goal of therapy: HbA1c < 6%

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8. Investigations

• Initial: USG
• Screening: Level I USG
• Diagnostic: TIFFA
• Karyotyping: NOT done (detects chromosomal anomalies, not GCA)

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9. Congenital Fetal Malformations

Prevention of GCA:

• Strict glucose control (HbA1c < 6.5% = nil risk)
• Switch to insulin before conception / on confirmation of pregnancy
• Folic acid 400 mcg/day
  • Begin 1 month before conception
  • Continue for 3 months post conception

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PART 3: Other Complications of Pre-GDM

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10. Other Complications

• PIH (Pregnancy Induced Hypertension)
• Polyhydramnios
• Infections (asymptomatic bacteriuria)
• ↑ IR throughout pregnancy
• Fetal macrosomia

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11. Management (Antenatal Visits)

• Measure weight
• Check BP
• Urine dipstick for proteinuria
• Blood glucose monitoring:
  • 2nd trimester: every 2 weeks
  • 3rd trimester: every week
• Fundal examination: rule out diabetic retinopathy

• Diabetic vasculopathy
• Development of PIH

Note: All above investigations are done in GDM except Fetal ECHO (no CVS anomaly suspicion in GDM).

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12. Treatment

Medical Management:

1. Weight counselling
2. Medical Nutrition Therapy (MNT) / diet modification
3. Insulin - DOC (Drug of Choice) for diabetes in pregnancy
4. Low-dose aspirin (to prevent PIH)

Obstetric Management:

• TOP/IOL (Termination / Induction of labour): ≥ 39 weeks
• Mode of delivery: Vaginal (preferred)
• Indication for C-section: Baby weight ≥ 4.5 kg

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PART 4: Gestational Diabetes (GDM)

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13. GDM Features

• Occurs due to ↑ IR in normoglycemic female
• Complications: Similar to Pre-GDM except no congenital anomalies (GCA)
• Follow-up: Same as Pre-GDM
• Investigations: Same as Pre-GDM except Fetal ECHO not done

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14. DIPSI Criteria (Diagnosis of GDM)

• 1st test: at 1st antenatal visit
• Repeat: at 24-28 weeks (minimum gap from 1st = 4 weeks)
• If 1st visit is after 28 weeks: Only 1 test

1. No fasting needed (universal screening)
2. Irrespective of previous meals
3. Give 75g glucose in 300 mL water (can add lime) - consume in 5-10 minutes
4. Check 2-hour PP levels using plasma-calibrated glucometer

• Within 30 minutes → Repeat test on another day
• After 30 minutes → Continue test

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40-40-20 Rule for GDM Diet Control

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Additional Dietary Guidelines in GDM

• Total calories: ~30-35 kcal/kg/day (based on pre-pregnancy weight)
• Carbohydrate restriction: 40-45% of total calories (complex carbs preferred)
• Protein: ~20-25%
• Fat: ~30-35%
• Frequent small meals are preferred over 3 large meals to avoid post-prandial glucose spikes
• No simple sugars / refined carbohydrates
• High fiber diet - slows glucose absorption

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Goal of Dietary Control (A1 GDM)

• FBS < 95 mg/dL
• 2hr PP < 120 mg/dL
• If targets not met on diet alone → escalate to insulin (move from A1 to A2 GDM)

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Note: This rule is specifically relevant for the Priscilla White Class A1 (GDM controlled on diet alone). If diet fails to control blood sugar, the patient is reclassified as A2 and started on insulin or metformin.

Sacral Agenesis (Caudal Regression Syndrome)

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Definition

• Comprehensive Clinical Nephrology, 7th Ed

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Alternate Name

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Cause / Pathogenesis

Key exam point: GDM does NOT cause congenital malformations because hyperglycemia starts at 24-28 weeks, AFTER organogenesis is complete.

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Classification (Renshaw / Partial-Complete)

• Campbell's Operative Orthopaedics, 15th Ed

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Clinical Features

Musculoskeletal:

• Characteristic "sitting Buddha" posture of lower limbs
• Foot deformities
• Knee flexion contractures with popliteal webbing
• Hip flexion contractures
• Dislocated hips
• Spinal-pelvic instability
• Scoliosis
• Bone prominence at the last vertebral segment (visible on inspection of back)
• Gross motion between vertebral prominence and pelvis

Neurological:

• Motor power intact down to level of lowest vertebra with pedicles
• Sensation is preserved at up to 3 dermatome levels lower than functional motor control
• Even severe cases may retain some function

Visceral:

• Genitourinary anomalies (very common)
  • Neurogenic bladder → urinary incontinence, recurrent UTIs
• Anorectal anomalies
  • Stool incontinence

Outcome:

• Significant orthopedic disability (similar to paraplegia)
• Mental function is typically preserved

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Antenatal Diagnosis

Ultrasound findings:

• Abrupt termination of spine at lumbosacral region on USG
• Echolucent mass caudal to defect (accumulated fetal urine)
• In axial view: cord insertion seen anteriorly but spine absent posteriorly
• 3D fetal MRI or 3D skeletal imaging used for confirmation

Screening:

• Detected on TIFFA / targeted anomaly scan at 18-20 weeks
• Amniocentesis + microarray / NIPT considered for karyotype
• Karyotyping is NOT the primary tool (it detects chromosomal anomalies, not GCA)

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HbA1c Risk Correlation

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Prevention

• Strict glycemic control before conception (HbA1c < 6.5%)
• Switch to insulin before/at conception
• Folic acid 400 mcg/day starting 1 month before conception

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Quick Exam Summary

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Fetal Monitoring - Complete Explanation

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Why Fetal Monitoring?

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Methods of Fetal Monitoring

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1. Non-Stress Test (NST)

• At least 2 FHR accelerations in a 20-30 minute period
• Each acceleration must:
  • Rise ≥ 15 beats/min above baseline
  • Last ≥ 15 seconds

• Acceleration of ≥ 10 beats/min lasting ≥ 10 seconds (smaller accelerations are normal in younger fetuses)

• Fetal sleep cycle (most common - normal cause)
• Prematurity
• Fetal growth restriction (FGR)
• Maternal medications (narcotics, magnesium sulfate)
• CNS abnormality or prior CNS injury
• True fetal compromise

Important: A non-reactive NST with preserved FHR variability and no decelerations is most likely a sleep cycle, NOT fetal compromise. Always back up with BPP.

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2. Biophysical Profile Score (BPS/BPP)

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3. Amniotic Fluid Volume (AFV) Assessment

• Transducer held vertical to maternal abdomen
• Measure the maximum vertical depth of a clear fluid pocket
• Rotate 90° to confirm it is a true 3D pocket
• The 2×2 pocket rule: pocket must be ≥ 2 cm deep in at least 2 intersecting planes

• Normal AFI: 8-24 cm
• Oligohydramnios: AFI < 5 cm
• Polyhydramnios: AFI > 24 cm

Avoid using continuous color Doppler when measuring - can falsely suggest oligohydramnios by mistaking cord loops for fluid.

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4. Umbilical Artery Doppler Velocimetry

• Diabetic vasculopathy
• Development of PIH

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5. Fetal Heart Rate (FHR) Monitoring / Cardiotocography (CTG)

• Category I (Normal): Baseline 110-160, moderate variability, no late/variable decels
• Category II (Indeterminate): Does not fit I or III
• Category III (Abnormal): Sinusoidal pattern OR absent variability with recurrent late/variable decelerations → immediate action

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6. Growth Scan (Fetal Biometry on USG)

• Done 3-weekly (to rule out polyhydramnios and macrosomia)
• At least 2 growth scans:
  • At 28-30 weeks
  • At 34-36 weeks
  • Minimum gap between scans: 3 weeks

• BPD (Biparietal Diameter)
• HC (Head Circumference)
• AC (Abdominal Circumference)
• FL (Femur Length)
• Estimated Fetal Weight (EFW)

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Summary Table: Fetal Monitoring Schedule in Diabetes

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Key Exam Points

• Creasy & Resnik's Maternal-Fetal Medicine, Principles and Practice

• The Harriet Lane Handbook (Johns Hopkins, 23rd ed.)
• Red Book 2021 (Committee on Infectious Diseases)

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What I Can Do Instead

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Cardiovascular System - Pediatric Summary

(Ghai-style, cross-referenced with Robbins, Rosen's Emergency Medicine, Sabiston Surgery, Braunwald's Heart Disease)

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OVERVIEW OF CONGENITAL HEART DISEASE (CHD)

• Incidence: ~8 per 1000 live births
• Most common congenital malformation in children overall
• CHD is divided into:

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ACYANOTIC CHD - LEFT TO RIGHT SHUNTS

1. Ventricular Septal Defect (VSD)

• Most common CHD overall
• Hole in the interventricular septum → oxygenated blood shunts L → R → ↑ pulmonary blood flow

• Small VSD: Loud pansystolic murmur at lower left sternal border (LLSB) - "maladie de Roger" - asymptomatic
• Large VSD: Heart failure in infancy (tachypnea, poor feeding, failure to thrive), recurrent chest infections
• Pulmonary hypertension → if long-standing → Eisenmenger syndrome (shunt reversal R→L → cyanosis)

• CXR: Cardiomegaly, ↑ pulmonary vascular markings
• ECG: Left ventricular hypertrophy (LVH); biventricular hypertrophy in large VSD
• ECHO: Diagnostic - shows defect, size, direction of shunt

• Small VSD: Spontaneous closure (especially muscular type, by age 2-3 years)
• Large VSD with heart failure: Anti-failure treatment → surgical closure / device closure (catheter-based)
• Penicillin prophylaxis for prevention of infective endocarditis (pre-procedure)

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2. Atrial Septal Defect (ASD)

• Hole in the interatrial septum → L → R shunt at atrial level

• Often asymptomatic in childhood
• Wide, fixed splitting of S2 - hallmark sign
• Soft ejection systolic murmur at pulmonary area (↑ flow across pulmonary valve)
• Recurrent chest infections, exercise intolerance in large ASD

• CXR: Cardiomegaly, ↑ pulmonary vascular markings, dilated pulmonary artery
• ECG: Right axis deviation, right bundle branch block (rSR' in V1) - incomplete RBBB typical of ASD
  • Ostium primum: Left axis deviation (LAD)
• ECHO: Confirms defect

• Secundum ASD: Device closure (Amplatzer occluder) - catheter-based, age 2-5 years
• Primum/sinus venosus: Surgical repair
• Spontaneous closure possible for small defects in infancy

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3. Patent Ductus Arteriosus (PDA)

• Failure of closure of ductus arteriosus (connects main pulmonary artery to descending aorta) after birth
• Normally closes within 24-72 hours after birth (functionally) and by 2-3 weeks anatomically

• Continuous "machinery" murmur at left infraclavicular area / upper left sternal border (Gibson murmur)
• Bounding peripheral pulses, wide pulse pressure
• Heart failure in large PDA
• In premature infants: Respiratory distress, ventilator dependence

• CXR: Cardiomegaly, ↑ pulmonary vascular markings
• ECG: LVH
• ECHO: Color Doppler shows continuous L→R flow through ductus

• Premature infants: Indomethacin (PG inhibitor - promotes ductal closure) OR Ibuprofen
• Term infants/children: Device closure (catheter-based coil/occluder) - treatment of choice
• Surgical ligation if device closure not possible

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ACYANOTIC CHD - OBSTRUCTIVE LESIONS (No Shunt)

4. Pulmonary Stenosis (PS)

• Obstruction at pulmonary valve level
• Most common obstructive CHD
• Mild PS: Asymptomatic; Severe: RVH, dyspnea, syncope

• Mild: No treatment
• Moderate-severe: Balloon valvuloplasty (catheter-based) - treatment of choice

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5. Coarctation of Aorta (CoA)

• Narrowing of descending aorta, typically just distal to origin of left subclavian artery (near ductus)
• Associated with Turner syndrome and bicuspid aortic valve

• Radio-femoral delay (weak/absent femoral pulses vs strong radial pulses)
• Hypertension in upper limbs, hypotension in lower limbs
• "3" sign on CXR (notching at aortic knuckle)
• Rib notching on CXR (due to collateral vessels - intercostal arteries)
• In neonates: Severe heart failure, shock when ductus closes

• Neonates: PGE1 to keep ductus open → emergency surgical repair
• Older children: Balloon dilation / stenting or surgical resection

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CYANOTIC CHD - DECREASED PULMONARY BLOOD FLOW

6. Tetralogy of Fallot (TOF)

• Most common cyanotic CHD beyond infancy
• Accounts for ~5% of all CHD

• Cyanosis (degree depends on severity of RVOTO)
• "Pink TOF" (acyanotic) - mild RVOTO, predominantly L→R shunt
• Tet spells (hypercyanotic spells): Sudden severe cyanosis on crying/feeding/exertion
  • Mechanism: ↓ SVR or ↑ RVOTO → ↑↑ R→L shunt → profound hypoxia → acidosis → worsening cyanosis (vicious cycle)
  • Squatting relieves tet spell - increases SVR, decreases R→L shunt
• Clubbing (chronic hypoxemia → polycythemia)
• Single S2 (pulmonary component absent/soft)
• Ejection systolic murmur at left sternal border (due to RVOTO, NOT VSD)

1. Knee-chest position (squatting equivalent)
2. Oxygen
3. Morphine (reduces hyperpnea, sedates)
4. IV fluids (↑ preload)
5. Propranolol (relaxes RVOTO)
6. Sodium bicarbonate (corrects acidosis)
7. Phenylephrine (↑ SVR)

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7. Pulmonary Atresia / Tricuspid Atresia

• Complete absence of pulmonary valve / tricuspid valve
• Survival depends on PDA and/or ASD
• PGE1 infusion to keep ductus open - immediate management
• Surgical palliation: BT shunt (Blalock-Taussig) → staged Fontan procedure

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CYANOTIC CHD - INCREASED PULMONARY BLOOD FLOW (MIXING LESIONS)

8. Transposition of Great Arteries (TGA)

• Most common cyanotic CHD presenting in neonatal period
• Aorta arises from RV; Pulmonary artery arises from LV → complete parallel circuits (incompatible with life unless mixing exists)
• Survival depends on: ASD, VSD, or PDA (for mixing)

• Profound cyanosis from birth
• CXR: Egg-on-side appearance + narrow mediastinum (great vessels lie one in front of other)
• No murmur typically (unless associated VSD)

• Immediate: PGE1 + balloon atrial septostomy (Rashkind procedure) - creates ASD for mixing
• Definitive: Arterial switch operation (Jatene procedure) within first 2 weeks of life

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9. Total Anomalous Pulmonary Venous Connection (TAPVC)

• All pulmonary veins drain into right side (systemic venous system) instead of left atrium
• Cyanosis + ASD essential for survival

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RHEUMATIC FEVER (RF) AND RHEUMATIC HEART DISEASE (RHD)

• GAS pharyngitis → host immune response → molecular mimicry
• Antibodies against streptococcal M protein cross-react with cardiac antigens
• CD4+ T cells + antibodies → damage to pericardium, myocardium, valves
• Aschoff bodies - pathognomonic granulomas in myocardium
• Streptococci are completely absent from lesions (pure immune-mediated)

• Pancarditis - all three layers affected
• Mitral valve most commonly affected (mitral regurgitation in acute RF)
• RHD: Chronic fibrotic valvular disease - mitral stenosis (virtually the only cause)
  • Valve involvement frequency: Mitral > Aortic > Tricuspid > Pulmonary

• Drug: Benzathine Penicillin 1.2 MU IM every 3-4 weeks

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HEART FAILURE IN CHILDREN

• Tachycardia, tachypnea
• Poor feeding (feeding = exercise for infants)
• Failure to thrive / poor weight gain
• Excessive sweating during feeding
• Hepatomegaly
• Pulmonary crepitations

• Diuretics: Furosemide
• ACE inhibitors: Captopril
• Digoxin (inotrope)
• Treat underlying cause

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INFECTIVE ENDOCARDITIS (IE)

• Infection of cardiac endothelium / valves
• Most common organism: Streptococcus viridans (subacute); Staph aureus (acute)
• CHD is the biggest risk factor in children (VSD, PDA, TOF most common)

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QUICK EXAM SUMMARY TABLE

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Investigations to Diagnose Diabetes in Pregnancy

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A. For Pre-Gestational Diabetes (Overt Diabetes)

All are "clinically done" - no special glucose load required.

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B. For Gestational Diabetes (GDM) - DIPSI Criteria

Testing Schedule:

Procedure:

Give 75g glucose in 300 mL water (lime can be added)
           ↓
     Consume in 5-10 minutes
           ↓
Check 2-hour PP levels using
plasma-calibrated glucometer

If Patient Vomits:

DIPSI Diagnostic Cut-offs:

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C. WHO / Other Criteria (for reference)

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D. Additional Investigation - HbA1c

• Not used to diagnose GDM but used as risk assessment for Gross Congenital Anomalies (GCA) in Pre-GDM
• Also used to monitor long-term glycemic control
• Goal of therapy in pregnancy: HbA1c < 6%

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E. Confirming GDM vs Pre-GDM Post-Delivery

• Repeat sugar level at 6 weeks postpartum
• GDM resolves within 6 weeks → if sugar still high = Pre-GDM (was overt diabetes all along)

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Quick Summary

Investigations to Diagnose Diabetes in Pregnancy

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1. Pre-Gestational Diabetes - Diagnostic Criteria

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2. GDM - DIPSI Criteria (Govt. of India)

DIPSI Schedule

DIPSI Results

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3. If Patient Vomits During Test

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4. HbA1c - Risk of Congenital Anomalies

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5. Post-Delivery Confirmation