🔶
🔸 Medical management
Medical Nutrition Therapy (MNT)
• Recommended calorie intake is about 30 cal/kg/day divided over 3 meals and 3 snacks. The aim is to blunt the post
prandial hyperglycemia.
• Bed time snack should contain complex carbohydrate and protein to prevent late night hypoglycemia and early
🔸
morning starvation ketosis.
Exercise
• Light exercise especially of the upper part of the body.
• 20min daily atleast
🔸
• Least mechanical stress should be on the trunk.
Insulin
• Indicated when MNT fails.
• Self administration should be encouraged
• Ideally, 3 premeal injections of rapid acting regular insulin (aspart and lispro)
• The requirements increase and pregnancy advances
• Mild cases, mixture of rapid and intermediate acting, given twice daily (30:70)
The total first dose of insulin is calculated according to the patient’s weight as follow : 0.7-1.0 IU /K G/DAY
▫ In the first trimester .......... weight x 0.7
▫ In the second trimester........ weight x 0.8
▫ In the third trimester........... weight x 0.9
Monitoring
• Self monitoring by glucometer and capillary blood glucose or venous plasma levels.
• Aim is to keep the fasting plasma level at 5.1 mmol/L (95mg/dl)
• 2 hours post prandial 6.6mmol/L ( 130 )
• Women using daily self monitoring had less macrosomic infants.
• Ideal monitoring is 4 times a day including fasting, post breakfast, post lunch and post dinner with additional
testing w henever she is symptomatic
🔶Obstetric Management
🔸 Antepartum
• Nuchal translucency is assessed at 11-14 w eeks
Definition:
• Metabolic disease characterized by hyperglycemia resulting from defect on insulin
• Anomaly scan at 18-20 weeks
secretion, insulin action or both
• Grow th scan done monthly at third trimester (28,32,36 weeks)
• Look for macrosomia (increased in abdominal circumference w ith increased fetal subcutaneous fat) and
🔸
polyhydramnios Glucose Regulation during Healthy Pregnancy
Antepartum fetal surveillance and non stress testing and biophysical profile may help prevent still birth and • During healthy pregnancy, the mother’s body undergoes aseries of physiological changes
unnecessary preterm delivery and detect fetal compromise. in order to support the demands of the growing fetus. These include adaptations to the
• Antepartum corticosteroid to enhance lung maturity are not contraindicated in pregnancy cardiovascular, renal, hematologic, respiratory, and metabolic systems .
• One important metabolic adaptation is in insulin sensitivity. Over the course of gestation,
🔸
• Doppler studies is indicated in case of diabetes complicated by preeclamsia and grow th restriction.
insulin sensitivity shifts depending on the requirements of pregnancy. Duringearly gestation,
▪️ Intrapartum
Timing of delivery
•Early delivery is indicated if there is presence of fetal or maternal complications or if the glycemic index control is
insulin sensitivity increases, promoting theuptake of glucose into adipose stores in
preparation for theenergy demands of later pregnancy
poor. • However, as pregnancy progresses, a surge of local and placentalhormones, including
• Women on insulin are best delivered after 38 w eeks. estrogen, progesterone, leptin, cortisol, placental lactogen, and placental growth hormone
Management together promote a state of insulin resistance. As a result, blood glucose is slightly
▪️
•Previous term still birth is an indication for early delivery
Type of Delivery: • Tight glycemic control is the elevated, and this glucose is readily transported across theplacenta to fuel the growth of
the fetus.
🔹
• Diabetes per se is not an indication for C-section and V Dmaybe allow ed if no complications. cornerstone in the management
• This mild state of insulin resistance also promotes endogenous glucose production and
1 Vaginal delivery: • Divided into Medical and Obstetric
•No maternal or fetal complications the breakdown of fat stores, resulting in a further increase in blood glucose and free fatty
management acid (FFA) concentrations, in order to maintain glucose homeostasis, pregnant women
• The cervix is favorable, average baby size, vertex presentation with no CPD
•Induction of labour compensate for these changes through hypertrophy and hyperplasia of pancreatic β-cell.
•Continuous CT G monitoring is mandatory.
Introduction
🔹
•Shoulder dystocia should be anticipated
🔹
• Human Placental Lactogen
🔹
2 Caesarean: Affects protein, fat & carbohydrate metabolism.
🔹
•If there is maternal or fetal complications Increase lipolysis --> increased FFA -->increase in insulin resistance
• Macrosomia (On US increasing AC or fetal w eight > 4000g) FFA used for maternal metabolism so that glucose & amino acids are available for the fetus.
🔸 Intrapartum Glycemic control:
•Euglycemic state should be maintained.
• Plasma cortisol also increases leading to insulin resistance.
• So pancreas is forced to produce more insulin and plasma glucose level fall.
• There is decrease in renal tubular threshold for glucose within glmerular filteration rate, so most
•Morning dose of insulin is skipped in elective CS pregnant women will have glycosuria
•Mother should get a limited amount of glucose duringlabour *RENAL GLUCOSURIA* BUT blood glucose level is normal.
•Hourly glucose monitoring is done. • Pregnancy is characterized by “Fasting Hypoglycemia” and “Post-prandial Hyperglycemia”.
•Once into active labour, she can be started on the sliding scale of insulin using an Insulin & Dextrose infusion •Insulin resistance in late pregnancy is a normal physiological adaptation that shifts maternal
🔸
regimen. energy metabolism from carbohydrate to lipid oxidation & thereby spares glucose for the fetus.
Neonatal Care: •Gestational diabetes occurs w hen the pancreas despite increased insulin production cannot
•Blood glucose levels closely monitored for 48hrs counter the insulin resistance caused by pregnancy hormones.
•Early breastfeeding is advocated
•Cord clamped early to prevent neonatal polycythemia.
🔸
•Avoid heat loss and look for congenital abnormalities.
Postpartum care:
🔹
Classification:
Preexisting or pregestational diabetes refers to type
•Prophylactic antibiotics to minimize infections
•Most women w ith GDM will no longer require insulin Types of Pregnancy Diabetes
🔹
1or 2 diabetes diagnosed before conception.
Gestational diabetes mellitus (GDM) is defined as any
degree of glucose intolerance w ith onset or first recognition
•At 6-12 w eeks do OGTT
🔹
• Pregestational or O vert Diabetes (10% ) during pregnancy.
•Lifelong screening at least every 3 years • Gestational diabetes (90% ) Overt diabetes in pregnancy is defined as
hyperglycemia first recognized during pregnancy w hich
meets the diagnostic threshold of diabetes in non-pregnant
🔸
Counseling and Contraception
🔸Counseled about the risk of future diabetes and receive lifestyle advice.
adults according to ADA criteria for diagnosis of diabetes
🔸
🔸
Encouraged to continue on diet and exercise.
Annual OGTT
🔸Low
Barrier methods are safe.
dose Combined OCPs, injectable progestogens and IUD can all be safely
used in women who had GDM.
• Carbohydrate intolerance of variable severity,
with onset or first recognition during the
DIABETES IN GESTATIONAL DIABETES
present pregnancy.
• GDM usually manifests in the latter half of
pregnancy so no effect on organogenesis and
PREGNANCY does not cause congenital defects.
🔷
🔹 Maternal complications • The main problem is macrosomia
• Reverts to normal follow ing delivery
🔹 Preeclampsia
Polyhydramnios:
-Due to maternal hyperglycemia in 20%
-Leads to fetal hyperglycemia and polyuria
• To remember that women are already diabetic at the time of
🔹
-Osmosis is another factor
Infections N eonatal complications▫ U sually macrosomic, has increased adiposity, increased skinfold thickness and conception
• Hence, prove for congenital abnormalities
🔹
visceromegaly (liver).▫ Plethoric appearance because of polycythemia
🔹 Risk of operative delivery
• Management is similar to GDM
• Preconceptional and early pregnancy care is important.
🔹 Genital tract trauma (macrosomia)
Puerperal sepsis and wound infections PREGESTATIONAL OR OVERT
• Scanning :HbA1c < 6
🔷
🔹 Fetal Complications
Abortions and congenital anomalies are a major problem of pregestational diabetes and GDM usually appears only after 20
DIABETES Screening
• Universal screening- all the women are screened
• Selective screening- only women with the risk factors.
🔹
weeks.
🔹AllThisthecanfetal and neonatal complications are due to the fetal Hyperinsulinemia.
Advantage of screening:
• Reduces perinatal mortality & morbidity
🔹Miscarriage: More in uncontrolled pregestational diabetes
be explained by the Pederson Hypothesis
• Picks up those w omen likely to develop typeII diabetes
🔹Congenital malformations: in the future.
•More in uncontrolled pregestational diabetes
•Hyperglycemia, ketosis and O2 free radical toxicityare the causative agents
-Cardiac defects (transposition of great vessels & VSD) 🔷
🔹 OGTT (oral glucose tolerance test)
-Neural tube defects (anencephaly and spina bifida)
🔹
🔹
Done at 24-28 weeks
🔹
-Caudal regression syndrome or sacral agenesis (rare) but is a congenital defect specific to diabetes. Done after an overnight fasting of atleast 8hours
Unexplained intrauterine death (IUD):
🔹Two75g of glucose in 100ml water
🔷
-Due to fetal hypoxia readings taken after 1hr and the next 1hr
-Fetal hyperglycemia and hyperinsulinaemia increase the O 2 demand of fetus.▫ Glycosylated Hb binds O2 more avidly but Diagnosis:
releases less O2 • Fasting > or equal 5.1 mmol/L ( ≥ 95 )
•Fetal polycythemia & hyperviscosity • 1 hour > or equal 10 mmol/L ( ≥ 180 )
• 2 hours > or equal 8.5 mmol/L ( ≥ 150 )
🔹Prematurity
•In overt DM w ith vasculopathy, placental insufficiency can lead to IUD especially in association with preeclampsia.
Women with GDM should be screened for persistant diabetes
🔹Macrosomia: 6-12w eeks post partum. They have high risk of life long
diabetes so screen every 3 yrs.
•Most common complication▫ Increase in IGF I and II
•Increase adiposity in insulin dependent area as trunk and shoulders. COMPLICATIONS OF DIABETES
tests
🔷
🔹 One Step Test or Spot Test
🔹 Intrauterine Grow th R estriction (IUGR ) 🔹
•Good glycemic control reduces the risk No need for fasting.
IN PREGNANCY Given 75g of glucose in 300ml w ater irrespective of last
-In Pregestational diabetes with vascular complications (retinopathy & nephropathy)
🔹
meal.
🔹Blood
🔹
-Disturbance in maternal fuels during organogenesis could also be the cause. glucose assessed at 2 hours
Neonatal complications Diagnosis of GDM if > 7.7 mmol/L ( ≥ 140 )
-Usually macrosomic, has increased adiposity, increased skinfold thickness and visceromegaly (liver).
🔷 Two Step procedure
🔹
- Plethoric appearance because of polycythemia
•50 g glucose challenge test follow ed by a 100g OGTT if the 1
Respiratory Distress Syndrome: hour plasma glucose is 7.7 mmol/L or more. ( ≥ 140 )
- More common in overt diabetes delivered by CS •The fasting plasma glucose level is determined following
-Occur at all gestational ages. 100g of oral glucose and plasma glucose level estimated at
-Fetal hyperinsulinemia impairs surfactant production in the lung. 1,2 & 3hours
🔹
-This leads to delay in lung maturity and RDS. •FBS 5.2 mmol/L ( 95 ) 1 hour 10 mmol/L ( 180 )
Hypoglycaemia: •2 hour 8.6 mmol/L ( 155 ) 3 hour 7.7 mmol/L ( 140 )
🔹DueHypocalcaemia:
-Fetal hyperinsulinemia causes hypoglycaemia (plasma glucose level to be less than 2.2 mmol/L).
🔹
to transient hypoparathyroidism, serum calcium level below 0.38 mmol/L
Hyerbilirubinaeimia :
🔹 Hyperviscosity Syndrome:
- Due to Polycythaemia w ith hemolysis , can be due to prematurity
- Due to increased erythropoiesis and polycythemia
🔹
- Renal vain thrombosis and necrotizing entrocolitis also result from polycythemia.
Hypertrophic cardiomyopathy:
by fatema okoff
- May progress to heart failure
- Echocardiography-->demonstrate Septal hypertrophy (transient and resolve soon)
- If regress by 6 months -->No permanent myocardial damage
🔹
-Rarely, it is severe and cause CCF in the first few days of life
Birth trauma:
-Due to macrosomia and Shoulder dystocia due to disproportionate grow th of the shoulders
- Shoulder dystocia. This results in Erb’s and K lumpke’s paralysis & fracture of the clavicle and humerus
🔹late effect
• Obesity
• Early onset type II diabetes
• Cardiovascular disease
🔸 Medical management
Medical Nutrition Therapy (MNT)
• Recommended calorie intake is about 30 cal/kg/day divided over 3 meals and 3 snacks. The aim is to blunt the post
prandial hyperglycemia.
• Bed time snack should contain complex carbohydrate and protein to prevent late night hypoglycemia and early
🔸
morning starvation ketosis.
Exercise
• Light exercise especially of the upper part of the body.
• 20min daily atleast
🔸
• Least mechanical stress should be on the trunk.
Insulin
• Indicated when MNT fails.
• Self administration should be encouraged
• Ideally, 3 premeal injections of rapid acting regular insulin (aspart and lispro)
• The requirements increase and pregnancy advances
• Mild cases, mixture of rapid and intermediate acting, given twice daily (30:70)
The total first dose of insulin is calculated according to the patient’s weight as follow : 0.7-1.0 IU /K G/DAY
▫ In the first trimester .......... weight x 0.7
▫ In the second trimester........ weight x 0.8
▫ In the third trimester........... weight x 0.9
Monitoring
• Self monitoring by glucometer and capillary blood glucose or venous plasma levels.
• Aim is to keep the fasting plasma level at 5.1 mmol/L (95mg/dl)
• 2 hours post prandial 6.6mmol/L ( 130 )
• Women using daily self monitoring had less macrosomic infants.
• Ideal monitoring is 4 times a day including fasting, post breakfast, post lunch and post dinner with additional
testing w henever she is symptomatic
🔶Obstetric Management
🔸 Antepartum
• Nuchal translucency is assessed at 11-14 w eeks
Definition:
• Metabolic disease characterized by hyperglycemia resulting from defect on insulin
• Anomaly scan at 18-20 weeks
secretion, insulin action or both
• Grow th scan done monthly at third trimester (28,32,36 weeks)
• Look for macrosomia (increased in abdominal circumference w ith increased fetal subcutaneous fat) and
🔸
polyhydramnios Glucose Regulation during Healthy Pregnancy
Antepartum fetal surveillance and non stress testing and biophysical profile may help prevent still birth and • During healthy pregnancy, the mother’s body undergoes aseries of physiological changes
unnecessary preterm delivery and detect fetal compromise. in order to support the demands of the growing fetus. These include adaptations to the
• Antepartum corticosteroid to enhance lung maturity are not contraindicated in pregnancy cardiovascular, renal, hematologic, respiratory, and metabolic systems .
• One important metabolic adaptation is in insulin sensitivity. Over the course of gestation,
🔸
• Doppler studies is indicated in case of diabetes complicated by preeclamsia and grow th restriction.
insulin sensitivity shifts depending on the requirements of pregnancy. Duringearly gestation,
▪️ Intrapartum
Timing of delivery
•Early delivery is indicated if there is presence of fetal or maternal complications or if the glycemic index control is
insulin sensitivity increases, promoting theuptake of glucose into adipose stores in
preparation for theenergy demands of later pregnancy
poor. • However, as pregnancy progresses, a surge of local and placentalhormones, including
• Women on insulin are best delivered after 38 w eeks. estrogen, progesterone, leptin, cortisol, placental lactogen, and placental growth hormone
Management together promote a state of insulin resistance. As a result, blood glucose is slightly
▪️
•Previous term still birth is an indication for early delivery
Type of Delivery: • Tight glycemic control is the elevated, and this glucose is readily transported across theplacenta to fuel the growth of
the fetus.
🔹
• Diabetes per se is not an indication for C-section and V Dmaybe allow ed if no complications. cornerstone in the management
• This mild state of insulin resistance also promotes endogenous glucose production and
1 Vaginal delivery: • Divided into Medical and Obstetric
•No maternal or fetal complications the breakdown of fat stores, resulting in a further increase in blood glucose and free fatty
management acid (FFA) concentrations, in order to maintain glucose homeostasis, pregnant women
• The cervix is favorable, average baby size, vertex presentation with no CPD
•Induction of labour compensate for these changes through hypertrophy and hyperplasia of pancreatic β-cell.
•Continuous CT G monitoring is mandatory.
Introduction
🔹
•Shoulder dystocia should be anticipated
🔹
• Human Placental Lactogen
🔹
2 Caesarean: Affects protein, fat & carbohydrate metabolism.
🔹
•If there is maternal or fetal complications Increase lipolysis --> increased FFA -->increase in insulin resistance
• Macrosomia (On US increasing AC or fetal w eight > 4000g) FFA used for maternal metabolism so that glucose & amino acids are available for the fetus.
🔸 Intrapartum Glycemic control:
•Euglycemic state should be maintained.
• Plasma cortisol also increases leading to insulin resistance.
• So pancreas is forced to produce more insulin and plasma glucose level fall.
• There is decrease in renal tubular threshold for glucose within glmerular filteration rate, so most
•Morning dose of insulin is skipped in elective CS pregnant women will have glycosuria
•Mother should get a limited amount of glucose duringlabour *RENAL GLUCOSURIA* BUT blood glucose level is normal.
•Hourly glucose monitoring is done. • Pregnancy is characterized by “Fasting Hypoglycemia” and “Post-prandial Hyperglycemia”.
•Once into active labour, she can be started on the sliding scale of insulin using an Insulin & Dextrose infusion •Insulin resistance in late pregnancy is a normal physiological adaptation that shifts maternal
🔸
regimen. energy metabolism from carbohydrate to lipid oxidation & thereby spares glucose for the fetus.
Neonatal Care: •Gestational diabetes occurs w hen the pancreas despite increased insulin production cannot
•Blood glucose levels closely monitored for 48hrs counter the insulin resistance caused by pregnancy hormones.
•Early breastfeeding is advocated
•Cord clamped early to prevent neonatal polycythemia.
🔸
•Avoid heat loss and look for congenital abnormalities.
Postpartum care:
🔹
Classification:
Preexisting or pregestational diabetes refers to type
•Prophylactic antibiotics to minimize infections
•Most women w ith GDM will no longer require insulin Types of Pregnancy Diabetes
🔹
1or 2 diabetes diagnosed before conception.
Gestational diabetes mellitus (GDM) is defined as any
degree of glucose intolerance w ith onset or first recognition
•At 6-12 w eeks do OGTT
🔹
• Pregestational or O vert Diabetes (10% ) during pregnancy.
•Lifelong screening at least every 3 years • Gestational diabetes (90% ) Overt diabetes in pregnancy is defined as
hyperglycemia first recognized during pregnancy w hich
meets the diagnostic threshold of diabetes in non-pregnant
🔸
Counseling and Contraception
🔸Counseled about the risk of future diabetes and receive lifestyle advice.
adults according to ADA criteria for diagnosis of diabetes
🔸
🔸
Encouraged to continue on diet and exercise.
Annual OGTT
🔸Low
Barrier methods are safe.
dose Combined OCPs, injectable progestogens and IUD can all be safely
used in women who had GDM.
• Carbohydrate intolerance of variable severity,
with onset or first recognition during the
DIABETES IN GESTATIONAL DIABETES
present pregnancy.
• GDM usually manifests in the latter half of
pregnancy so no effect on organogenesis and
PREGNANCY does not cause congenital defects.
🔷
🔹 Maternal complications • The main problem is macrosomia
• Reverts to normal follow ing delivery
🔹 Preeclampsia
Polyhydramnios:
-Due to maternal hyperglycemia in 20%
-Leads to fetal hyperglycemia and polyuria
• To remember that women are already diabetic at the time of
🔹
-Osmosis is another factor
Infections N eonatal complications▫ U sually macrosomic, has increased adiposity, increased skinfold thickness and conception
• Hence, prove for congenital abnormalities
🔹
visceromegaly (liver).▫ Plethoric appearance because of polycythemia
🔹 Risk of operative delivery
• Management is similar to GDM
• Preconceptional and early pregnancy care is important.
🔹 Genital tract trauma (macrosomia)
Puerperal sepsis and wound infections PREGESTATIONAL OR OVERT
• Scanning :HbA1c < 6
🔷
🔹 Fetal Complications
Abortions and congenital anomalies are a major problem of pregestational diabetes and GDM usually appears only after 20
DIABETES Screening
• Universal screening- all the women are screened
• Selective screening- only women with the risk factors.
🔹
weeks.
🔹AllThisthecanfetal and neonatal complications are due to the fetal Hyperinsulinemia.
Advantage of screening:
• Reduces perinatal mortality & morbidity
🔹Miscarriage: More in uncontrolled pregestational diabetes
be explained by the Pederson Hypothesis
• Picks up those w omen likely to develop typeII diabetes
🔹Congenital malformations: in the future.
•More in uncontrolled pregestational diabetes
•Hyperglycemia, ketosis and O2 free radical toxicityare the causative agents
-Cardiac defects (transposition of great vessels & VSD) 🔷
🔹 OGTT (oral glucose tolerance test)
-Neural tube defects (anencephaly and spina bifida)
🔹
🔹
Done at 24-28 weeks
🔹
-Caudal regression syndrome or sacral agenesis (rare) but is a congenital defect specific to diabetes. Done after an overnight fasting of atleast 8hours
Unexplained intrauterine death (IUD):
🔹Two75g of glucose in 100ml water
🔷
-Due to fetal hypoxia readings taken after 1hr and the next 1hr
-Fetal hyperglycemia and hyperinsulinaemia increase the O 2 demand of fetus.▫ Glycosylated Hb binds O2 more avidly but Diagnosis:
releases less O2 • Fasting > or equal 5.1 mmol/L ( ≥ 95 )
•Fetal polycythemia & hyperviscosity • 1 hour > or equal 10 mmol/L ( ≥ 180 )
• 2 hours > or equal 8.5 mmol/L ( ≥ 150 )
🔹Prematurity
•In overt DM w ith vasculopathy, placental insufficiency can lead to IUD especially in association with preeclampsia.
Women with GDM should be screened for persistant diabetes
🔹Macrosomia: 6-12w eeks post partum. They have high risk of life long
diabetes so screen every 3 yrs.
•Most common complication▫ Increase in IGF I and II
•Increase adiposity in insulin dependent area as trunk and shoulders. COMPLICATIONS OF DIABETES
tests
🔷
🔹 One Step Test or Spot Test
🔹 Intrauterine Grow th R estriction (IUGR ) 🔹
•Good glycemic control reduces the risk No need for fasting.
IN PREGNANCY Given 75g of glucose in 300ml w ater irrespective of last
-In Pregestational diabetes with vascular complications (retinopathy & nephropathy)
🔹
meal.
🔹Blood
🔹
-Disturbance in maternal fuels during organogenesis could also be the cause. glucose assessed at 2 hours
Neonatal complications Diagnosis of GDM if > 7.7 mmol/L ( ≥ 140 )
-Usually macrosomic, has increased adiposity, increased skinfold thickness and visceromegaly (liver).
🔷 Two Step procedure
🔹
- Plethoric appearance because of polycythemia
•50 g glucose challenge test follow ed by a 100g OGTT if the 1
Respiratory Distress Syndrome: hour plasma glucose is 7.7 mmol/L or more. ( ≥ 140 )
- More common in overt diabetes delivered by CS •The fasting plasma glucose level is determined following
-Occur at all gestational ages. 100g of oral glucose and plasma glucose level estimated at
-Fetal hyperinsulinemia impairs surfactant production in the lung. 1,2 & 3hours
🔹
-This leads to delay in lung maturity and RDS. •FBS 5.2 mmol/L ( 95 ) 1 hour 10 mmol/L ( 180 )
Hypoglycaemia: •2 hour 8.6 mmol/L ( 155 ) 3 hour 7.7 mmol/L ( 140 )
🔹DueHypocalcaemia:
-Fetal hyperinsulinemia causes hypoglycaemia (plasma glucose level to be less than 2.2 mmol/L).
🔹
to transient hypoparathyroidism, serum calcium level below 0.38 mmol/L
Hyerbilirubinaeimia :
🔹 Hyperviscosity Syndrome:
- Due to Polycythaemia w ith hemolysis , can be due to prematurity
- Due to increased erythropoiesis and polycythemia
🔹
- Renal vain thrombosis and necrotizing entrocolitis also result from polycythemia.
Hypertrophic cardiomyopathy:
by fatema okoff
- May progress to heart failure
- Echocardiography-->demonstrate Septal hypertrophy (transient and resolve soon)
- If regress by 6 months -->No permanent myocardial damage
🔹
-Rarely, it is severe and cause CCF in the first few days of life
Birth trauma:
-Due to macrosomia and Shoulder dystocia due to disproportionate grow th of the shoulders
- Shoulder dystocia. This results in Erb’s and K lumpke’s paralysis & fracture of the clavicle and humerus
🔹late effect
• Obesity
• Early onset type II diabetes
• Cardiovascular disease
