This document discusses diabetes mellitus in pregnancy. It defines diabetes and discusses its prevalence and classifications. It covers gestational diabetes mellitus (GDM), risk factors for GDM, screening and diagnostic methods for GDM, and complications of diabetes in pregnancy for both mother and baby. It outlines management of diabetes in pregnancy including diet, insulin therapy, glycemic control during labor, and care of the newborn.
Definition
Incidence
Types
Diabetogenic effect of pregnancy
Metabolic changes during pregnancy
Risk of uncontrolled DM on pregnancy
Diagnosis and evaluation
Medical management
Nursing management
Definition of Diabetes mellitus:It is inability to metabolize glucose properly. It is a chronic systemic disease, manifesting metabolic and vascular changes affecting every organ in the body.
a. Pregestational (preexisting) diabetes
Occurs when have type 1 or type 2 diabetes before becoming pregnant.
1-Type I Insulin-dependent (IDDM) (Insulin deficient).
2-Type II Non-Insulin dependent (NIDDM) (Insulin resistant).
b. Gestational diabetes mellitus (GDM).
Occurs diabetes when becoming pregnant.
a. Pregestational (preexisting) diabetes
Occurs when have type 1 or type 2 diabetes before becoming pregnant.
1-Type I Insulin-dependent (IDDM) (Insulin deficient).
2-Type II Non-Insulin dependent (NIDDM) (Insulin resistant).
b. Gestational diabetes mellitus (GDM).
Occurs diabetes when becoming pregnant.
Diabetes may appear only during pregnancy due to :-
1-Increased levels of antiinsulinas (estrogen, progesteron, human placental lactogen, and prolactine).
2-Decreased renal threshold for glucose (glucose loss in urine).
During early stage of pregnancy: Maternal hypoglycemia.
After the fourth month: increase glucose level in the blood due to placental hormones
During labor: liability to hypoglycaemia.
After delivery: glucose level return to prepregnant state.
Gestational Diabetes
Risk Factors
Maternal age >25
Family history
Glucosuria
Prior macrosomia
Previous unexplained stillbirth
Risk of uncontrolled diabetes on pregnancy
A- Maternal effect:
On pregnancy On labor On puerperium
-Abortion - premature -puerperal sepsis
-PET labor -PPH
-Polyhydramnios - Inertia - Abnormal
-Pressure symptom - Operative lactation
-Infection delivery
-Retinopathy
Risk of uncontrolled diabetes on fetus
1- Abortion
2- Congenital anomalies
Open neural defect, CHD, renal anomaly, sacral agenesis, small left colon syndrome(Approximately 40% to
50% of infants with this disorder have diabetic mothers, almost all of whom are insulin dependent , , imperforated anus.
3- Macrosomia
Fetal hyperglycaemia causes increase insulin secretion and lead to increase fetal fat deposition
Open neural defect
sacral agenesis
Macrosomia
Macrosomia
Macrosomia
Risk of uncontrolled diabetes on fetus
4- Intrauterine fetal death due to:
Congenital malformation, ketoacedosis, hypoglycaemia, superimposed PET.
5- Neonatal hypoglycemia
After delivery, glucose concentration fail, while neonatal insulin level remain high lead to neonatal hypoglycemia (Tremors, pallor, apnea, cyanosis)
Risk of uncontrolled diabetes on fetus
7- Hyperbilirubinaemia
Due to immature liver
8- Neonatal death due to:
Congenital anomalies
Definition
Incidence
Types
Diabetogenic effect of pregnancy
Metabolic changes during pregnancy
Risk of uncontrolled DM on pregnancy
Diagnosis and evaluation
Medical management
Nursing management
Definition of Diabetes mellitus:It is inability to metabolize glucose properly. It is a chronic systemic disease, manifesting metabolic and vascular changes affecting every organ in the body.
a. Pregestational (preexisting) diabetes
Occurs when have type 1 or type 2 diabetes before becoming pregnant.
1-Type I Insulin-dependent (IDDM) (Insulin deficient).
2-Type II Non-Insulin dependent (NIDDM) (Insulin resistant).
b. Gestational diabetes mellitus (GDM).
Occurs diabetes when becoming pregnant.
a. Pregestational (preexisting) diabetes
Occurs when have type 1 or type 2 diabetes before becoming pregnant.
1-Type I Insulin-dependent (IDDM) (Insulin deficient).
2-Type II Non-Insulin dependent (NIDDM) (Insulin resistant).
b. Gestational diabetes mellitus (GDM).
Occurs diabetes when becoming pregnant.
Diabetes may appear only during pregnancy due to :-
1-Increased levels of antiinsulinas (estrogen, progesteron, human placental lactogen, and prolactine).
2-Decreased renal threshold for glucose (glucose loss in urine).
During early stage of pregnancy: Maternal hypoglycemia.
After the fourth month: increase glucose level in the blood due to placental hormones
During labor: liability to hypoglycaemia.
After delivery: glucose level return to prepregnant state.
Gestational Diabetes
Risk Factors
Maternal age >25
Family history
Glucosuria
Prior macrosomia
Previous unexplained stillbirth
Risk of uncontrolled diabetes on pregnancy
A- Maternal effect:
On pregnancy On labor On puerperium
-Abortion - premature -puerperal sepsis
-PET labor -PPH
-Polyhydramnios - Inertia - Abnormal
-Pressure symptom - Operative lactation
-Infection delivery
-Retinopathy
Risk of uncontrolled diabetes on fetus
1- Abortion
2- Congenital anomalies
Open neural defect, CHD, renal anomaly, sacral agenesis, small left colon syndrome(Approximately 40% to
50% of infants with this disorder have diabetic mothers, almost all of whom are insulin dependent , , imperforated anus.
3- Macrosomia
Fetal hyperglycaemia causes increase insulin secretion and lead to increase fetal fat deposition
Open neural defect
sacral agenesis
Macrosomia
Macrosomia
Macrosomia
Risk of uncontrolled diabetes on fetus
4- Intrauterine fetal death due to:
Congenital malformation, ketoacedosis, hypoglycaemia, superimposed PET.
5- Neonatal hypoglycemia
After delivery, glucose concentration fail, while neonatal insulin level remain high lead to neonatal hypoglycemia (Tremors, pallor, apnea, cyanosis)
Risk of uncontrolled diabetes on fetus
7- Hyperbilirubinaemia
Due to immature liver
8- Neonatal death due to:
Congenital anomalies
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
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The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
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Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
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2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
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- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
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- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
2. DEFINITION
Diabetes mellitus is defined a a carbohydrate disturbance
characterised by hyperglycaemia with peripheral insulin deficiency or
insulin resistance.
5. Etilogical classification.
Type 1 insulin dependent diabetes
Type 2 non insulin dependent diabetes
Other specific types-
1. Genetic mutration of beta cell function
2. Genetic defect in insulin action.
3. Genetic syndrome
4. Disease of exocrine pancreas
5. Drug or chemical induced
6. Infections
• Gestational diabetes mellitus.
6. Classification in pregnancy
Type 1 Diabetes:Diabetes resulting from beta cell destruction,usually
leading to absolute insulin deficiency.further classified as with vascular
complications and without vascular complications.
Type 2 Diabetes:Diabetes from inadequate insulin secretion in the face of
increased insulin resistance.further classified as with vascular
complications and without vascular complications.
Other types of Diabetes:genetic in origin ,associated with pancreatic
disease or chemically induced.
7. Glycosuria during pregnancy
Detected on Random urine samples in 5-50%.
Increased GFR +impaired tubular reabsorptive capacity for
filtered glucose.
Decreases renal threshold.
12. RISK FACTORS
Age over 30 yrs
Past history of GDM
Family history of diabetes.
Bad obstetric history
Prior history of macroscomic baby.
Previous still birth.
Previous fetal anomalies.
Unexplained perinatal loss.
History of pcos.
Polyhydraminos
Recurrent vaginal
candidiasis.
Recurrent urinary tract
infection.
Obesity ,more than 90 kg.
Congenital fetal anomalies.
Pre eclampsia.
Persistent Glycosuria.
FACTORS IN HISTORY FACTORS IN PP
14. TWO STEP APPROACH
GLUCOSE CHALLENGE TEST:
1. TIME:24-28 WEEKS
2. No fasting is required.
METHOD:50 gms of glucose to patient
Check blood sugar levels
After 1 hour
Less than 140 mg/dl 140-180 mg/dl More than 180 mg/dl
Normal
Do diagnostic test
(i.e)GTT
Diabetes
confirmed.
15. GLUCOSE TOLERANCE TEST
Perform a three hour 100 gram oral glucose tolerance test
• Overnight fasting is required,of 8-10 hours with previous 3 days of unrestricted diet (150 gms of
carbohydrate per day ).fasting blood sugar sample is taken as first sample .
Give 100 gms of glucose to patient
2nd Sample:1 hr Post prandial
3rd Sample:2 hr post prandial
4th Sample:3 hr post prandial.
If any two or more than two values are abnormal
Confirms Diabetes
16. DIPSI
Proposed single step test.
Hardly affects daily routine of women.
No fasting is needed.
Both screening and diagnostic procedure.
Whenever a female comes for antenatal visit
Irrespective of previous meals,Give 75gms of oral glucose
After 2 hours
Blood sugar levels
>=140mg/dl but <200
>=120mg/dl
>=200mg/dl
Overt diabetes
GDM
Glucose intolerance
18. MATERNAL COMPLICATIONS
DURING PREGNANCY DURING LABOUR DURING PUERPERIUM
• Miscarriages
• Infections including UTI
and pyelonephritis
• Vaginal candidiasis
• Polyhydraminos
• Gestational hypertension
and pre eclampsia
• Ketoacidosis
• Worsening of
nephropathy with or
withour renal failure
• Worsening of diabetic
retinopathy
• Pre term labour
• hyperglycemia
• Ketoacidosis
• Prolonged labor
• Shoulder dystocia
• Increased incidence of
instrumental delivery
• Increased incidence of
operative delivery
• Maternal soft tissue
injuries,perineal
tears,vaginal
lacerations,cervical
tears
• Postpartum
hemorrhage
• Subinvolution of
uterus
• Puerperal sepsis
• Failed lactation.
19. FETAL COMPLICATIONS
FETAL COMPLICATIONS NEONATAL COMPLICATIONS
• Increased spontaneous
abortion rate
• Congenital malformations
• Fetal macrosomia
• Fetal growth restriction
• Intrauterine fetal death
• Shoulder dystocia
• Fetal birth injuries like
brachial plexus injuries.
• Respiratory distress
syndrome
• Hypoglycemia
• Hypocalcemia
• Hyperbilirubinemia
• Hypomagnesemia
• Hyperviscosity syndrome
• Hypertrophic cardiomyopathy
• Transient tachypnoea of new
born
• Birth asphyxia
• Birth injuries
• Long term cognitive
development of infant
• Perinatal mortality
• Late effects and inheritance
of diabetes.
20. PEDERSONS HYPOTHESIS
Maternal hyperglycemia
Excessive glucose transfer to fetus
Fetal hyperglycemia
Beta cells of fetal pancreas undergo hypertrophy in response to blood sugar
levels
Fetal hyperinsulinemia and increased IGF-1 and IGF-2
Fetal macrosomia
d/t deposition of
fats,glycogen and
proteins
Other neonatal
metabolic
complicatoions
Neonatal
hypoglycemia
Inhibition of surfactant
production
Increased
erythropoiesis,hy
perviscosity
syndrome
Fetal
cardiomyopathy
Increased fetal
metabolism
Thrombosis of renal
and other
vreins,necrotising
enterocolitis
RDS
Shoulder dystocia
,birth injuries
22. PRE PERGNANCY COUNSELLING
For better outcome,euglycemia to be maintained during peri conceptional period and throughout pregnancy.
They should be attended by an endocrinologist,obstetrician and dietician.
Should conceive only when diabetes is well under control.
Periconceptional folic acid 400 mcg/day is given to prevent neural tube defects and to be continued in first
trimester.
Proper advice about diet and insulin is given to these women.
Women controlled on OHA should be started with insulin therapy for better outcome and to prevent congenital
malformations.
Women with PCOS who conceived on metformin should continue to take metformin throughout pregnancy for a
better outcome.
As per ADA,recommended peri conceptional glucose control using insulin to achieve FBS between 80-110 ,2
hour PPBS <155 mg/dl.
23. ANTENATAL CARE
VISITS:every 4 weeks up to 20 weeks ,every 2
weeks until 30 weeks and weekly thereafter.
DIET:30 calories /kg body weight.The total calorie
intake is split into 3 small meals and 3-4 snacks to
minimise fluctuations in blood sugar levels.
Education:to be explained about the utmost need of
glycemic control to minimise complications.usually
the women can be taught to give their own
injections.She should also be explained about the
early symptoms of hypoglycemia and its
management by consuming some biscuits
CARBOHYDRATES:
• 175-200 gm
• 3+ meal should be
consumed to
compensate for urinary
loss and fetal growth.
24. History taking:Careful history taking including any symptoms of diabetes and its
complivcations and various complications of pregnancy should be asked in each AN
visit.
General physical examination:to be done and pallor,pulse,blood pressure,jugular venous
pressure,respiratory and cardiovascular system are checked at each visit.Fundus
examination to rule out diabetic retinopathy.
Abdominal examination:confirm the POG to look for the cause of increased fundal height
,fetal presentation and fetal heart sounds.
25. INVESTIGATIONS
Blood pressure on each visit
Weight on each visit.
Complete hemogram including hemoglobin and total leucocyte count.
Urine examination for glucose ,proteins,specific gravity,ketones,microscopy and culture
Kidney function tests
Hepatic function tests in case of gestational hypertension or pre eclampsia.
Fundus examination to rule out hypertensive or diabetic retinopathy.
ECG if cardiac involvement in pre gdm only.
Blood sugar estimation.
Fetal evaluation:
Maternal serum alpha protein levels at 16 weeks of gestation are increased in neural tube defects .(normally values are to be less in a
diabetic )
26. Targetted ultrasonography at 18-20 weeks to evaluate fetal growth
and well being ,NTD and anomalies.
Fetal echocardiography at 22-24 weeks of gestation due to 5 fold
increase in cardiac anomalies.
Fetal kick chart daily.
Regular non stress test.
Biophysical profile.
Doppler velocimetry.
27. Insulin therapy
Indications:
1. All type 1 diabetes.
2. Gestational diabetes not controlled by diet.
3. Type 2 diabetes pt s who were on OHA before pregnancy.
PRINCIPLES:
1. Frequent changes in needs of insulin during pregnancy.
2. Changes are made in small increements of 2 units at a
time.
3. A combination of short acting and long actiong insulin is
given 2-3 doses/ day.
28. MANAGEMENT OF LABOR ON INSULIN
With glood glycemic control and fetal surveillance to detect uteroplacental insufficiency,more
pregnant diabetes are allowed to reach term and go into spontaneous labor.
Patients with vascular disease are delivered early if hypertension worsens or if there is FGR,
Factors influencing the timing of delivery are Control of diabetes,condition of cervix ,previous
obstetric history anf fetal compromise.
Delivery is planned at 38 wseeks to avoid unexplained IUD.
29. INDUCTION.
Induction of labor is usually by prostaglandin gel or oxytocin drip
and artificial rupture of membranes.
Protocol used is:
Any patient on long acting insulin should receive the dose of
insulin the night before expected delivery and be admitted to the
ward an evening prior to delivery.
When patient on isulin is in labor,skip morning dose of insulin.
30. ACOG 2018 management during labor
Morning dose of insulin is skipped.
Start intravenous infusion of normal saline.
In active labor or when blood sugar levels drop to 70 mg/dl ,5% dextrose drip
is started at rate of 100-150 ml/hour with the aim of blood glucose at about
100 mg/dl.
Blood glucose levels are chrecked every hour with bedside glucometer to
adjust dose of insulin and dextrose.
Regu;ar insulin is given by intravenous infusion using pump at rate of 1.25
U/hr if glucose levels >100mg/dl.
Sliding scale to be followed.
31. BLOOD GLUCOSE INSULIN DOSE
<100mg/dl No insulin
100-140 1 U/hr(4 units of insulin in 1 litre of 5%
dextrose at 32 drops/min)
140-180 1.5 U/hr(6 units of insulin in 1 litre of 5%
dextrose at 32 drops/min)
180-220 2 U/hr(8 units of insulin in 1 litre of 5%
dextrose at 32 drops/min)
>220 2.5 U/hr(10 units of insulin in 1 litre of 5%
dextrose at 32 drops/min)
32. Antibiotics to be given prophylactically.
In labour,continuous cardiotocography if available should be
performed .
Active management of labor is encouraged.
Instrumental delivery may be required.
Durind delivery of placenta,the insulin infusion rate should be halved
in women who were diabetic pre pregnancy and intravenous insulin
and dextrose is continued until mother eats.
In GDM,insulin may be stopped after delivery,Blood sugars to be
checked every 2-4 hourly for 24 hrs.
33. INDICATIONS OF CESAREAN DELIVERY
Malpresentaions.
Proliferative retinopathy.
Pregnancy complicated by pre eclampsia.
Macrosomia.
Previous caesarean
Fetal distress prior to or during labor.
Bad obstetric history.
Elderly primigravida
HBA1c>6.4%
34. MANAGEMENT IN GDM
The aim is to keep fasting plasma glucose at less than 95 mg/dl and 2 hour ppbs less than 120 mg
/dl.
1. DIET RESTRICTION:recommended daily calorie intake in pregnant women with GDM:
BMI(kg/m2) Calorie intake(kcal/kg/day) Weight gain (kgs)
16.5-18.4 35 11.4-15.9
18.5-24.9 30 11.4-15.9
25-30 22-25 6.8-11.4
>40 12-14 7
ACOG (2017)recommends carbohydrate intake of 40%,protein 20% and fats 40% of total calorie.
35. Exercise:mild to moderate exercises for 30 mins improve insulin sensitivity at
skeletal muscles,which improves glycemic control wich overall reduces insulin
requirement.
Regular monitoring of blood glucose levels is to be done.
Insulin therapy:insulin is the first line of agent for persistent hyperglycemia in
GDM.human insulin therapy is initiated if fasting plasma glucose exceeds 105mg/dl
or 2hours PP exceeds 140 mg/dl despite diet therapy.A total dose of 20-30 units
divided into 2/3rd morning dose while rest 1/3 rd insulin is given at night.
OHA:Usually to be avoided in pregnancy.
Starting dose of Glyburideis 2.5mg orally with morning meal ,increased by 2.5 mg per
week to 10 mg once a day.Later it can be increased to a maximum dose of 10 mg
twice daily,beyond which insulin is started.similarly metformin given for PCOS can be
safely continued .
36. CARE OF NEWBORN
A neonatologist or pediatrician should attend to the new born.
The newborn should be transferred to nursery for 48 hours to manage any
neonatal complications at the earliest.
Baby may be macrosomic and plethoric in poorly controlled diabetes,hence
baby to be carefully examined for APGAR score,any asphyxiaand
congenital malformations.
Baby s blood sugar to be done at birth,1 hour,6 hours,12 hours,24 hours,48
hours and 72 hours as neonatal hypoglycemia is very frequent.
Early and more frequent breast feeding.
Vitamin K1to be given intramuscularly.
37. CONTRACEPTION.
Barrier method is safe and ideal.
Low dose combined OCP,injectable progestogens and IUCD
can be used in women who had GDM.
In overt , low dose OCP to be used with caution.progestogen
only pill can be given.
IUCD was avoided for fear of infection in the past but WHO
recommends it now.
Permanent sterilisation to be done if family is completed.