metabolic condition in obstetrics and gynaecological nursing

Thangamjayarani 881 views 81 slides Jun 18, 2024
Slide 1
Slide 1 of 81
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40
Slide 41
41
Slide 42
42
Slide 43
43
Slide 44
44
Slide 45
45
Slide 46
46
Slide 47
47
Slide 48
48
Slide 49
49
Slide 50
50
Slide 51
51
Slide 52
52
Slide 53
53
Slide 54
54
Slide 55
55
Slide 56
56
Slide 57
57
Slide 58
58
Slide 59
59
Slide 60
60
Slide 61
61
Slide 62
62
Slide 63
63
Slide 64
64
Slide 65
65
Slide 66
66
Slide 67
67
Slide 68
68
Slide 69
69
Slide 70
70
Slide 71
71
Slide 72
72
Slide 73
73
Slide 74
74
Slide 75
75
Slide 76
76
Slide 77
77
Slide 78
78
Slide 79
79
Slide 80
80
Slide 81
81

About This Presentation

OG nursing


Slide Content

METABOLIC CONDITIONS

INTRODUCTION Total metabolism is increased due to the needs of the growing uterus and the foetus. Basal metabolic rate is increased to the extent of 30% higher that of the averages for the non pregnant women. Early gestation can be viewed as an anabolic state in the mother with an increased in insulin sensitivity. In the second half of gestation the rapid foetal growth and the higher cardiovascular and respiratory work increase basal metabolic work.

DEFINITION: METABOLISM Metabolism is the chemical reaction in the body cell that change food into energy. METABOLIC CHANGES DURING PREGNANCY : Total metabolism is increased due to the needs of growing fetus and the uterus. It increased to the extent of 30% higher than that of the average for the non pregnant women.

PROTIEN METABOLISM There is a positive nitrogenous balance throughout pregnancy On average, 500 gm protein retained by the end of pregnancy As the breakdown of amino acids to urea is suppressed, the blood urea levels falls 15.20 mg %. Blood uric acid and creatinine level either unchanged or fall slightly. Amino acids actively transported across the placenta to fetus . Pregnancy is an anabolic state.

The recommended protein during pregnancy I Trimester – 46g/day II & III trimester – 71g/day Protein deficiency during pregnancy Poor growth - IUGR Muscular weakness Poor hair growth

CONTD., Low serum albumin which result in edema Embryonic loss Reduced postnatal growth Protein increase during pregnancy Preeclampsia Kidney disease

CARBOHYDRATE METABOLISM Transfer increased amount of glucose from mother to the fetus is needed throughout pregnancy. Insulin secretion is increased (hyperplasia and hypertrophy of beta cells of pancreas) Sensitivity to insulin is decreased. Plasma insulin increased, thus ensures continuous supply of glucose to fetus .

Increased in insulin secretion also favours lipogenesis (fat storage). During maternal fasting, there is hypoglycaemia, hyperinsulinemia and hyperlipidaemia. Lipolysis takes action and generates fatty acids for gluconeogenesis and fuel supply. Effects Diet that reduced carb were 30% more likely to have babies with neural tube defects. Gestational diabetic mellitus

FAT METABOLISM An average of 3-4 kgs of fat is stored during pregnancy, mostly in the abdominal wall, breast, hip and thigh. Lipids and lipoproteins increase appreciably during the later half of pregnancy due to increased oestrogen, progesterone, HPL and Leptin levels. Fat affect pregnancy – Over weight during pregnancy increase the chance of preterm birth, still birth. Baby: Neural tube defect.

LIPID METABOLISM HDL level increases by 15%, LDL is utilised for placental steroid synthesis. This hyperlipidaemia normal pregnancy is not atherogenic. The activity of lipoprotein lipase is increased changes in the lipid components are tableted below,

NON PREGNANT PREGNANCY NEAR TERM CHANGE Total lipid (mg/100ml) 650 1000 +50% LDL and cholesterol (mg/100ml) 180 260 +40% HDL (mg/100ml) 60 70 +15% Triglycerides (mg/100ml) 80 160 +50%

IRON METABOLISM Total iron requirement during pregnancy is estimated 1000mg. The amount of the iron absorbed from the diet and that mobilized from the store is inadequate to meet the demand. Absorption through the gut is enhanced during pregnancy. Absence of iron supplementation can cause drop in hemoglobin, serum iron and serum ferritin concentration. Placenta transfers adequate iron to the fetus, despite severe maternal iron deficiency

CALCIUM METABOLISM CALCIUM METABOLISM AND SKELETAL CHANGES: Increased demand of Ca by the growing fetus to the extent of 28 g. Daily requirement of calcium is about 1-1.5 g. Ca absorption from intestine and kidneys are doubled due to rise in level 1,25 dihydroxy cholecalciferol Relaxation of pelvic ligaments and muscles occurs because of the influence of estrogen and relaxin reaches maximum during last weeks of the pregnancy

Increased lumber lordosis during later months of the pregnancy due to enlarged uterus produces backache and wadding gait. Abnormal; Hypercalcemia- IUGR Hypocalcemia Pre eclampsia, LBW, Preterm delivery. Neonatal death

WATER METABOLISM During early months of pregnancy there is marked diuresis, sweating and a weight loss of approximately 2.5 kgs. During later months (5-6 month onwards) of pregnancy excess of water is retained in the fetus, placenta, amniotic fluid, breast, uterus and other tissues. The retention of water is due to fall in plasma protein concentration. Retention of sodium due to steroidal sex hormones.

METABOLIC DISORDERS HYPER AND HYPOTHYROIDISM PHENYL KETONURIA DIABETIC MELLITUS OBESITY HYPEREMESIS GRAVINDARUM

HYPEREMESIS GRAVINDARUM Hyperemesis gravindarum can lead to weight loss, dehydration, hyponatremia, hypokalaemia, alkalosis and in severe cases metabolic acidosis. It may lead to severe metabolic abnormalities including acute kidney injury (AIC) and electrolyte and acid base disturbance.

HYPER AND HYPOTHYROIDISM HYPOTHYROIDISM: The pregnancy related hormones human chorionic gonadotropin (HCG) and oestrogen cause increased thyroid hormone leads in the blood. Auto immune thyroiditis is the commonest causes of hypothyroidism during pregnancy.

HYPERTHYROIDISM: Physiological changes to pregnancy such as increase in cardiac output, oxygen consumption and heat production, many mimic mild thyrotoxicosis. Autoimmune hyperthyroidism due to thyroid stimulating antibodies is the commonest cause. Other causes are toxic nodular goiter and trophoblastic disease. Hyperemesis gravidarum may be associated with hyperthyroidism.

PHENYLKETONURIA Phenylketonuria (PKU) is a rare autosomal recessive metabolic disorder characterised by the body’s inability to utilize the essential amino acid phenylalanine Untreated and poorly controlled phenylamine level are associated with IUGR and other fetal abnormalities ( mental retardation, congenital heart disease).

OBESITY Cause: Over weight and obesity before conception. Excess food intake Lack of physical activity , genetics and medicines. EFFECTS: For mother Gestational hypertension- High blood pressure that starts during the second half of pregnancy is called gestational hypertension. Overweight in pregnancy increasing chances are in relation to: miscarriage. gestational diabetes. high blood pressure and pre-eclampsia. For Baby : Birth defect such as CHD and neural tube defect.

DIABETIC MELLITUS IN PREGNANCY DEFINITION: Diabetes mellitus is a chronic metabolic disorder due to either insulin deficiency or due to peripheral tissue resistance to the action of insulin. INCIDENCE 1-4% of all pregnancies are complicated by diabetic mellitus 90% of them are gestational diabetic mellitus 50% of women with GDM will became overt diabetics (type 2) over a period of 5-20 years

CLASSIFICATION Type I – IDDM Is a characterised by young age onset (juvenile) and absolute insulinopenia . Type II – NDDM Is a characterised by late age onset, overweight women and peripheral tissue insulin resistance. Genetic predisposition is also observed. Type III – GESTATIONAL DIABETES MELLITUS During pregnancy in which carbohydrate intolerance that developed during pregnancy, regardless of severity. Overt diabetes : Mother with symptoms of diabetic mellitus & casual glucose concentration 200mg/dl or more

GESTATIONAL DIABETES

GESTATIONAL DIABETES MELLITUS DEFINITION: The term includes cases with abnormal carbohydrate tolerance with onset or first detected during the present pregnancy. Risk factors positive family history of diabetes Having previous birth of overweight baby of 4kg or more. Previous still birth with pancreatic islet hyperplasia revealed on autopsy Unexplained perinatal loss.

Presence of polyhydramnios or recurrent vaginal candidiasis in present pregnancy. Persistent glycosuria Age over 30 Obesity Ethnic group (East Asian, Pacific island ancestry)

SCREENING

SCREENING ROUTINE SCREENING: Maternal history collection Physical examination Laboratory tests Routine prenatal blood test Liver function test Thyroid function test Glycosylated haemoglobin

FETAL: Ultrasonography FOR RISK: Foetal kick counts FHR CST Biophysical profile Screening strategy for detection of GDM are Low risk Average risk High risk

Low risk: Absence of any risk factors as mentioned above routinely required glucose tolerance test . Average Risk: Some risk factors perform screening test. High Risk: Blood glucose test as soon as feasible.

Time Mg/dl m.mol /L Fasting 95 5.3 1 hour 180 10.0 2 hours 155 8.6 3 hours 140 7.8 GDM is diagnosed when any two values are met or elevated. Criteria for diagnosis of GDM with underground coral glucose (O’ Sullivan Mohan modified by Carpenter and Coustan ) Table I GTT: Venous plasma (mg/dl)

Table II Criteria for diagnosis of impaired glucose tolerance and diabetes with 75 gm oral glucose (American diabetic association) Venous whole blood value 15% then the plasma. M mol/l.mg% x 0.0555 Plasma (mg%) Time Normal tolerance Impaired glucose tolerance Diabetes Fasting <110 >110 and <126 >126 2 hours post glucose <140 >140 and <200 >200

An excellent screening test is to obtain plasma glucose level one hour after a 50 g glucose load administered at any time of the day without regard to the time since the last meal. It is a well validated and widely applied screening procedure for women between 24 - 28 weeks of gestation. Cut-off value > 140 mg/dl identifies 80% women with GDM Cut-off value > 130 mg/dl identifies 90% women with GDM. GLUCOSE CHALLENGE TEST

PATHOPHYSIOLOGY Fetoplacental hormone(Progesterone, oestrogen Cortisol, Prolactin, HPL) Increased insulin resistance Compensatory increase in insulin secretion Pancreas Insulin Normal pregnancy Hormone produced by placenta Increased sugar level Gestational diabetes To counteract Leading to Unable to produce enough

OVERT DIABETES A patient with symptoms of diabetes mellitus and casual plasma glucose concentration 200mg / dL or more is considered overt diabetic. The condition may be pre-existing or detected for the first time during present pregnancy. According to American Diabetic Association diagnosis is positive if the fasting plasma glucose exceeds 126 mg/dl the 2 hour post glucose (75 gm) value exceeds 200mg / dl

CLASSIFICATION Fetal and maternal outcome of diabetic pregnancy depends on severity of the disease and its duration. Priscilla White's classification was originally used to assess the perinatal outcome and to formulate the obstetric management. Patients with poor glycemic control and vasculopathy are at increased risk of complication like IUD, IUGR, Pre-eclampsia and Ketoacidosis.

WHITE’S CLASSIFICATION OF PREGNANT DIABETIC WOMEN CLASS AGE OF ONSET, DURATION (YEARS), VASCULAR DISEASE, INSULIN NEED A Gestational diabetes, Any age onset or duration A1: Managed by diet alone; A2: Insulin needed B Onset at age > 20, Duration < 10, No vascular disease, Insulin - needed. C Onset at age 10-19, Duration 10-19, No vascular disease, Insulin needed D Onset at age < 10, Duration > 20 , Vascular disease present, Insulin needed. F Any age onset or duration, Nephropathy, Insulin needed. R Any age onset or duration, Proliferative retinopathy, Insulin needed. H Any age onset or duration, coronary artery disease (heart), Insulin needed. T Any age onset or duration, Renal transplant, Insulin needed.

EFFECTS OF DIABETES ON PREGNANCY Complications of diabetes: Maternal Fetal MATERNAL - During pregnancy: Abortion - Uncontrolled diabetes. Preterm labor - due to infection or polyhydramnios. Infection - specially urinary tract infection. Increased incidence of pre-eclampsia (25%) is associated even in absence of vascular lesion.

Polyhydramnios (25-50%) is a common association. Large baby, large placenta, fetal hyperglycemia leading to polyuria, increased glucose concentration of liquor irritating the amniotic epithelium or increased osmosis, are some of the probabilities. Maternal distress may be due to the combined effects of an oversized fetus and polyhydramnios. Diabetic retinopathy microaneurysms, hemorrhages and proliferative retinopathy are related to duration of diabetes as well as with glycemic control. Diabetic nephropathy - may lead to renal failure. Ketoacidosis

DURING/LABOUR There is increased incidence of: (1) Prolongation of labor due to big baby. (2) Shoulder dystocia - Shoulder dystocia is due to disproportionate growth with increased shoulder/head ratio (3) Perineal injuries. (4) Postpartum hemorrhage. (5) Operative interference.

PUERPERIUM: (1) Puerperal sepsis. (2) Lactation failure.

FETAL HAZARDS Foetal macrosomia (30-40%) probably results from : (a) Maternal hyperglycaemia Hypertrophy & Hyperplasia of the foetal islets of Langerhans Increased secretion of foetal insulin Stimulate carbohydrate utilisation and accumulation of fat involved insulin like growth factors (IGF-I and II) Foetal macrosomia

(b) Elevation of maternal free fatty acid (FFA) In diabetes leads to its increase transfer to their fetus Acceleration of triglyceride synthesis Adiposity

CONGENITAL MALFORMATION Is related to the severity of diabetes affecting organogenesis, in the first trimester. The proposed factors associated with teratogenesis are: (a)Genetic susceptibility. (b) Hyperglycemia. (c) Arachidonic acid deficiency. (d) Ketone body excess. (e) Somatomedin inhibition. (f)Free oxygen radical excess

MAJOR BIRTH DEFECTS IN INFANTS OF DIABETIC MOTHERS CNS and skeletal: Neural tube defects Anencephaly Microcephaly Sacral agenesis

Cardiac VSD, ASD Coarctation of aorta Transposition of great vessels Cardiomegaly

Renal Renal agenesis Hydronephrosis Ureteral duplication Gastrointestinal Duodenal atresia Anorectal atresia Others Single umbilical artery

EARLY DETECTION OF FETAL ANOMALIES Estimation of glycosylated haemoglobin A (HbA1c) before 14 weeks reflect the quality of diabetic control over the previous 3 months. Overall risk of fetal malformations are increased when the level of HbAIc is high (normal < 8 percent). Maternal serum a fetoprotein level at 16 weeks and a detailed high resolution ultrasonography of the fetus including fetal echocardiography at 20-22 weeks are advocated.

Birth injuries (brachial plexus) are associated with prolonged labour and shoulder dystocia due to macrosomic baby. Fetal hazards: Growth restriction is less commonly observed and is associated with maternal vasculopathy. Unexplained fetal death: Due to hypoxia and lactic acidemia. It is observed more in patients with poor glycemic control, vasculopathy, pre eclampsia, ketoacidosis and fetal macrosomia. Fetal hyperglycemia and hyper insulinemia increase fetal oxygen demand & fetal polycythemia, hyper viscosity.

NEONATAL COMPLICATIONS INCLUDE (a) Hypoglycaemia (b) Respiratory distress syndrome (c) Hyperbilirubinemia (d) Polycythaemia (e) Hypocalcaemia (f) Hypomagnesemia (g) Cardiomyopathy.

PERINATAL MORTALITY Perinatal mortality is increased 2-3 times. The neonatal deaths are principally due to hypoglycemia, respiratory distress syndrome, polycythemia and jaundice.

MANAGEMENT Pre-conceptional counselling : Goal is to achieve tight control of diabetes before the onset of pregnancy. Fetal congenital anomalies or malformations are significantly low (0.8-2%) in women who received pre-conceptional counselling. Women taught for self glucose monitoring. Appropriate advice about diet and insulin is given.

PRINCIPLES IN THE MANAGEMENT (1) Careful antenatal supervision and control of the diabetes, so as to maintain the glucose level as near to physiological level as possible. (2) To find out the optimum time and method of delivery. (3) Arrangement for the care of the newborn.

ANTENATAL CARE Antenatal supervision should be at monthly intervals up to 20 weeks and thereafter 2 weeks intervals. At times patient needs admission for stabilization of blood glucose and for monitoring the fetus. The daily calorie requirement is about 30-35 K Cal per kg of body weight. Diet should come carbohydrate 50%, protein 20% and fat 25-30%. Fat may be curtailed, if the patient is obese. Fiber containing diet is increased. Frequent blood sugar estimation is required.

Sonographic evaluation pregnancy (at 4-6 weeks interval) is extremely helpful, not only to diagnose varieties of congenital malformation of fetus but also to detect fetal macrosomia or growth restriction (rare). Assessment of fetal well being is to be made from 28 weeks onwards Biophysical profile (twice weekly) should be performed when there is abnormal NST Doppler umbilical artery velocimetry is useful in cases with vasculopathy.

INSULIN THERAPY Diabetes is first detected during pregnancy and cannot be controlled by diet alone it should be treated with insulin A post prandial plasma glucose level of more than 140 mg% even on diet control is an indication of insulin therapy. Glycemic goals should be around 90 mg/dl before meals and not to exceed 120 mg/dl. 2 hours after meals During the stabilization process of the insulin dose, frequent blood sugar estimation specially at night may be recovery using glucose meter

A pregnancy advances, "a double mixed regime" may be employed. The mother should receive three to four daily injections of a regular and an intermediate acting insulin (isophane), the latter is to be given before dinner. The aim is to maintain the blood sugar level as near to normal as possible without causing troublesome hypoglycemia. Oral antidiabetic drugs are avoided during pregnancy. These drugs cross the placenta and may have teratogenic effect or produce neonatal hypoglycemia

ADMISSION In uncomplicated cases, the patient is admitted at 34-36 weeks. Early hospitalization facilities: (1) Stabilization of diabetes (2) Minimizes the incidence of pre-eclampsia, polyhydramnios and preterm labor. (3) To select out the appropriate time and method of delivery.

TERMINATION OF PREGNANCY The termination should be done after 37 completed weeks. Facilities of an equipped neonatal care unit should be available. Early delivery maybe considered when there is vascular complication (hypertension) or evidences of fetal compromise on antepartum monitoring.

INDUCTION OF LABOUR The indications are (1) Multipara with a good obstetric history. (2) Young primigravidae without any obstetric abnormality. (3) Presence of congenital malformation of the fetus.

CAESAREAN SECTION The indications are: Elderly primigravida Multigravida with a bad obstetric history Diabetes with complications or difficult to control. Obstetric complications like pre-eclampsia, polyhydramnios, malpresentation. Fetal macrosomia (> 4 kg) As such 50% of diabetic mothers are delivered by caesarean section.

PLACE OF AWAITING SPONTANEOUS ONSET OF LABOUR AT TERM Young primigravidae or multipara with good obstetric history Diabetes well controlled either by diet or insulin with good obstetric history Fetal monitoring: Constant watch to note the fetal condition is mandatory, preferably with continuous electronic fetal monitoring. Fetal scalp blood pH sampling is done whenever indicated.

Labour should not be allowed for more than an arbitrary 12 hours and should be augmented by low rupture the membranes and oxytocin or delivered by Caesarean section. Shoulder dystocia may be a problem. The cord should be clamped immediately after delivery to avoid hypervolemia. Examination of the placenta and cord: Placenta is large, the cord is thick and there is increased incidence of a single artery. Microscopically, villi show oedema and excessive syncytial knots, numerous cytotrophoblasts and thickened basement membrane.

DIABETIC KETOACIDOSIS Pathology is insulin resistance → lipolysis enhanced ketogenesis → fall in plasma HCO3 and PH < 7.30 It may be precipitated with the use of ẞ mimetic agents ( Isoxuprine ) and corticosteroids.

MANAGEMENT Is done in an acute care unit. Parameters to assess are : degree of acidosis, alterations in the level of arterial blood gas, blood glucose, ketones and electrolytes. IV Insulin 0.2 - 0.4 units/kg (loading dose) 2.0 – 10.0 units/h (maintenance with frequent capillary glucose measurement). Fluids -Isotonic Nacl 4-6 L in first 12 hours. 5% Dextrose in normal saline when blood glucose is 200mg /dl Potassium : if reduced or normal - infusion 15-20mEq /h Bicarbonate : if PH < 7.10 add 44 mEq to IL of 0.45 normal saline.

PUERPERIUM Antibiotics should be given prophylactically to minimize infection. Insulin requirement falls traumatically following delivery. She is to revert to the insulin regime as was prior to pregnancy. A fresh blood glucose level after 24 hours will help to adjust the dose of insulin. Women who breast feed should have additional 500 Kcal daily in diet. In lactating women insulin dose is lower.

CARE OF THE BABY A neonatologist should be present at the time of delivery. The baby should preferably kept in a neonatal care unit and to remain vigilant for at least 48 hours, to detect and to treat electively any complication likely to arise. Asphyxia is anticipated and be treated effectively. To look for any congenital malformation.

All babies should have blood glucose checked within 2 hours of birth. All babies should receive 1 mg vitamin K intramuscularly. Early breast feeding within 1/2 - 1 hour is advocated and to be repeated at three to 4 th hourly intervals thereafter to minimize hypoglycemia and hyperbilirubinemia.

CONTRACEPTION Barrier method of contraceptives is ideal for spacing of births. Low dose combined pills containing third generation progestins are effective and have got minimal effect on carbohydrate metabolism. Progestin only pill is suitable alternative. The IUCD is avoided for fear of pelvic infection. Permanent stabilization is considered when family is completed.

SUMMARY So far, we have discussed metabolic changes, types of metabolic condition, definition of diabetic mellitus, incidence, classification, risk factors, pathophysiology, effects of diabetes in pregnancy, investigations, management of diabetes in pregnancy.

CONCLUSION Metabolic condition are crucial for the proper development of fetus . Diverse biomolecules including glucose, fatty acids, cholesterol, ketone bodies and hormones maintain proper balance in these metabolic adaptations during pregnancy.

THEORY APPLICATION GENERAL SYSTEM THEORY INPUT The student lack of knowledge regarding Metabolic conditions. THROUGH PUT Taking lecture class on Metabolic conditions. OUTPUT The students gain knowledge regarding Metabolic conditions. FEED BACK

JOURNAL APPLICATION AUTHOR: Solanga dabou (2021) Conducted a cross sectional steady to determine the prevalence and determinants of metabolic syndrome among pregnant women at the Dschang district hospital in the West region of Cameron. A sample of 604 pregnant women was considered. The Study revealed that the metabolic syndrome was 17.88% low level of HDL Cholesterol 66.23% and hypertriglyceridemia 28%. Grand multiparous shows higher risk of presenting metabolic syndrome compared to nulliparous shows higher risk of presenting metabolic syndrome on pregnant women in the Dschang Health District is 17.88% and its major determinants is pre gestational obesity.

ASSIGNMENT Write an assignment on effect of diabetes mellitus on pregnancy.

BIBLIOGRAPHY: Dutta. D.C. (2004) Text book of obstetrics 6 th edition. New central book agency, Calcutta. Bhaskar Nima (2012) midwifery and obstetrical nursing Bangalore EMMESS medical publishers. Jacob Annamma (2015) A comprehensive Text book of Midwifery & Gynaecological nursing. Fourth edition New Delhi Jaypee Brothers Medical publishers (P) Ltd. Neelam kumari (2011) A text book of midwifery and gynaecological nursing S. Vikes & company medical publishers, Jalendhar city. http://www.bmj.com/ on 22 jan 2022.
Tags