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Obesity in O&G Practice

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    1. Height and weight indices
      • Height and weight tables
      • Ponderal index— square of height divided by cube root of weight
      • Body mass index (BMI)/Quetelet index= body weight in kg divided by square of the height in meter. Normal range is 18.5—24.9 kg/m2.
      • These do not consider lean body mass.
    2. Subscapular and triceps skin fold thickness greater than the standard by 20% or more.
    3. Empirical definitions
      • Weight greater than 90kg in pregnancy regardless of pre-pregnancy weight and height
      • Morbid obesity- weight greater than 115 kg

    Edema

    Hypertensive disease of pregnancy

    DM

    Difficulty in abdominal palpation

    Difficulty in auscultation of the fetal heart

    Macrosomia- shoulder dystocia, traumatic delivery, and birth asphyxia

    Post-term pregnancy

    Increased indications for induction of labor due to prolonged pregnancy or medical disorders.

    Potential technical problems in managing obese mothers

    • Difficult to use ultrasonography accurately to date pregnancy or detect fetal anomalies
    • Large cuffs required to measure blood pressure accurately
    • Woman may have reduced awareness of fetal movements
    • Prolonged labor due to macrosomia, uterine inertia
    • Perinatal mortality and morbidity
    • Higher risk of cesarean deliveries
    • Failure of lactation
    • Thromboembolism
    • Urinary tract infection
    • Postpartum hemorrhage
    • Wound complications- wound sepsis, wound dehiscence, burst abdomen
    • External electronic fetal monitoring can be problematic
    • Surgery is technically difficult, requiring more assistants or larger operating table
    • Regional and general anesthesia can be challenging
    • Wound care can be compromised in the event of cesarean section.

    • Overweight = 25—29.9 kg/m2
    • Class I = 30—34.9
    • Class II = 35—39.9
    • Class III = 40 or more

    Effects span the female reproductive career i.e. from menarche to menopause.

    There is a positive correlation between body mass index (BMI) and increased rate of hirsuitism, cycle disturbance, and infertility.

    These effects include—

    • Hirsutism
    • Amenorrhoea
    • Menstrual irregularities
    • Anovulation
    • Infertility
    • Miscarriages
    • Post-menopausal carcinomas

    It is associated with

    • Early onset of puberty
    • Menstrual irregularities during adolescence and
    • Polycystic ovary syndrome

    The impact of body fat distribution on miscarriage rates appears to warrant pre- conceptual advice concerning weight loss.

    The presence of obesity, and the related hyperinsulinemia is thought to be responsible for early pregnancy loss.

    Miscarriages

    The impact of body fat distribution on miscarriage rates appears to warrant pre- conceptual advice concerning weight loss.

    The presence of obesity, and the related hyperinsulinemia is thought to be responsible for early pregnancy loss.

    Polycystic ovary (PCO) syndrome was initially described by Stein and Leventhal in 1935 as a syndrome of

    • Obesity
    • Hirsuitism
    • Anovulation and infertility, and associated with
    • Enlarged and polycystic ovaries.

    PCOS may be an incidental finding on a routine ultrasound scan in a woman of normal weight with regular menstrual cycles.

    The principal abnormality in women with PCOS is one of anovulation manifested by oligomenorrhea or secondary amenorrhea.

    Diagnostic criteria

    Accepted criteria describe ovarian morphology with more than 10 peripheral cysts in a single plane, sized between 2-8 mm, arranged in an echodense stroma.

    This sonographic appearance of PCO may occur together, or in isolation with a biochemical imbalance, which classically involves metabolic and hormonal changes.

    Biochemical indicators of syndrome

    Concentrations of luteinizing hormone (LH) are elevated in 45-75% of cases in a reported series, and a raised testosterone is seen in 80% of patients.

    Features of Polycystic Ovary Syndrome

    • Polycystic ovaries on ultrasonography
    • Menstrual disturbances (amenorrhea, oligomenorrhea)
    • Acne, acanthosis nigricans, hirsutism
    • Obesity, central fat distribution
    • Infertility
    • Glucose intolerance, diabetes mellitus
    • Increased circulating androgen levels
    • Insulin resistance, increased luteinizing hormone

    Etiopathogenesis

    The etiology of polycystic ovaries has long remained elusive, and there is increasing evidence that the primary abnormality is excessive ovarian androgen production.

    Obesity has consistently been shown to increase the prevalence of hirsuitism and anovulation when compared to lean women with PCOS.

    Hyperinsulinemia due to insulin resistance

    In obese women, hyperinsulinemia is a secondary disorder, resulting in a decrease in and IGFBP-1 levels SHBG (insulin inhibit their synthesis in the liver), creating an increase in free androgens, which are in turn converted to estrone due to the excessive adipose tissue.

    Obese women produce more estrogen by extraglandular conversion of androgens than do non-obese subjects and, therefore, have a greater excess circulating estrone over estradiol concentrations than lean women.

    Secondly, as concentrations of SHBG are much lower in obese women, there is an increased free biologically active fraction of estradiol (SHBG transports androgens and estrogens in the blood and regulate their access to target tissue).

    Therapeutic weight loss has been found to improve the symptoms and endocrine profile of women with PCOS.

    Encourage lifestyle modifications

    Thereafter, consider ovulation induction if patient desires contraception

    Progestogens may be offered every two months to ensure endometrial shedding in those with oligomenorrhea

    Consider Mirena and screening for endometrial hyperplasia.

    Laboratory Tests

    • Glucose tolerance
    • Lipid profile
    • Androgens (testosterone, free testosterone)
    • Prolactin and LH
    • FSH and thyroid hormones
    • Ovarian ultrasonography

    Breast cancer and endometrial cancer are increased by long term estrogen replacement therapy. The incidence of endometrial carcinoma is increased in women who are obese, nulliparous and infertile.

    The increased peripheral conversion of androgens to estrogens, and the resultant effect of the unopposed estrogen upon the endometrium is thought to be responsible.

    The cancer most frequently associated with obesity is that of the endometrium. The risk of endometrial cancer is 2-3 times higher in overweight and obese women.

    Obesity also adversely affects survival in most studies.

    With regard to ovarian cancer the evidence is inconsistent.

    Risks for postmenopausal breast cancer have been identified as obesity, late age at menopause, a family history of breast disease and an early age at menarche.

    There is increased risk of thrombosis and coronary heart disease in the obese at menopause.

    Obesity protects against osteoporosis.

    Obesity can aggravate symptoms of pelvic organ prolapse, stress urinary incontinence and increase the risk of endometrial polyps and symptomatic fibroids.

    Reduce calorie intake to < 1000kcal/day to achieve weight loss of 5-10% in the non-pregnant obese.

    Use of insulin sensitizers.

    Regular antenatal screening for glucose intolerance, hypertension, macrosomia and excessive weight gain should be routine in the obese pregnant women.

    Weight loss not recommended in pregnancy, gain should be restricted.

    Weight loss postpartum must also be encouraged

    Daily exercise of moderate intensity in combination with diet is better than either alone.

    Modification of lifestyle.

    Weight loss drugs - limited because of side effects and does not achieve attainment of normal body weight.

    Ideal diet

    • Carbohydrate -50%
    • Protein- 15-20%
    • Fat- <30%

    Weight loss Drugs.

    • Amphetamine related drugs e.g. phentermine, phendimetrazine, benzphentamine
    • Serotonin and norepinepherine reuptake inhibitor e.g sibutramine
    • Sertonergic agent e.g. fluoxetine
    • Lipase inhibitor e.g. orlistat
    • Cannabinoid receptor agonist e.g. rimonabant

    Preconceptional care

    Obese women should receive pre-pregnancy counselling (via clinics for sub-fertility, recurrent miscarriage, or diabetes; via obstetric pre-pregnancy clinics; or via a general practitioner) and folic acid.

    Encourage obese women to lose weight before conceiving, and use contraception while aiming for target weight (fertility rises as BMI decreases).

    Advise on the importance of healthy diet and exercise and the need to avoid excessive weight gain (refer to dietician if necessary)

    During ANC

    Avoid weigh reduction and excessive weight gain

    Screen for medical conditions

    Fetal surveillance with obstetric USS

    Consider low dose aspirin in the presence of additional risk factors (obesity is associated with increased risk of pre-eclampsia); assess thrombosis risk and provide thromboprophylaxis if needed.

    Recommend detailed anomaly scan and serum screening for congenital abnormality.

    During labor

    Close fetal monitoring using the cardiotocograph

    Fetal weight estimation

    Evaluate for cephalopelvic disproportion and prepare for shoulder dystocia.

    Surgeries

    Bariatric surgeries

    • Gastric banding
    • Sleeve gastrectomy
    • Gastric bypass
    • Duodenal switch

    Surgical risk from obesity in gynecology

    • Infection
    • Thromboembolism
    • Surgical difficulty
    • Failure to complete surgery
    • Bleeding
    • Organ damage
    • Anesthetic problems
    • Cannulation
    • Airway and ventilation
    • Lifting and moving the woman
    • Analgesia
    • Nausea and vomiting

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