User:Jsinghal/Complications of pregnancy
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[edit]Gestational diabetes
[edit]Gestational diabetes is when a woman without a history of diabetes develops high blood sugar levels after 20 weeks of pregnancy.[1] There are many non-modifiable and modifiable risk factors that lead to the devopment of this complication. Non-modifiable risk factors include a family history of diabetes, advanced maternal age, and ethnicity. Modifiable risk factors include maternal obesity. There is an elevated demand for insulin during pregnancy which leads to increased insulin production from pancreatic β cells. The elevated demand is a result of increased maternal calorie intake and weight gain, and increased production of prolactin and growth hormone. Gestational diabetes increases risk for further maternal and fetal complications such as development of pre-eclampsia, need for cesarean delivery, preterm delivery, polyhydramnios, macrosomia, shoulder dystocia, fetal hypoglycemia, hyperbilirubinemia, and admission into the neonatal intensive care unit. The increased risk is correlated with the how well the gestational diabetes is controlled during pregnancy with poor control associated with worsened outcomes. A multidisciplinary approach is used to treat gestational diabetes and involves monitoring of blood-glucose levels, nutritional and dietary modifications, lifestyle changes such as increasing physical activity, maternal weight management, and medication such as insulin [2].
Hyperemesis gravidarum
[edit]Hyperemesis gravidarum is the presence of severe and persistent vomiting, causing dehydration and weight loss. It is similar although more severe than the common morning sickness. It is estimated to affect 0.3–3.6% of pregnant women and is the greatest contributor to hospitalizations under 20 weeks of gestation. Most often, nausea and vomiting symptoms during pregnancy resolve in the first trimester, however, some continue to experience symptoms. Hyperemesis gravidarum is diagnosed by the following criteria: greater than 3 vomiting episodes per day, ketonuria, and weight loss of more than 3kg or 5% of body weight. There are several non-modifiable and modifiable risk factors that predispose women to development of this condition such as female fetus, psychiatric illness history, high or low BMI pre-pregnancy, young age, African American or Asian ethnicity, type I diabetes, multiple pregnancies, and history of pregnancy affected by hyperemesis gravidarum. There are currently no known mechanisms for the cause of this condition. This complication can cause nutritional deficiency, low pregnancy weight gain, dehydration, and vitamin, electrolyte, and acid-based disturbances in the mother. It has been shown to cause low birth weight, small gestational age, preterm birth, and poor APGAR scores in the infant. Treatments for this condition focus on preventing harm to the fetus while improving symptoms and commonly include fluid replacement and consumption of small, frequent, bland meals. First-line treatments include ginger and acupuncture. Second-line treatments include vitamin B6 +/- doxylamine, antihistamines, dopamine antagonists, and serotonin antagonists. Third-line treatments include corticosteroids, transdermal clonidine, and gabapentin. Treatments chosen are dependent on severity of symptoms and response to therapies.
Pelvic girdle pain
[edit]Pelvic girdle pain (PGP) disorder is pain in the area between the posterior iliac crest and gluteal fold beginning peri or postpartum caused by instability and limitation of mobility. It is associated with pubic symphysis pain and sometimes radiation of pain down the hips and thighs. For most pregnant individuals, PGP resolves within 3 months following delivery, but for some it can last for years, resulting in a reduced tolerance for weight bearing activities. PGP affects around 45% of individuals during pregnancy: 25% report serious pain and 8% are severely disabled [3]. Risk factors for complication development include multiparity, increased BMI, physically strenuous work, smoking, distress, history of back and pelvic trauma, and previous history of pelvic and lower back pain. This syndrome results from a growing uterus during pregnancy that causes increased stress on the lumbar and pelvic regions of the mother, thereby, resulting in postural changes and reduced lumbopelvic muscle strength leading to pelvic instability and pain. It is unclear whether specific hormones in pregnancy are associated with complication development. PGP can result in poor quality of life, predisposition to chronic pain syndrome, extended leave from work, and psychosocial distress. Many treatment options are available based on symptom severity. Non-invasive treatment options include activity modification, pelvic support garments, analgesia with or without short periods of bed rest, and physiotherapy to increase strength of gluteal and adductor muscles reducing stress on the lumbar spine. Invasive surgical management is considered a last-line treatment if all other treatment modalities have failed and symptoms are severe [4].
Hypothyroidism
[edit]Hypothyroidism (commonly caused by Hashimoto's disease) is an autoimmune disease that affects the thyroid by causing low thyroid hormone levels. Symptoms of hypothyroidism can include low energy, cold intolerance, muscle cramps, constipation, and memory and concentration problems[5]. It is diagnosed by the presence of elevated levels of thyroid stimulation hormone or TSH. Patients with elevated TSH and decreased levels of free thyroxine or T4 are considered to have overt hypothyroidism. While those with elevated TSH and normal levels of free T4 are considered to have subclinical hypothyroidism[6]. Risk factors for developing hypothyroidism during pregnancy include iodine deficiency, history of thyroid disease, visible goiter, hypothyroidism symptoms, family history of thyroid disease, history of type 1 diabetes or autoimmune conditions, and history of infertility or fetal loss. Various hormones during pregnancy affect the thyroid and increase thyroid hormone demand. For example during pregnancy, there is increased urinary iodine excretion as well as increased thyroxine binding globulin and thyroid hormone degradation which all increase thyroid hormone demands [7]. This condition can have a profound effect during pregnancy on the mother and fetus. The infant may be seriously affected and have a variety of birth defects. Complications in the mother and fetus can include pre-eclampsia, anemia, miscarriage, low birth weight, still birth, congestive heart failure, impaired neurointellectual development, and if severe, congenital iodine deficiency syndrome[5][7]. This complication is treated by iodine supplementation, levothyroxine which is a form of thyroid hormone replacement, and close monitoring of thyroid function[7].
Peripartum cardiomyopathy
[edit]Peripartum cardiomyopathy is a heart failure caused by a decrease in left ventricular ejection fraction (LVEF) to <45% which occurs towards the end of pregnancy or a few months postpartum. Symptoms include shortness of breath in various positions and/or with exertion, fatigue, pedal edema, and chest tightness. Risk factors associated with the development of this complication include maternal age over 30 years, multi gestational pregnancy, family history of cardiomyopathy, previous diagnosis of cardiomyopathy, pre-eclampsia, hypertension, and African ancestry. The pathogenesis of peripartum cardiomyopathy is not yet known, however, it is suggested that multifactorial potential causes could include autoimmune processes, viral myocarditis, nutritional deficiencies, and maximal cardiovascular changes during which increase cardiac preload. Peripartum cardiomyopathy can lead to many complications such as cardiopulmonary arrest, pulmonary edema, thromboembolisms, brain injury, and death. Treatment of this condition is very similar to treatment of non-gravid heart failure patients, however, safety of the fetus must be prioritized. For example, for anticoagulation due to increased risk for thromboembolism, low molecular weight heparin which is safe for use during pregnancy is used instead of warfarin which crosses the placenta[8].
Basic Template for subheadings:
1) overview of complication
2) diagnosis criteria
3) risk factors
4) pathogenesis
5) what complications it causes
6) treatments
References
[edit]- ^ "Pregnancy complications". womenshealth.gov. 2016-12-14. Retrieved 2018-11-07.
- ^ Lende, Michelle; Rijhsinghani, Asha (2020-12-21). "Gestational Diabetes: Overview with Emphasis on Medical Management". International Journal of Environmental Research and Public Health. 17 (24): 9573. doi:10.3390/ijerph17249573. ISSN 1660-4601. PMC 7767324. PMID 33371325.
{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ Wu, W. H.; Meijer, O. G.; Uegaki, K.; Mens, J. M. A.; van Dieën, J. H.; Wuisman, P. I. J. M.; Östgaard, H. C. (2004-11). "Pregnancy-related pelvic girdle pain (PPP), I: Terminology, clinical presentation, and prevalence". European Spine Journal. 13 (7): 575–589. doi:10.1007/s00586-003-0615-y. ISSN 0940-6719. PMC 3476662. PMID 15338362.
{{cite journal}}: Check date values in:|date=(help)CS1 maint: PMC format (link) - ^ Walters, Charlotte; West, Simon; Nippita, Tanya A (2018-07-01). "Pelvic girdle pain in pregnancy". Australian Journal of General Practice. 47 (7): 439–443. doi:10.31128/AJGP-01-18-4467.
- ^ a b "Thyroid Disease & Pregnancy | NIDDK". National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved 2022-03-12.
- ^ Sullivan, Scott A. (2019-06). "Hypothyroidism in Pregnancy". Clinical Obstetrics & Gynecology. 62 (2): 308–319. doi:10.1097/GRF.0000000000000432. ISSN 0009-9201.
{{cite journal}}: Check date values in:|date=(help) - ^ a b c Taylor, Peter N.; Lazarus, John H. (2019-09-01). "Hypothyroidism in Pregnancy". Endocrinology and Metabolism Clinics of North America. Pregnancy and Endocrine Disorders. 48 (3): 547–556. doi:10.1016/j.ecl.2019.05.010. ISSN 0889-8529.
- ^ Davis, Melinda B.; Arany, Zolt; McNamara, Dennis M.; Goland, Sorel; Elkayam, Uri (2020-01). "Peripartum Cardiomyopathy". Journal of the American College of Cardiology. 75 (2): 207–221. doi:10.1016/j.jacc.2019.11.014.
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