9 1 2 Weeks Book Pdf PORTABLE

9 1 2 Weeks Book Pdf PORTABLE

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Involution, a part of postpartum physiology, is the term given to the process of reproductive organs returning to their prepregnant state. Immediately following the delivery, the uterus, and the placental site contracts rapidly to prevent further blood loss. This rapid uterine contraction can lead to abdominal pain or cramps after childbirth. At this point, the uterus has an increased tone, feels firm, and weighs 1000 gms, and at the end of the first week, it weighs 500 gms, and by six weeks, it weighs approximately 50 gms. The female may complain. Initially, the contraction of the uterus is due to a substantial reduction in myometrial cell size; it constricts the blood vessels and limits the bleeding. The subsequent decrease in size is due to autolysis and infarction of uterine blood vessels.[10][11][12] The withdrawal of estrogen and progesterone leads to an increase in the activity of uterine collagenase and other proteolytic enzymes, accelerating the process of autolysis.[13] The intima and elastic tissues in the uterine blood vessels also undergo fibrosis and hyaline degeneration, leading to infarction and shedding of more uterine cells, which are removed by macrophages. The superficial and basal layers of the endometrium become necrotic and sloughed.[14] The endometrium is usually fully restored within 2 to 3 weeks.[15]

The lochia is the vaginal discharge that originates from the uterus, cervix, and vagina. The lochia is initially red and comprised of blood and fragments of decidua, endometrial tissues, and mucus and lasts 1 to 4 days. The lochia then changes color to yellowish or pale brown, lasting 5 to 9 days, and is comprised mainly of blood, mucus, and leucocytes. Finally, the lochia is white and contains mostly mucus, lasting up to 10 to 14 days. The lochia can persist up to 5 weeks postpartum. The persistence of red lochia beyond one week might be an indicator of uterine subinvolution. The presence of an offensive odor or large pieces of tissue or blood clots in lochia or the absence of lochia might be a sign of infection.[16][17][18] The cervix and vagina may be edematous and bruised in the early postpartum period and gradually heal back to normal.[19]

Once the ovarian function resumes, rugae start to appear in the vagina, usually by the third week in females that are not breastfeeding. Similarly, the postpartum vaginal epithelium, which appears atrophic under the microscopic exam, is restored in 6 to 10 weeks, but the recovery delays in breastfeeding females due to low estrogen levels. The patient may develop perineal edema, lacerations, tears, or undergo an episiotomy in the immediate postpartum period that may lead to discomfort and pain.[20][21]

The onset of the first menstrual period following delivery is variable and depends if the mother is lactating or not. If the mother is not breastfeeding, then the menstrual function returns by the sixth to eighth week postpartum in most of the cases. The duration of anovulation depends on the frequency and intensity of breastfeeding and is attributed to high serum prolactin levels associated with suckling.[24] Elevated serum prolactin levels inhibit the ovarian response to the follicular stimulating hormone, suppress the release of luteinizing hormone, suppressing the secretion of gonadotropins even further. This approach offers a natural method of contraception to the lactating female. In lactating females, menstruation usually reappears in 4 to 5 months, and in some cases, can be as late as 24 months. However, ovulation can commence in the absence of menstruation, and pregnancy can occur.[25][26][27] Non-lactating mothers should use contraceptive measures after three weeks, and lactating mothers after three months of delivery.[28] The level of human chorionic gonadotropin that mimics stimulating thyroid hormone falls dramatically after delivery. Consequently, the thyroid gland volume regresses to the pre-pregnant state by 12 weeks, and the thyroid function returns to normal by four weeks postpartum.[29][30] The diabetogenic effects of pregnancy are due to the production of placental insulinase, corticotropin-releasing hormone, and human placental lactogen.[31] The insulin sensitivity begins to increase after delivery and becomes restored within 2 to 3 days following delivery.[32] However, in obese females, postpartum normalization of insulin sensitivity may take 15 to 16 weeks.[33]

The bladder wall may become edematous, hyperemic, and the bladder might be overdistended without the urge to pass urine.[34] The retention of urine in the first few days after labor may be due to the laxity of the abdominal musculature, tone of pelvic floor muscles, atony of bladder, compression of urethra by edema or hematoma, reflex inhibition of micturition due to genitourinary trauma.[35][1][35] Conversely, urinary incontinence, especially urge incontinence, affects 30% of postpartum females and is attributed most commonly to psychological stress associated with childbirth.[36] The mother may complain of painful micturition or dysuria that could be due to tears, laceration of the cervix or vagina, or episiotomy. During pregnancy, the compressive forces of the gravid uterus and the progesterone-induced decrease in ureteral tone, peristalsis, and contraction pressure lead to the dilation of the calyceal system, increasing the volume of kidneys by 30% from the pre-pregnant state.[37][38][37] The dilated ureters and renal pelvis usually return to the pre-pregnant state within four-eight weeks. There is an increased risk of developing urinary tract infections. It is important to counsel the mother to void every 3 to 4 hours.[39]

There is a shift of fluid from extravascular to intravascular space, corresponding to 6 to 8 liters of total body water. Furthermore, the persistent activity of the renin-angiotensin-aldosterone system (RAAS) during pregnancy leads to an excess of 950 mEq of sodium.[40] In the postpartum period, there is increased serum levels of the atrial natriuretic peptide (1.5 times normal) that inhibits aldosterone, angiotensin II and vasopressin and promotes urinary sodium excretion. There is brisk diuresis in the first two weeks after childbirth, and it is not uncommon to have a urinary output of 3000 cc/day. The amount of loss is usually in line with the amount of fluid retained during pregnancy. The glomerular filtration rate returns to baseline at eight weeks postpartum.[39] Lactosuria is not uncommon on the third or fourth day of the start of lactation.[41]

The hematocrit may initially drop due to blood loss associated with delivery but starts to rise again plasma volume decreases due to diuresis and hemoconcentration.[42] The hematocrit values return to normal in 3-5 days postpartum as plasma volume starts to increase. The discrepancy in hemoglobin values in the postpartum phase is due to the variability in the plasma volume due to fluid shifts. Studies evaluating the longitudinal values of hemoglobin in the postpartum phase indicate that it takes at least 4-6 months to restore the pregnancy-induced dip in hemoglobin to non-pregnant states.[43] The patient may develop leucocytosis (approximately 25,000/mm^3) due to the stress associated with labor. The white blood cell count returns to pre-pregnant values within four weeks.[44] The gestational thrombocytopenia resolves in 4 to 10 days after delivery as platelet count increases in response to platelet consumption during delivery.[44][45] During pregnancy, the fibrinogen, factor VII, VIII, X, XII, von Willebrand's factor, and ristocetin activity increase significantly as gestation progresses to prepare for delivery and prevent excess blood loss.[46] In the early postpartum period, the fibrinogen levels are still high, and platelets begin to rise to normal values. The tissue plasminogen, an enzyme responsible for clot lysis, doesn't rise or normalize in the early postpartum period. During pregnancy, the hypercoagulable state resolves gradually after birth, as clotting factor levels normalize in 8 to 12 weeks postpartum.[47][48] The changes in the coagulation system confer an increased risk for thromboembolic phenomena that are approximately ten-fold during pregnancy and twenty-fold during the early postpartum period.[49][50] Furthermore, the in vitro tests to assess or predict the possibility of thromboembolism, such as d-dimer tests, fibrin degradation products assay, are less reliable in the immediate postpartum period.[51]

There are significant structural and hemodynamic alterations in the peripartum period. Cardiac output increases throughout pregnancy. However, in the immediate postpartum period, following delivery, there is an increase in circulating blood volume from the contraction of the uterus and an increase in preload from the relief of inferior vena cava obstruction, leading to an increase in stroke volume and heart rate leading to a 60 to 80% rise in cardiac output, which rapidly declines to pre-labor values in 1 to 2 hours following delivery and to pre-pregnancy values in two weeks postpartum.[52][53] An increase in serum levels of progesterone and relaxin, a peptide hormone produced by corpus luteum and placenta, promotes systemic vasodilation leading to a progressive decrease in systemic vascular resistance (SVR). SVR decreases by 35 to 40% during pregnancy and increases to pre-pregnant levels in 2 weeks postpartum. There is also a decrease in systemic blood pressure by 5 to 10 mm Hg during pregnancy. Diastolic blood pressure decreases more than systolic blood pressure. The systemic blood pressures start to rise during the third trimester and return to prepregnant va