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Physiology, Postpartum Changes

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Last Update: November 14, 2022.


The postpartum period is the period after delivery of conceptus when maternal physiological and anatomical changes return to the nonpregnant state. The postpartum period, also known as puerperium, starts following the expulsion of the placenta until complete physiological recovery of various organ systems. The postpartum period divides into three arbitrary phases, i.e., acute phase  - the first 24 hours after delivery of the placenta, early – up to 7 days, and late – up to 6 weeks to 6 months. Each phase has its unique clinical considerations and challenges.[1][2]

Organ Systems Involved

General Physiological Changes

There is generalized physical fatigue immediately after delivery. The pulse rate may be elevated a few hours after childbirth due to excitement or pain and usually normalizes on the second day. The blood pressure could be elevated due to pain or excitement but is generally in the normal range.[3] A significant decrease (> 20% below baseline) in blood pressure could be a sign of postpartum hemorrhage or septic shock.[4] Conversely, high blood pressure could be a sign of pain or pre-eclampsia.[5]

The temperature is slightly elevated up to 37.2C (99F) along with increased shivering, sweating, or diaphoresis in the first 24 hours and normalizes within 12 hours.[3][6] The temperature rise is attributable to the systemic absorption of metabolites accumulated due to muscle contractions. There could be a transient temperature rise (by 0.5C) on the third or fourth day due to breast engorgement. The respiratory rate also begins to fall back to the pre-pregnancy level within 2 to 3 days. A rise of temperature beyond the third day or over the upper limit is usually a sign of infection.[7][8][9][7] There is a weight loss of 5 to 6 kg due to the expulsion of products of gestation and accompanying blood loss. Further weight loss of 2 to 3 kg can be attributed to the brisk diuresis. The weight loss due to diuresis may continue up to 6 months after delivery.


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 secretion from the breasts called colostrum increases after childbirth. Colostrum is rich in protein, vitamins and immunoglobulins, and other humoral factors (lactoferrin) and provides an immunological defense to the newborn.[22] The mammogenesis or preparation of breasts for lactation starts during pregnancy and entails ductal and lobuloalveolar hyperplasia and hypertrophy.[23] The high levels of estrogen and progesterone make the breast tissue unresponsive to prolactin. Still, as their levels decrease the following childbirth dramatically, the prolactin begins its milk secretory activity in mammary glans. The lactogenesis or milk secretion starts the third or fourth day postpartum. The neural arch of lactation involves ascending afferent impulses from nipple and areola, activated by suckling or stimulation of nipples, which pass via thoracic sensory nerves to the paraventricular and supraoptic nuclei of the hypothalamus, promoting the synthesis and secretion of Oxytocin from the posterior pituitary. Oxytocin affects the contraction of myoepithelial cells, leading to galactokinesis or milk expression from the mammary ducts. This release is also known as "milk ejection," or milk let down reflex." The milk ejection reflex can be inhibited by pain, anxiety, depression, breast engorgement, or depression. Prolactin maintains galactopoiesis, defined as the maintenance of effective and continuous lactation. A healthy mother secretes 500-800 ml of milk per day, which requires 700kcal/ day. The fat stores of up to 5 kg gained during pregnancy can provide enough calories to make up for any nutritional deficit during lactation. It is not unusual to develop nipple soreness, mastitis during this phase.[24][25]


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 values at 16 weeks postpartum.[54] Heart rate increases in a linear fashion during pregnancy by 10 to 20 bpm over baseline and returns to pre-pregnant levels 6 weeks postpartum.[55][55] There is ventricular remodeling during pregnancy, and left ventricular wall thickness and mass increase by 28% to 52% above pre-pregnancy values. A few recent studies also report an increase in right ventricular volume and mass by 40% during pregnancy. The physiological hypertrophy of the ventricular system reverts to the pre-pregnant state in 4 weeks postpartum.[56][57] Cardiac contractility and ventricular ejection fraction don't undergo any significant change during the entire peripartum period.[55] 


The mother may develop flatulence or constipation due to intestinal ileus (induced by pain or presence of placental hormone relaxin in the circulation), loss of body fluids, laxity of abdominal wall, and hemorrhoids.[58][59] The postpartum constipation is due to the progesterone-induced decrease in gastrointestinal transit time.[58] The compressive effects of the gravid uterus on the stomach, a decrease in lower esophageal sphincter tone due to high progesterone levels, and hypersecretion of acid due to high gastrin levels cause an increase in the incidence of acid reflux during pregnancy. After delivery, the levels of progesterone and gastrin drop within 24 hours, and the acid reflux and associated symptoms resolve in the next three to four days.[60][61][62][63]


Hyperpigmentation is the most commonly reported skin change during pregnancy, affecting 85% to 90% of females.[64] The hypothesis is that melanocytes are sensitive to elevated levels of estrogen, progesterone, and endorphins during pregnancy. Humoral factors produced by the placenta lead to the upregulation of tyrosine kinase, promoting further melanin synthesis.[65][66] The pigment changes accompanying pregnancy (melasma and linea nigra) usually disappear by 6 to 8 weeks.[67] Elevated estrogen during pregnancy can lead to telangiectasis and spider angiomata.[68] Venous dilation and increased hydrostatic pressure due to the gravid uterus can lead to nonpitting edema and varicosities in lower extremities, which returns to baseline in the postpartum period.[69] The nails undergo symmetrical, uniform hyperpigmentation during pregnancy that fades away in the postpartum period.[70] The abdominal muscles are overstretched during pregnancy and strained during labor and are slow to regain their normal tone and elasticity, returning to pre-pregnancy levels by 6 to 8 weeks. The patient may have divarication of recti, and the striae or stretch marks over the abdomen and legs might not disappear.[66]

Clinical Significance

Human physiology is significantly altered during pregnancy and in the postpartum period. The physician should be aware of the physiological changes associated with the postpartum period. The clinician should be able to tell the difference between healthy and abnormal to effectuate a diagnostic and therapeutic algorithm, especially in cases of acute emergencies such as postpartum hemorrhage, sepsis, amniotic fluid embolism, or uterine inversion. Furthermore, one should be aware of the hormonal changes related to the puerperium and lactation to formulate an effective contraception plan in the postpartum period. Thromboprophylaxis in the postpartum period is a constant topic of debate due to the high incidence of venous thromboembolism in the postpartum period, and females are risk-stratified into low-risk, medium-risk and, high-risk. Females with a history of no coagulation anomalies or low-risk don't require any thromboprophylaxis. Intermediate-risk females should be instituted thromboprophylaxis after delivery up to 7 days of puerperium. The females that are high risk receive thromboprophylaxis throughout pregnancy and up to 7 days of postpartum. The conduct of anesthesia for surgery also varies according to the timeline post-delivery. Patients undergoing surgery under general anesthesia within 48 hours of delivery should be treated as full stomach and should receive anti-aspiration measures, including non-particulate antacid and rapid sequence induction of anesthesia.

Review Questions


Romano M, Cacciatore A, Giordano R, La Rosa B. Postpartum period: three distinct but continuous phases. J Prenat Med. 2010 Apr;4(2):22-5. [PMC free article: PMC3279173] [PubMed: 22439056]
Brown JS, Posner SF, Stewart AL. Urge incontinence: new health-related quality of life measures. J Am Geriatr Soc. 1999 Aug;47(8):980-8. [PubMed: 10443860]
Bystrova K, Matthiesen AS, Vorontsov I, Widström AM, Ransjö-Arvidson AB, Uvnäs-Moberg K. Maternal axillar and breast temperature after giving birth: effects of delivery ward practices and relation to infant temperature. Birth. 2007 Dec;34(4):291-300. [PubMed: 18021144]
Nathan HL, El Ayadi A, Hezelgrave NL, Seed P, Butrick E, Miller S, Briley A, Bewley S, Shennan AH. Shock index: an effective predictor of outcome in postpartum haemorrhage? BJOG. 2015 Jan;122(2):268-75. [PubMed: 25546050]
Matthys LA, Coppage KH, Lambers DS, Barton JR, Sibai BM. Delayed postpartum preeclampsia: an experience of 151 cases. Am J Obstet Gynecol. 2004 May;190(5):1464-6. [PubMed: 15167870]
Benson MD, Haney E, Dinsmoor M, Beaumont JL. Shaking rigors in parturients. J Reprod Med. 2008 Sep;53(9):685-90. [PubMed: 18839822]
Alekseev NP, Vladimir II, Nadezhda TE. Pathological postpartum breast engorgement: prediction, prevention, and resolution. Breastfeed Med. 2015 May;10(4):203-8. [PMC free article: PMC4410447] [PubMed: 25774443]
Woodd SL, Montoya A, Barreix M, Pi L, Calvert C, Rehman AM, Chou D, Campbell OMR. Incidence of maternal peripartum infection: A systematic review and meta-analysis. PLoS Med. 2019 Dec;16(12):e1002984. [PMC free article: PMC6903710] [PubMed: 31821329]
Hamadeh G, Dedmon C, Mozley PD. Postpartum fever. Am Fam Physician. 1995 Aug;52(2):531-8. [PubMed: 7625327]
Negishi H, Kishida T, Yamada H, Hirayama E, Mikuni M, Fujimoto S. Changes in uterine size after vaginal delivery and cesarean section determined by vaginal sonography in the puerperium. Arch Gynecol Obstet. 1999 Nov;263(1-2):13-6. [PubMed: 10728621]
Mulic-Lutvica A, Bekuretsion M, Bakos O, Axelsson O. Ultrasonic evaluation of the uterus and uterine cavity after normal, vaginal delivery. Ultrasound Obstet Gynecol. 2001 Nov;18(5):491-8. [PubMed: 11844171]
Sokol ER, Casele H, Haney EI. Ultrasound examination of the postpartum uterus: what is normal? J Matern Fetal Neonatal Med. 2004 Feb;15(2):95-9. [PubMed: 15209115]
Cyganek A, Wyczalkowska-Tomasik A, Jarmuzek P, Grzechocinska B, Jabiry-Zieniewicz Z, Paczek L, Wielgos M. Activity of Proteolytic Enzymes and Level of Cystatin C in the Peripartum Period. Biomed Res Int. 2016;2016:7065821. [PMC free article: PMC4745279] [PubMed: 26904684]
Anderson WR, Davis J. Placental site involution. Am J Obstet Gynecol. 1968 Sep 01;102(1):23-33. [PubMed: 5672474]
SHARMAN A. Post-partum regeneration of the human endometrium. J Anat. 1953 Jan;87(1):1-10. [PMC free article: PMC1244561] [PubMed: 13022577]
Sherman D, Lurie S, Frenkel E, Kurzweil Y, Bukovsky I, Arieli S. Characteristics of normal lochia. Am J Perinatol. 1999;16(8):399-402. [PubMed: 10772198]
Oppenheimer LW, Sherriff EA, Goodman JD, Shah D, James CE. The duration of lochia. Br J Obstet Gynaecol. 1986 Jul;93(7):754-7. [PubMed: 3755355]
Chi C, Bapir M, Lee CA, Kadir RA. Puerperal loss (lochia) in women with or without inherited bleeding disorders. Am J Obstet Gynecol. 2010 Jul;203(1):56.e1-5. [PubMed: 20417483]
McLAREN HC. The involution of the cervix. Br Med J. 1952 Feb 16;1(4754):347-52. [PMC free article: PMC2022557] [PubMed: 14896142]
Christianson LM, Bovbjerg VE, McDavitt EC, Hullfish KL. Risk factors for perineal injury during delivery. Am J Obstet Gynecol. 2003 Jul;189(1):255-60. [PubMed: 12861171]
Albers L, Garcia J, Renfrew M, McCandlish R, Elbourne D. Distribution of genital tract trauma in childbirth and related postnatal pain. Birth. 1999 Mar;26(1):11-7. [PubMed: 10352050]
Thapa BR. Health factors in colostrum. Indian J Pediatr. 2005 Jul;72(7):579-81. [PubMed: 16077241]
Lamote I, Meyer E, Massart-Leën AM, Burvenich C. Sex steroids and growth factors in the regulation of mammary gland proliferation, differentiation, and involution. Steroids. 2004 Mar;69(3):145-59. [PubMed: 15072917]
Crowley WR. Neuroendocrine regulation of lactation and milk production. Compr Physiol. 2015 Jan;5(1):255-91. [PubMed: 25589271]
The World Health Organization Multinational Study of Breast-feeding and Lactational Amenorrhea. II. Factors associated with the length of amenorrhea. World Health Organization Task Force on Methods for the Natural Regulation of Fertility. Fertil Steril. 1998 Sep;70(3):461-71. [PubMed: 9757874]
Campbell OM, Gray RH. Characteristics and determinants of postpartum ovarian function in women in the United States. Am J Obstet Gynecol. 1993 Jul;169(1):55-60. [PubMed: 8333476]
Campino C, Ampuero S, Díaz S, Serón-Ferré M. Prolactin bioactivity and the duration of lactational amenorrhea. J Clin Endocrinol Metab. 1994 Oct;79(4):970-4. [PubMed: 7962307]
Jackson E, Glasier A. Return of ovulation and menses in postpartum nonlactating women: a systematic review. Obstet Gynecol. 2011 Mar;117(3):657-662. [PubMed: 21343770]
Gaberšček S, Osolnik J, Zaletel K, Pirnat E, Hojker S. An Advantageous Role of Spectral Doppler Sonography in the Evaluation of Thyroid Dysfunction During the Postpartum Period. J Ultrasound Med. 2016 Jul;35(7):1429-36. [PubMed: 27208199]
Stagnaro-Green A, Abalovich M, Alexander E, Azizi F, Mestman J, Negro R, Nixon A, Pearce EN, Soldin OP, Sullivan S, Wiersinga W., American Thyroid Association Taskforce on Thyroid Disease During Pregnancy and Postpartum. Guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and postpartum. Thyroid. 2011 Oct;21(10):1081-125. [PMC free article: PMC3472679] [PubMed: 21787128]
Sonagra AD, Biradar SM, K D, Murthy D S J. Normal pregnancy- a state of insulin resistance. J Clin Diagn Res. 2014 Nov;8(11):CC01-3. [PMC free article: PMC4290225] [PubMed: 25584208]
Ryan EA, O'Sullivan MJ, Skyler JS. Insulin action during pregnancy. Studies with the euglycemic clamp technique. Diabetes. 1985 Apr;34(4):380-9. [PubMed: 3882502]
Sivan E, Chen X, Homko CJ, Reece EA, Boden G. Longitudinal study of carbohydrate metabolism in healthy obese pregnant women. Diabetes Care. 1997 Sep;20(9):1470-5. [PubMed: 9283800]
Rogers RG, Leeman LL. Postpartum genitourinary changes. Urol Clin North Am. 2007 Feb;34(1):13-21. [PubMed: 17145356]
Snooks SJ, Swash M, Mathers SE, Henry MM. Effect of vaginal delivery on the pelvic floor: a 5-year follow-up. Br J Surg. 1990 Dec;77(12):1358-60. [PubMed: 2276018]
Viktrup L, Lose G, Rolff M, Barfoed K. The symptom of stress incontinence caused by pregnancy or delivery in primiparas. Obstet Gynecol. 1992 Jun;79(6):945-9. [PubMed: 1579319]
Au KK, Woo JS, Tang LC, Liang ST. Aetiological factors in the genesis of pregnancy hydronephrosis. Aust N Z J Obstet Gynaecol. 1985 Nov;25(4):248-51. [PubMed: 3869447]
Beydoun SN. Morphologic changes in the renal tract in pregnancy. Clin Obstet Gynecol. 1985 Jun;28(2):249-56. [PubMed: 4017319]
Cheung KL, Lafayette RA. Renal physiology of pregnancy. Adv Chronic Kidney Dis. 2013 May;20(3):209-14. [PMC free article: PMC4089195] [PubMed: 23928384]
Ogueh O, Clough A, Hancock M, Johnson MR. A longitudinal study of the control of renal and uterine hemodynamic changes of pregnancy. Hypertens Pregnancy. 2011;30(3):243-59. [PubMed: 21740248]
Andria M, Vargiu N. [Lactosuria in pregnancy and the puerperium]. Minerva Ginecol. 1968 May 15;20(9):773-6. [PubMed: 5738768]
Nicol B, Croughan-Minihane M, Kilpatrick SJ. Lack of value of routine postpartum hematocrit determination after vaginal delivery. Obstet Gynecol. 1997 Oct;90(4 Pt 1):514-8. [PubMed: 9380307]
Taylor DJ, Lind T. Red cell mass during and after normal pregnancy. Br J Obstet Gynaecol. 1979 May;86(5):364-70. [PubMed: 465384]
Chandra S, Tripathi AK, Mishra S, Amzarul M, Vaish AK. Physiological changes in hematological parameters during pregnancy. Indian J Hematol Blood Transfus. 2012 Sep;28(3):144-6. [PMC free article: PMC3422383] [PubMed: 23997449]
Shehata N, Burrows R, Kelton JG. Gestational thrombocytopenia. Clin Obstet Gynecol. 1999 Jun;42(2):327-34. [PubMed: 10370851]
Clark P, Brennand J, Conkie JA, McCall F, Greer IA, Walker ID. Activated protein C sensitivity, protein C, protein S and coagulation in normal pregnancy. Thromb Haemost. 1998 Jun;79(6):1166-70. [PubMed: 9657443]
de Boer K, ten Cate JW, Sturk A, Borm JJ, Treffers PE. Enhanced thrombin generation in normal and hypertensive pregnancy. Am J Obstet Gynecol. 1989 Jan;160(1):95-100. [PubMed: 2521425]
Eichinger S. D-dimer testing in pregnancy. Pathophysiol Haemost Thromb. 2003 Sep-2004 Dec;33(5-6):327-9. [PubMed: 15692237]
Jackson E, Curtis KM, Gaffield ME. Risk of venous thromboembolism during the postpartum period: a systematic review. Obstet Gynecol. 2011 Mar;117(3):691-703. [PubMed: 21343773]
Tepper NK, Boulet SL, Whiteman MK, Monsour M, Marchbanks PA, Hooper WC, Curtis KM. Postpartum venous thromboembolism: incidence and risk factors. Obstet Gynecol. 2014 May;123(5):987-996. [PubMed: 24785851]
Gherman RB, Goodwin TM, Leung B, Byrne JD, Hethumumi R, Montoro M. Incidence, clinical characteristics, and timing of objectively diagnosed venous thromboembolism during pregnancy. Obstet Gynecol. 1999 Nov;94(5 Pt 1):730-4. [PubMed: 10546719]
Robson SC, Hunter S, Boys RJ, Dunlop W. Serial study of factors influencing changes in cardiac output during human pregnancy. Am J Physiol. 1989 Apr;256(4 Pt 2):H1060-5. [PubMed: 2705548]
Soma-Pillay P, Nelson-Piercy C, Tolppanen H, Mebazaa A. Physiological changes in pregnancy. Cardiovasc J Afr. 2016 Mar-Apr;27(2):89-94. [PMC free article: PMC4928162] [PubMed: 27213856]
Nama V, Antonios TF, Onwude J, Manyonda IT. Mid-trimester blood pressure drop in normal pregnancy: myth or reality? J Hypertens. 2011 Apr;29(4):763-8. [PubMed: 21178781]
Grindheim G, Estensen ME, Langesaeter E, Rosseland LA, Toska K. Changes in blood pressure during healthy pregnancy: a longitudinal cohort study. J Hypertens. 2012 Feb;30(2):342-50. [PubMed: 22179091]
Umar S, Nadadur R, Iorga A, Amjedi M, Matori H, Eghbali M. Cardiac structural and hemodynamic changes associated with physiological heart hypertrophy of pregnancy are reversed postpartum. J Appl Physiol (1985). 2012 Oct 15;113(8):1253-9. [PMC free article: PMC3472485] [PubMed: 22923507]
Hill JA, Olson EN. Cardiac plasticity. N Engl J Med. 2008 Mar 27;358(13):1370-80. [PubMed: 18367740]
Glazener CM, Abdalla M, Stroud P, Naji S, Templeton A, Russell IT. Postnatal maternal morbidity: extent, causes, prevention and treatment. Br J Obstet Gynaecol. 1995 Apr;102(4):282-7. [PubMed: 7612509]
Shin GH, Toto EL, Schey R. Pregnancy and postpartum bowel changes: constipation and fecal incontinence. Am J Gastroenterol. 2015 Apr;110(4):521-9; quiz 530. [PubMed: 25803402]
Blouw R, Scatliff J, Craig DB, Palahniuk RJ. Gastric volume and pH in postpartum patients. Anesthesiology. 1976 Oct;45(4):456-7. [PubMed: 973697]
Lam KK, So HY, Gin T. Gastric pH and volume after oral fluids in the postpartum patient. Can J Anaesth. 1993 Mar;40(3):218-21. [PubMed: 8467543]
O'Sullivan GM, Sutton AJ, Thompson SA, Carrie LE, Bullingham RE. Noninvasive measurement of gastric emptying in obstetric patients. Anesth Analg. 1987 Jun;66(6):505-11. [PubMed: 3578862]
Vanner RG, Goodman NW. Gastro-oesophageal reflux in pregnancy at term and after delivery. Anaesthesia. 1989 Oct;44(10):808-11. [PubMed: 2589605]
Bieber AK, Martires KJ, Stein JA, Grant-Kels JM, Driscoll MS, Pomeranz MK. Pigmentation and Pregnancy: Knowing What Is Normal. Obstet Gynecol. 2017 Jan;129(1):168-173. [PubMed: 27926637]
Bieber AK, Martires KJ, Driscoll MS, Grant-Kels JM, Pomeranz MK, Stein JA. Nevi and pregnancy. J Am Acad Dermatol. 2016 Oct;75(4):661-666. [PubMed: 27646736]
Tyler KH. Physiological skin changes during pregnancy. Clin Obstet Gynecol. 2015 Mar;58(1):119-24. [PubMed: 25517755]
Motosko CC, Bieber AK, Pomeranz MK, Stein JA, Martires KJ. Physiologic changes of pregnancy: A review of the literature. Int J Womens Dermatol. 2017 Dec;3(4):219-224. [PMC free article: PMC5715231] [PubMed: 29234716]
Fernandes LB, Amaral WN. Clinical study of skin changes in low and high risk pregnant women. An Bras Dermatol. 2015 Nov-Dec;90(6):822-6. [PMC free article: PMC4689069] [PubMed: 26734862]
Engelhorn CA, Cassou MF, Engelhorn AL, Salles-Cunha SX. Does the number of pregnancies affect patterns of great saphenous vein reflux in women with varicose veins? Phlebology. 2010 Aug;25(4):190-5. [PubMed: 20656957]
Erpolat S, Eser A, Kaygusuz I, Balci H, Kosus A, Kosus N. Nail alterations during pregnancy: a clinical study. Int J Dermatol. 2016 Oct;55(10):1172-5. [PubMed: 27097299]

Disclosure: Gaurav Chauhan declares no relevant financial relationships with ineligible companies.

Disclosure: Prasanna Tadi declares no relevant financial relationships with ineligible companies.

Copyright © 2023, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK555904PMID: 32310364


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