• To describe the physiological processes that achieve haemostasis in the early puerperium.
• To discuss the timing of the physiological changes in the puerperium.
• To discuss the aetiology of the common problems experienced within the puerperium.
• To recognize signs of pathological conditions associated with the puerperium.
The puerperium has been traditionally defined as the 6-week period immediately following the birth of a baby and represents the period of time in which maternal physiology, particularly the reproductive system, returns to a near prepregnant state. It probably originates from the tradition of ‘churching’ or the ‘lying-in period’, which was a religious ceremony where women were accepted back into the church after a period of 40 days during which they were considered unclean. The time after childbirth is imbued with social, cultural and religious significance and, in many cultures, the puerperal woman is given special treatment. Two important landmarks are often observed: the cessation of lochial discharge (women often being considered ‘unclean’ when lochia is present) and the shrivelling and loss of the remnants of the umbilical cord from the infant. With the rise of medical dominance, the end of the puerperium was marked by the postnatal examination of the woman by a doctor. This has structured the traditional descriptions of the puerperium as a period of maternal recovery, underpinned by the medicalization of pregnancy. It is the midwife's responsibility to maintain a careful watch on the physiological changes in the puerperium and to recognize early signs of pathological conditions.
Chapter case study
Zak was born 2 days after his expected date of delivery and was the first son born to his proud parents, Zara and James. Zak was delivered at around 04:30 hours and Zara had laboured in a birthing pool attended by her named midwife. As labour had progressed quickly without complications, the midwife followed Zara's request for no active management in the third stage of labour. The midwife was unable to accurately estimate Zara's blood loss due to the waterbirth. Once out of the bath, the midwife assessed Zara's perineal trauma, which appeared to be a first-degree tear that was not bleeding and did not require suturing.
• How can the midwife effectively assess Zara's well-being following the delivery, given that she has been unable to estimate Zara's total blood loss?
• What factors that have occurred during Zak's delivery will optimize Zara's transition to parenthood?
The puerperium is sometimes considered to be the ‘Cinderella’ of midwifery and obstetrics as the excitement of the birth is over and after delivery the effects of pregnancy on maternal physiology receive little emphasis. There is not very much research into the timing or mechanisms of the changes in the puerperium. However, the puerperal woman can be very vulnerable to physiological stress, which can become pathological. The midwife's role is to observe and monitor the early changes and to be able to differentiate between those which are normal and abnormal.
A woman adapts to pregnancy progressively over a period of months, but after childbirth she suddenly no longer needs the physiological changes. During the puerperium, there is a marked decrease in the levels of oestrogen and progesterone within the maternal system. Although the placenta is the main source of progesterone in pregnancy, the corpus luteum continues to produce progesterone for several days into the puerperal period. The fall in concentrations of steroid hormones facilitates the initiation of lactation (see Chapter 16) and allows the physiological systems to return to their prepregnant state. In reality, the puerperium should be described as a transitional phase. It begins at the birth of a child and it ends with the return of fertility. Women do not return to the same physiological and anatomical state, however. The puerperium also, within a social context, represents many transitions for the parents, child and other members of the family. Many of the physiological changes within the puerperium, such as the establishment of parenting skills, lactation and feeding, are modified by the past and present social interactions of the individuals within the new family situation.
Physiological and structural changes
Involution of the uterus
Clinical observation and management of the puerperium is essentially based on the return of the uterus to its ‘normal’ size. The puerperium begins as soon as the placenta and membranes are expelled from the uterus together with a substantial proportion of the endometrium. Oxytocin released from the posterior pituitary gland induces strong intermittent myometrial contractions, and as the uterine cavity is empty the whole uterus contracts down fully and the uterine walls become realigned in apposition to each other. The myometrial spiral fibres that occlude the uterine blood vessels (see Chapter 13) constrict the blood supply to the placental site (Fig. 14.1). Uterine vascular resistance increases soon after delivery (Tekay and Jouppila, 1993).
(A) Myometrial spiral fibres around uterine blood vessels; (B) occlusion of blood supply to the placental site.
(Reproduced with permission from Sweet and Tiran, 1996.)
About an hour after delivery, the myometrium relaxes slightly but further active bleeding is prevented by the activation of the blood-clotting mechanisms, which are altered greatly during pregnancy to facilitate a swift clotting response. Haemostasis is achieved in three ways:
• Pressure: apposition of the uterine walls forming the T-shaped cavity
• Clotting mechanisms.
The midwife has the responsibility to inspect the placenta and membranes to assess that they are complete and that no tissue remains within the uterine cavity. Retained products impede the contraction of the uterus and may be the source of abnormal bleeding and cause secondary postpartum haemorrhage (secondary PPH) as they become the focus of infection. Retained products are often spontaneously voided usually associated with the passing of a blood clot, which facilitates the cleansing of the uterine cavity. Blood clots should always be checked for the presence of placental and membranous tissue.
Immediately after delivery, the uterus weighs about 900–1000 g and the fundus is palpable about 11–12 cm above the symphysis pubis (Howie, 1995) at around the level of the umbilicus. The placental site is raw and exposed. Initially, the uterus is continuous with the vagina with the cervix draping from the body of the uterus. Uterine involution is rapid so 50% of the total mass of the tissue is lost within a week (Howie, 1995). This physiological destruction of most of the uterine tissue is unique in adult life and the mechanisms are not clearly understood. It is suggested that 90% of uterine protein is degraded in the first 10 days of the puerperium (Hytten, 1995). There are rapid and marked changes in collagen and elastin content (Stone and Franzblau, 1995), and water and protein are lost. Involution results from a withdrawal of placental hormones and is thought to be mediated by hydrolytic and proteolytic enzymes released from myometrial cells, endothelial cells of blood vessels and macrophages. Cytoplasmic organelles are autodigested, and intracellular cytoplasm and extracellular collagen are reduced (Howie, 1995). The breakdown of protein from the myometrial cells releases the amino acid components into the circulation and thence into the urine; thus, a puerperal woman is in a state of negative nitrogen balance (see Chapter 12). The myometrial cells are thought to reduce in size (Fig. 14.2) rather than being destroyed and replaced, although there may be an ‘overshoot’ in uterine involution with rebuilding to the resting non-pregnant state. The uterus ultimately returns almost to its prepregnant size (Fig. 14.3), although the proportion of fibrous tissue present in the uterus is progressively increased with successive pregnancies.
Reduction in size of myometrial cells.
(Reproduced with permission from Miller and Hanretty, 1998.)
Return of uterus to a size close to the prepregnant dimensions: A nulliparous uterus; B parous uterus.
(Reproduced with permission from Miller and Hanretty, 1998.)
Initially, the cervix is soft, bruised and lacerated following a vaginal delivery (particularly so in primiparae and with premature labour). The cervix rapidly reforms and closes; by the end of the first puerperal week it will admit one finger. However, the cervix never returns to its original state and always shows evidence of parturition. The external os reforms with a slit rather than the nulliparous dimple (Fig. 14.4).
Reformation of the external os: (A) nulliparous cervix; (B) parous cervix.
(Reproduced with permission from Miller and Hanretty, 1998.)
The uterus involutes quite quickly, initially at about 1 cm/day; thus by the tenth day it should no longer be palpable above the symphysis pubis. Involution is slower in women who have undergone lower-segment caesarean section (LSCS), but it can be judged by a detectable decrease in fundal height. Subinvolution (a slow rate of uterine involution) may indicate retained products of conception (ERPC) and/or a secondary infection, which is usually found in conjunction with continued lochia rubra that may have an offensive odour. The uterus should be well contracted, hard and central; if it is higher than the umbilicus and soft on palpation (often described as ‘boggy’) then this may also indicate the presence of infection. The endometrial cavity is a potential space in non-pregnant women but gas is commonly detected in the endometrial cavity puerperally (Hytten, 1995).
The initiation of breastfeeding and the infant suckling in the early puerperium augments stimulation of oxytocin release. The oxytocin stimulates further contraction of the myometrium and so uterine evacuation. Involution of the uterus in breastfeeding mothers is more efficient. ‘After-pains’ associated with lactation are often experienced, particularly, by multiparous women who often complain of increased vaginal loss while feeding. Initially, oral analgesia such as paracetamol may be offered but the intensity of the pain usually subsides after about 24 h because expression of myometrial oxytocin receptors is reduced as a result of oestrogen withdrawal.
The superficial layer of the decidua becomes necrotic and is shed in the lochia in the first few days of the puerperium. The epithelium rapidly regenerates, re-forming an intact layer over most of the surface within 7–10 days of delivery. The placental site takes 3 weeks or longer to recover. The endometrium regenerates from the basal layers and grows in from the margins of the placental wound site and from glandular remnants within it (Howie, 1995).
Soft tissue damage and repair
It is not uncommon for soft tissue damage to occur during the delivery of a baby. Trauma to the female genital tract is described as follows:
• Superficial—this usually describes grazes to the skin where the epidermis has split owing to pressure of distension. These require no treatment; however, they often cause discomfort through stinging because of the disruption of the many nerve endings found within the superficial layer of the tissue. Voiding of urine can also be uncomfortable as the urine comes in contact with the grazes.
• First degree—this describes a tear in the skin and underlying superficial tissues (not including the muscle). Often the wound will heal spontaneously as the skin edges are usually in apposition. Ragged tears may result in the formation of excess scar tissue which can cause dyspareunia (pain during intercourse). Tears on the labia minora, a well-innervated area, can cause a lot of discomfort. If bilateral tears are present, suturing needs to be considered as the labia may fuse together if the tears are in close apposition forming a band of tissue over the vaginal opening.
• Second degree—when a tear involves perineal muscle damage it is described as being second degree. Usually these wounds are sutured to aid healing. Simple second degree tears are usually in the midline and involve one line of tearing. Some second degree tears can be complex with more than one tear line radiating in both lateral and downward directions involving larger amounts of muscle trauma.
• Episiotomy—this is a surgical incision to enlarge the introitus to facilitate the delivery of the baby which used to be thought to be beneficial and so done routinely. It falls into the same category as the second-degree tear. Although episiotomies can be performed in the midline, because of the increased risk of extension to a third degree tear and anal sphincter rupture they are usually performed to the side (mediolateral).
• Third degree—here the muscle of the anal sphincter is involved. Obstetric repair is essential so that the sphincter activity of the muscle is restored thus avoiding complications of faecal incontinence at a later time.
• Fourth degree—when the tear is extensive, the anal sphincter may become completely divided and the tear continues through the rectal mucosa. Specialist surgical repair is required to ensure the resumption of normal anal function.
Repair to the perineum involves the clinician suturing the perineum. There is a wide variety of suture materials and techniques for repair; however, suturing aims to achieve the following:
• Haemostasis—this is to ensure that any active bleeding points are ligated to minimize blood loss and the postnatal complication of a haematoma (formation of a blood clot within the wound) which can be extremely painful.
• Alignment—this is to bring the tissues back into alignment to optimize healing and to achieve a near pre-tear condition. If wounds are left gaping, alignment may not occur and as healing is by granulation this can result in the formation of scar tissue. This can result in a rigid misshapen perineum, which can cause dyspareunia (pain on intercourse).
The majority of perineal traumas can be described as being deep wounds as the tissue trauma involves layers below the epidermis and the dermis. Wound healing occurs in three phases: inflammation, tissue formation and tissue remodelling (see also Box 14.1). Some features of wound healing are common to all tissues; others are specific to the tissue involved. For instance, granulation tissue does not develop in the endometrium and the wounds do not heal with scarring. In this respect, there are similarities with fetal wounds which also heal without scarring suggesting that the process of endometrial remodelling is more a developmental mechanism than merely repair.
1. First is the inflammatory response; inflammation is a normal reaction to tissue trauma. Perineal inflammation can initially cause great discomfort for women in the very early postnatal period. An analgesic such as diclofenac sodium is useful as it acts as an anti-inflammatory agent (though it should be used with caution if the woman is asthmatic). Paracetamol and codeine-based products can also be used but codeine can cause or exacerbate bowel constipation so appropriate advice is required. However, a degree of inflammation is vital to ensure tissue healing, so analgesics should be used only when the response is severe and perineal pain restricts normal activity. The inflammation acts to isolate the damaged tissues, reducing the spread of infection. White blood cells, such as neutrophils and macrophages, invade the tissue owing to the increased vasodilatation in the surrounding blood vessels. These cells ingest any invading bacteria and break down any necrotic tissue within the wound.
2. The migratory phase involves the infiltration of the wound by mesenchymal cells that form fibroblasts, initially creating a scab over the open wound site. Following this, blood vessels grow into the wound and the wound is gradually filled from the bottom up by new tissue growth called granulation tissue.
3. There then follows a proliferative phase where epithelial cells grow under the scab. It concludes with the maturation of the new cells and the shedding of the scab.
The stages of wound healing
• Blood clot forms, reinforced with fibrin fibres.
• Acute inflammatory response occurs: polymorphs and macrophages migrate to site; high-protein exudate leads to local oedema.
1 week later
• Eschar dries out, hardens and eventually becomes detached.
• Wound contracts.
• Mitotic activity occurs in epidermal cells, which migrate over living tissue.
• New blood capillaries form from endothelial buds, bringing nutrients to healing tissue.
• New connective tissue, formed by fibroblasts, supports capillary loops.
6 months later
• Surface depression may still be visible at wound site; scar tissue becomes paler.
• Epithelialization is complete.
• Connective tissue is reorganized, less vascular and stronger.
The initial vaginal loss is termed the lochia rubra and consists of blood that has collected within the reproductive tract together with autolytic products of degenerated necrotic decidua from the placental site and any trophoblastic remains. The outward flow of blood lost at delivery and the subsequent discharge of lochia are important in removal of potential sources of ascending infection and, thus, protection of the placental wound site. The alkalinity of the lochia is also important in protecting the vulnerable site. Lochia is the normal discharge in the puerperium; it has a characteristic sweetish smell unless there is an infection.
Lochia may be described by its visual appearance (Box 14.2); normally, the lochia lightens progressively in both volume and colour. However, at about day 7 after delivery, the fibrinous mesh deposited over the placental site may be shed as part of the normal healing process so the vaginal loss may be transiently heavier and flushed with fresh blood. By day 10, the lochia is normally scant and pink in colour although discharge of lochia may persist for up to 6 weeks. Prolonged duration of lochia discharge suggests the placental wound site is not completely epithelialized or that the woman has some retained debris which is still disintegrating (Hytten, 1995). The duration of lochia discharge tends to be longer with the first pregnancy and is also related to birth weight.
• Lochia rubra (red)
– decidua and frank blood loss from placental site
– initially sterile then uterus begins to be colonized by vaginal flora
– red colour persists for about 3 days
• Lochia serosa (pink/brown)
– contains leukocytes, mucus, vaginal epithelial cells, necrotic decidua, non-pathological bacteria
– may be blood stained for 3–4 weeks
– characteristic sweetish odour
• Lochia alba (yellow–white)
– mostly serous fluid and leukocytes
– plus some cervical mucus and microorganisms
Heavy discharge of lochia with an offensive odour, maternal pyrexia and/or a feeling of general malaise can all indicate possible intrauterine infection. If the lochia remains abnormally heavy and further bleeding occurs, dilatation and curettage (D&C) to empty the uterine cavity may be necessary. The procedure is also termed evacuation of ERPC. The cervix is dilated and the retained products are scraped from the decidua. This procedure is not without complications, however. Excessive scraping can damage or remove the entire endometrium. If the basal layer of the endometrium is removed (see Chapter 2) then proliferation during the menstrual cycle fails to occur, affecting fertility; this is termed Asherman's syndrome.
Excessive blood loss, that is, more than 500 mL or any amount that jeopardizes the well-being of the mother, at and within 24 h of delivery is termed a primary postpartum haemorrhage (primary PPH). It is usually caused by failure of the myometrium to contract completely, or failure of the blood-clotting mechanisms, or both (see Chapter 13); PPH may be very serious (Box 14.3, Case study 14.1). Women may also loose significant amounts of blood from trauma to the genital tract and perineum. If there is excessive bleeding but the uterus is well contracted, examination of the genital tract and perineum should not be delayed to identify bleeding points and any trauma repaired as quickly as possible to minimize blood loss.
Disseminated intravascular coagulation
Disseminated intravascular coagulation (DIC) is a condition caused by abnormal activation of the clotting mechanisms. The blood-clotting factors are induced on a wide basis resulting in fibrin deposits being produced that line the major part of the vascular bed. Once this has occurred, bleeding continues owing to the absence of clotting factors, which were exhausted during the DIC phase and the activation of fibrinolysis. Liver dysfunction occurs in pre-eclampsia and may be associated with DIC and microangiopathic haemolysis (erythrocyte breakdown in small blood vessels). The acronym HELLP refers to Haemolysis, Elevated Liver enzymes and Low Platelet counts.
DIC is an extremely severe condition. Although such a life-threatening case would normally be managed by intensive care staff rather than by the midwifery unit, it is important that midwives are able to recognize the symptoms and implications of DIC, for example, the appearance of bruising on the skin not associated with trauma. In advanced cases, the observation of the failure blood to clot is significant of advanced DIC and warrants immediate intervention as this indicates a critical life-threatening situation.
Case study 14.1
Lucy is a 35-year-old primigravida who is delivered by emergency LSCS at 30 weeks' gestation owing to fulminating pre-eclampsia. Following delivery, the blood loss per vaginum is noted to be quite brisk and a Syntocinon (oxytocin) infusion is commenced in an attempt to control the bleeding. On investigation, it is discovered that Lucy's platelet count is extremely low and that the clotting time for her blood is greatly prolonged. A provisional diagnosis of DIC secondary to HELLP syndrome is made.
• What predisposing factors may have contributed to Lucy's condition?
• What intervention would Lucy require and what care would she need following this diagnosis?
Occasionally, there may be concealed bleeding, either into the peritoneum from ruptured blood vessels in the broad ligament or into the tissues forming large collections of blood clots called haematomas. Therefore, even in the absence of visible blood loss, women can still be physically in shock if concealed bleeding is present.
The risk of primary PPH is lower 24–72 h following delivery, but until involution of the uterus is complete there is a risk of a secondary PPH if there is an infection within the uterine cavity. The bleeding is usually due to the fibrinolytic action of bacteria such as haemolytic streptococcus. These bacteria are usually anaerobes (able to thrive in the absence of oxygen) and so specific antibiotic treatment with antibiotics such as metronidazole may be required.
In late pregnancy, most of the steroid hormones are derived from the placenta, although the corpus luteum and ovary continue to contribute some progesterone. Levels of progesterone and oestrogen fall to non-pregnant levels within 72 h of delivery. The placental protein hormones have a longer half-life so plasma levels fall more slowly. During pregnancy, production of the gonadotrophins is suppressed. Follicle-stimulating hormone (FSH) levels are restored to prepregnant concentrations within 3 weeks of delivery, but restoration of luteinizing hormone (LH) secretion takes longer, depending on the duration of lactation. Levels of oxytocin and prolactin also depend on lactational performance.
The haematological system and cardiovascular changes
The blood lost at delivery, accepted to be about 300–500 mL normally and about 1000 mL in caesarean sections, is adequately compensated for by the increase in blood volume acquired during pregnancy (see Chapter 11). Women can lose about 1000 mL of their predelivery blood volume before postnatal haemoglobin concentration is compromised (Letsky, 1998; Case study 14.2). Erythropoiesis isstimulated before and after delivery (Richter et al., 1995). Diuresis further decreases plasma volume in the first days, although as interstitial fluid is mobilized subsequently the plasma volume tends to increase transiently causing haemodilution of both haemoglobin and plasma proteins, such as clotting factors. It is this variability in blood lost at delivery and restoration of normal water balance that may result in raised concentrations of clotting factor and hypercoagulability. The tendency to coagulate is also affected by the loss of placental and fetal factors affecting clotting and water regulation (Blackburn, 2007).
Case study 14.2
Prior to delivery, Megan had a haemoglobin (Hb) concentration of 10.1 g/dL. At delivery, her blood loss is estimated at around 1000 mL. The midwife is quite concerned over this although Megan was asymptomatic. Prior to discharge on day 3, Megan's Hb concentration is rechecked and is estimated at being 9.8 g/dL.
• How can you account for the Megan's Hb concentration being relatively stable despite her suffering a postpartum haemorrhage?
• What advice/treatment would you give to Megan following her discharge?
Haemoglobin levels return to normal prepregnant levels within 4–6 weeks and white blood cell numbers fall to normal within a week of delivery (Blackburn, 2007). Platelet number increases in the first few days following delivery, thereafter falling gradually to prepregnant levels. Fibrinolytic activity is maximal for about 48 h after delivery in response to the removal of the placenta, which produces fibrinolytic inhibitors (Lanir et al., 2003). Clotting factors, which peaked in labour, gradually decrease. The net result is that the hypercoagulable state of pregnancy is increased in the early puerperium and then slowly returns to a prepregnant state over a few weeks. This period of prolonged hypercoagulability is why women are at significantly increased risk of thromboembolic episodes in the postnatal period.
In previous eras, wealthy women were advised to rest in bed after childbirth and received indulgent cosseting (Hytten, 1995). However, trials of early ambulation led to early mobility being highly recommended as it facilitates improved vena caval blood flow and rapid disposal of oedema and thus optimizes cardiovascular health. Mobilization is essential to optimize venous return and avoid stasis within the vascular bed, in order to minimize the risk of deep vein thrombosis (DVT) formation (see p. 373). Women who are unable to mobilize owing to obstetric complications, such as an LSCS, are given prophylactic treatment as the risks of DVT and complications are much increased. Women are advised to report any discomfort or swelling in the lower legs as this may indicate DVT formation (especially if one leg appears more swollen than the other although bilateral DVTs are possible); the risks of DVT progressively diminish.
The cardiovascular system is rendered transiently unstable by delivery owing to the blood loss and the ensuing compensatory mechanisms. During the brief period of instability of fluid balance in the first week after delivery, many women experience headaches. Initially, there is a marked increase in cardiac output as the uteroplacental flow is returned to the venous system and the gravid uterus no longer impedes the vena cava blood flow. This is augmented by the mobilization of extracellular fluid. Although pregnant women are normally able to tolerate normal blood lost at delivery, those women who had decreased vascular expansion during pregnancy, such as those with pre-eclampsia (see Chapter 11), may be less able to tolerate blood loss. Vaginal delivery is associated with a higher haemoglobin concentration than operative deliveries because vaginal delivery tends to have less blood loss and to promote diuresis more markedly (Blackburn, 2007).
Parameters of the cardiovascular system return towards prepregnant values but remain significantly different. Resolution of ventricular hypertrophy is slow. Vascular remodelling of pregnancy persists for at least a year after delivery and is enhanced by second and subsequent pregnancies (Clapp and Capeless, 1997). Because circulating blood volume and cardiac output fall early in the puerperium and the hypertrophied ventricle is slowly remodelled over a period of 4–6 months, the stroke volume remains relatively high for up to 12 weeks or longer (Blackburn, 2007). This means that heart rate falls in the puerperium, as the stroke volume contributes proportionately more to the decreased cardiac output. Thus, it is normal for puerperal women to exhibit bradycardia (a reduced pulse rate of about 60–70 beats per minute). A raised (or normal) pulse may indicate severe anaemia, venous thrombosis or infection (see below).
The decreased progesterone concentration following delivery of the placenta restores prepregnant sensitivity to carbon dioxide concentration promptly so partial pressures of carbon dioxide return to prepregnant levels. The diaphragm can increase its excursion distance once the gravid uterus no longer impedes it so full ventilation of the basal lobes of the lung is possible. Chest wall compliance, tidal volume and respiratory rate return to normal within 1–3 weeks. Changes in the elasticity of the rib cage may persist for months (Blackburn, 2007).
It is important that bladder function is assessed in the early postnatal period. The trauma experienced by the bladder during delivery usually results in oedema and hyperaemia of the bladder, which has reduced muscle tone in pregnancy. Effects on the bladder are increased by prolonged labour, use of forceps, analgesia and anaesthetic procedures and pressure of the descending presenting part during delivery. The resulting transient loss of bladder sensation, which may result in overdistension and incomplete emptying, can last from days to weeks. Bladder changes are associated with increased risk of urinary tract infections (UTI) in the puerperium. Trauma to the sphincter of the bladder increases the frequency of stress incontinence, which is marked by urine leakage occurring with coughing, laughing, sudden movement or exercise.
If bladder function is impaired, an indwelling catheter may be inserted to enable the damaged tissue to recover; however, catheterization itself increases the risk of a UTI. If the uterus can be palpated high up or is displaced over to one side following the woman voiding urine, this indicates that there is retention of urine as the full bladder displaces the uterus. This is compounded by the increased diuresis that occurs in the postnatal period due to the reduction of the increased plasma volume acquired during pregnancy. It is normal for women to have frequency of micturition as long as they are voiding large amounts of urine each time. Frequency involving just small amounts of urine being voided may indicate a degree of urinary retention. Further assessment of bladder function by ultrasound scanning will confirm if an abnormal amount of residual urine is present following micturition.
Pain associated with micturition may indicate a UTI. Dilation of the ureters, overdistension of the bladder and instrumental or operative deliveries all increase the risk of infection. By day 10, full bladder function should be observed and assessed; there should be no evidence of unprovoked urinary incontinence.
Parameters of the renal system, such as renal plasma flow, glomerular filtration rate and plasma creatinine, are usually back to normal non-pregnant levels by the 6-week check. Urinary excretion of mineral and vitamins is normal within the first week after delivery. Plasma renin and angiotensin levels adjust to the loss of fetal hormones affecting their control so levels fall and then increase before returning back to normal (Blackburn, 2007). This fluctuation in hormone levels affecting water retention, together with the redistribution of body fluid, results in rapid and sustained natriuresis and diuresis, which is particularly marked between the second and fifth day after delivery. Fluid and electrolyte balance is normal with 21 days after delivery. Oxytocin, which has antidiuretic hormone (ADH)-like activity, falls after delivery, augmenting diuresis. The voiding volume increases and many women experience night sweats in the puerperium, which also increase fluid loss. Pregnancy-induced changes in the urinary system may persist for several months. Although the dilated smooth muscle of the urinary tract appears normal within a week of delivery, it remains potentially distensible. The kidneys return to their prepregnant size within 6 months of pregnancy.
Gastrointestinal system and defaecation
During labour, gastric motility is reduced, particularly in association with pain, fear and narcotic drugs. The reduced tone of the lower oesophageal sphincter, reduced gastric motility and increased gastric acidity result in delayed gastric emptying. The tone and pressure of the lower oesophageal sphincter are normal by 6 weeks after delivery. However, in the early puerperium, the reduced gastrointestinal muscle tone and motility and the relaxed abdomen can increase gas distension and constipation immediately after delivery. Gallbladder muscle tone and contractility is enhanced after delivery so the gallbladder may expel small gallstones that developed during pregnancy (Blackburn, 2007).
The first bowel movements usually occur within 2 or 3 days following delivery. This may become complicated by the presence of haemorrhoids, which are associated with evacuation problems. Haemorrhoids are common during late pregnancy because of the effects of progesterone on vascular smooth muscle tone. Usually haemorrhoids resolve quickly after birth and cause only minor discomfort in the postnatal period. Sometimes, particularly if they are severe, owing to displacement by the passage of the presenting part through the birth canal, they can become traumatized and localized thrombosis can occur. This can be further complicated if constipation develops and the woman, because of perineal trauma, resists opening her bowels. Problems with constipation are increased by intestinal atony, lax abdominal musculature, irregular food intake and dehydration in labour. By day 10, the woman should have achieved normal bowel function. Faecal incontinence may indicate anal sphincter damage or inadequate repair.
Although weight is lost at delivery of the products of conception, many women experience a weight gain in the first couple of days following delivery. This is due to a combination of increased adrenocorticotrophin (ACTH), ADH and stress, all of which increase sodium and water retention. Women who have a higher blood loss at delivery tend to gain slightly more weight during the early days of the puerperium as water is retained for compensatory expansion of their blood volume. Weight usually starts to fall from the fourth day after delivery as diuresis increases. Weight is lost steadily, usually over a period of several months. Postpartum weight retention is affected by changes in lifestyle during and after pregnancy rather than by pregnancy itself (Ohlin and Rossner, 1994). Weight loss tends to be greater with lower parity, maternal age and lower prepregnant weight. Lactation and maternal nutrition also affect the rate of weight loss (see Chapter 16).
Other structural changes
Immediately after delivery, the vagina is smooth, soft and oedematous. The elasticity of the tissue returns within a few days. As the vagina is extremely well vascularized, episiotomies and tears usually heal well. The rugae of the vagina re-form in the third week but are less prominent than prior to pregnancy. The labia regress to a less prominent and fleshy state than in nulliparous women. The fall in oestrogen at delivery results in the vaginal epithelium becoming thinner and many women experience problems with vaginal lubrication immediately after delivery. Tags of the hymen remain and are renamed carunculae myrtiformes (Fig. 14.5).
(Reproduced with permission from Miller and Hanretty, 1998.)
Pelvic floor muscle strength and neuromuscular control are impaired to a greater extent in women who deliver vaginally and experience more mechanical trauma, particularly in the first week of the puerperium (Peschers et al., 1997); however, for most women, muscular tone and strength are normal within 2 months. Weakened circumvaginal muscles are associated with perineal outcome, episiotomy, length of second stage of labour, the weight of the baby and pushing techniques (Cosner et al., 1991). Problems associated with a lax ineffective pelvic floor such as uterine prolapse, urinary incontinence and prolapse of the rectum are more likely as parity increases. Pelvic floor exercises help to restore the muscle tone and function of the pelvic floor; specialist advice from an obstetric physiotherapist may be required for persistent problems with incontinence.
The abdominal wall may remain soft and flabby for several weeks. Severe stretching, for instance in a multiple pregnancy or with polyhydramnios, can result in permanently lax muscles. The softened pelvic joints and ligaments slowly return to normal over a period of a few months. Relaxation of pelvic joints may cause backache in the puerperium. The striae gravidarum become paler over a period of several months but fade rather than completely disappear.
Pregnancy-induced changes in the skin spontaneously regress or fade, though hyperpigmentation and melasma may persist in women with darker skin and hair. Hair loss may be marked following delivery and initial regrowth may be initially less abundant. Corneal sensitivity and pressure return to normal within 2 months of delivery. Nasal congestion and effects on the ear and larynx are restored to prepregnant status within a few days of delivery.
In the first 24 h following delivery, body temperature may increase slightly (to 38˚C) in response to the stress of labour, particularly dehydration. This temperature fluctuation is normally transient; a persistent raised temperature may indicate infection (see below).
The puerperium is associated with disrupted sleep patterns, particularly immediately after delivery (Swain et al., 1997). The first 3 days can be extremely difficult for the mother compounded by fatigue accumulated during labour and being unable to rest comfortably due to perineal pain (see Case study 14.3). Postpartum perineal pain correlates well with the duration of the second stage of labour (Thranov et al., 1990). Euphoria, urinary, breast and perineal discomfort and infant disturbances can all lead to reduced sleep, which may affect memory and psychomotor tasks. Theoretically, sleep patterns are close to normal within 2 or 3 weeks of delivery but breastfeeding mothers obviously have more disrupted sleep (Quillin, 1997).
Case study 14.3
Sandra is a first-time mother who delivered a healthy male infant 3 days ago. She went home on the day of the birth as she appeared to be coping well with breastfeeding and caring for her infant. The community midwife visits at lunchtime on the third day to find a very distressed mother, partner and infant. They have had no sleep and the baby has been very fractious and wakeful.
• What are the possible physiological causes that have contributed to this situation?
• What would reassure the midwife that everything was normal and what support, help and advice could the midwife give to the family during this difficult period?
Usually by day 10 the mother and baby have established a feeding cycle. Although fatigue is common and normal, the mother should be developing strategies to cope with this, such as daytime sleeps. The mother should be independently caring for herself and the baby and interacting fully with members of her family and other people. Offspring provide their mothers with stimuli that elicit behavioural responses and emotional reactions; comparative studies suggest that these nurturing responses are evolutionarily conserved (Stern, 1997).
Many women experience a lack of libido (sex drive) during the first few months following delivery. This may be complicated by trauma to the reproductive tract during delivery. Sexual desire, expression and satisfaction may be reduced after delivery. Sexual activity may be affected by fatigue, altered body image, marital adjustment, dyspareunia, lactation, traditional taboos, vaginal bleeding or discharge, insufficient lubrication or fear of waking the baby.
Return to fertility
In pregnancy, ovarian function is suppressed by the high level of placental steroids. Women who do not breastfeed begin to menstruate, on average, about 55–60 days after delivery and to ovulate at about 40–50 days after delivery (Wang and Fraser, 1994), whereas lactation can delay ovulation to 30–40 weeks after delivery and menstruation to 8–15 months, depending on the duration and extent of breastfeeding. Although ovarian activity is almost invariably suspended, there have been reported cases of women who conceive within 2 weeks of giving birth (Hytten, 1995). The return to fertility exhibits similar hormonal profiles as puberty with a circadian pattern of LH secretion. A proportion of women become pregnant during lactational amenorrhoea but the degree of suppression of fertility depends on infant-feeding patterns and perhaps on maternal nutrition. Lactational effects on fertility are reduced as the spaces between the feeds increase and as the baby receives supplementary feeding. Where the number of sucking episodes is 10–20 per day, as is normal in many developing countries, resumption of ovarian activity is unlikely. With 5–6 feeds per day, the duration of feeds is important in suppressing ovulation. However, lactational amenorrhoea appears to reduce the likelihood of conception for a few months (Lewis et al., 1991), although it is probably more successful in achieving birth spacing.
Many women purposely choose to limit the number of children they wish to have. There are many economical and social issues that impinge on this; however, it is important to recognize that there are some women for whom certain (or all) methods of contraception are not acceptable on cultural and religious grounds. The return of fertility is very difficult to assess as factors such as breastfeeding, cultural and religious practice, genetic variation and disease may all compound the identification of return of the fertility cycle. It is important to emphasize that ovulation precedes menstruation so amenorrhoea does not guarantee the absence of fertility.
The role of the midwife
In the UK, most women are discharged from midwifery care by day 10; however, the midwife may visit up to day 28 in the postnatal period if required. Once the midwife is satisfied that the physiological transition is progressing normally then the discharge can be completed. The health visitor and general practitioner (GP) continue care of the mother and baby. The responsibilities of the midwife in the puerperium and at discharge include giving advice to women on a number of issues including infant feeding, parent craft, pelvic floor exercises, contraception and sources of psychological support.
Complications of the puerperium
Hypercoagulability of pregnancy probably evolved to protect women from excessive bleeding associated with miscarriage and delivery (James, 2009). However, the increase in potential clot formation can have a physiological disadvantage both in pregnancy and following delivery because thrombi (blood clots) can form within the venous system. During the third trimester, the pregnant woman develops a pronounced state of hypercoagulation, such that her blood is more likely to clot than it would in the non-pregnant state and the effects of progesterone on venous muscle tone increase stasis of flow and decrease venous capacitance. In addition, mechanical obstruction by the uterus can decrease venous outflow and women may become less mobile. The risk of thromboembolic disorders in pregnancy is about six times higher than previously, and increases further in the puerperium. This is enhanced by a decrease in fibrinolytic activity (the breakdown of fibrin forming a blood clot) and raised concentration of clotting factors. Vascular trauma during delivery and haemoconcentration of the blood from physiological diuresis following delivery augments the increase in clotting factors. Some women may suffer from protein C and protein S deficiencies, these proteins are anticoagulants and so in pregnancy and the postnatal period these women are at greater risk of developing DVT (Mahmoodi et al., 2010). The risk of thrombosis persists for at least 8 weeks following deliver (James, 2009).
Thrombophlebitis is inflammation due to the formation of a thrombus (clot) in a superficial vein. The commonest site of thrombus formation is in the saphenous vein supplying the calf of the leg. Symptoms include a tender reddened area over the thrombosed vein and possibly a small increase in pulse and temperature. Motility and elevating the legs at rest reduce the risk of thrombus formation; compression stockings may be helpful. Thrombophlebitis is unlikely to progress to pulmonary embolism (PE).
Deep vein thrombosis
DVT is less common but carries the risk of a clot dislodging, which can cause PE. Hypercoagulability is increased with increased maternal age, parity, dehydration following delivery and delivery by caesarean section. Risk factors include immobility, pelvic or leg trauma, obesity, pre-eclampsia, caesarean section, instrument-assisted delivery, haemorrhage, multiparity, varicose veins, a previous history of a thromboembolic event and hereditary or acquired thrombophilias (Colman-Brochu, 2004). It has been observed clinically that there is an increased risk of DVT in the left leg, especially after a caesarean section, because blood flow velocity is reduced to a greater extent (Macklon and Greer, 1997). DVT may cause no symptoms or the woman may experience pain and swelling over the affected area and occasionally pyrexia. There may be marked differences in calf size or, in extreme cases, circulation to the leg below the thrombosis may be affected so the leg appears cold and white and possibly oedematous. DVT is confirmed by Doppler ultrasound or impedance plethysmography.
PE is an obstetric emergency that may follow DVT or occur without warning. PE is a condition that contributes towards maternal mortality associated with pregnancy (Bourjeily et al., 2010). If a thrombus (a fragment of the blood clot) breaks away and enters the venous system, it is then carried in the venous system to the right side of the heart and the pulmonary circulation. As the pulmonary arteries reduce in size, the thrombus may occlude arterial vessels within the lungs, causing major damage. Symptoms are sudden collapse, acute severe chest pain, dyspnoea, cyanosis, haemoptysis and shock. A woman with a PE will require intensive treatment and care.
A PE is more common in the postnatal period compared to the antepartum period. This may be due to the physiological reversal of haemodilution happening much faster (usually by day 3) than the physiological reversal of increased clotting factors which may take up to 6 weeks to return to prepregnancy values.
Women assessed to be at increased risk of thrombus formation are treated with prophylactic anticoagulants, such as heparin and synthetic analogues such as enoxaparin. DVT is usually treated with heparin and, if required, long-term anticoagulation therapy with drugs such as warfarin is commenced. Warfarin use in pregnancy is contraindicated as it is transported across the placenta; but postnatal women who choose to breastfeed can have warfarin treatment as it not secreted in significant levels in the breast milk.
Postpartum thyroid disorders
Transient thyroid disorders are fairly common during the postpartum period (Okosieme et al., 2008). Postpartum women, especially if older than 35, are at increased risk of developing Graves' disease and postpartum thyroid disorder (PPTD) transiently affects 6–9% of postpartum women. It is thought that PPTD is probably due to changes in the immune system as it switches back to being Th1 dominated (see Chapter 10). The syndrome is biphasic (Weetman, 2010). The initial effects are thyrotoxicosis with thyroid cell destruction and excessive release of stored thyroid hormone from the damaged thyroid tissue causing mild hyperthyroidism for 2–4 weeks. This is followed by a period of hypothyroidism as the damage to the thyroid progresses, which usually lasts 2–4 months. Typical symptoms are mild and include fatigue, cold intolerance, hair damage and weight gain with high TSH and low free T4 levels. Normal thyroid function is established in most women with PPTD within a year but a proportion of women remain hypothyroidic (Stuckey et al., 2010). The condition may recur in subsequent pregnancies (Weetman, 2010) and the risk of developing permanent hypothyroidism is increased.
Risk of infection
In the puerperium, the woman is at increased risk of infection, particularly that associated with the genital tract, urinary system, breast and any site of thrombophlebitis. The placental wound site, lacerations and incisions of the perineum and the lax urinary system are especially vulnerable. The lochia provides ideal culture conditions for microorganisms. Other predisposing factors include anaemia, fatigue, malnutrition, traumatic delivery and the presence of retained tissue in the uterus. Both maternal and neonatal infection (see Chapter 15) may be caused by endogenous or exogenous organisms (Box 14.4).
Examples of microorganisms causing puerperal infection
• Escherichia coli
• Clostridium perfringens
• Streptococcus faecalis
• Pseudomonas aeruginosa
• β-Haemolytic streptococci
• Staphylococcus aureus
Common symptoms of infection include:
• pyrexia (up to 40 °C)
• tachycardia (up to 140 beats per minute)
• subinvolution of the uterus
• malaise, lower abdominal pain and back pain
• heavy offensive-smelling lochia.
Less common symptoms usually associated with severe sepsis (Dellinger et al., 2008) are:
• altered mental status
• marked oedema and positive fluid balance with acute oliguria
• hyperglycaemia in the absence of diabetes
– markers of inflammation such as high WBC count, high plasma C-reactive protein or procalcitonin levels
– haemodynamic variables such as arterial hypotension or hypoxia, signs of organ dysfunction, coagulation abnormalities and/or thrombocytopenia, high creatinine, ileus (absent bowel sounds)
– markers of impaired tissue perfusion such as hyperlactataemia or decreased capillary refill (or mottling).
Infection in the acute phase can inhibit lactation. When choosing antibiotics to treat infection in the puerperium, one needs to take into consideration whether the woman is breastfeeding and the potential effect of the transfer of the drug into breast milk.
Breast discomfort and after-pains
The establishment of lactation is covered in detail in Chapter 16; however, it is worth mentioning here two common problems that can occur during this period in relation to breastfeeding.
• If the baby has been incorrectly positioned, often because it is fractious or hungry and wanting to feed constantly, the nipple may become sore, cracked and bleed as a consequence. A break in the integrity of the nipple skin increases the risk of mastitis (localized and ascending infection usually caused by Staphylococcus aureus). Women experiencing early feeding problems need a lot of help and support. The baby needs to ‘fix’ or ‘latch on’ properly in order to provide adequate nipple stimulation to establish the feeding cycle.
• Sometimes the breasts become engorged or extended. Initially, this may be a venous cause due to the increased vascularization of the breast. However, when milk production increases (described as the milk ‘coming in’), the breast may initially be overproductive. The breasts may overfill with milk causing them to become distended and hardened, which may be uncomfortable or painful. The baby may need help achieving an appropriate position; however, once the feeding cycle is established the demand/supply balance is achieved and the breast engorgement problems will resolve.
The majority of deliveries within the UK have the third stage actively managed as opposed to passive or physiological management where the women deliver the placenta naturally (see Chapter 13). However, the administration of an anti-tocolytic (or ‘uterotonic’) drug such as Syntometrine (which contains ergometrine and oxytocin) may cause side effects following completion of the third stage; for example:
• nausea and vomiting
• transient rise in blood pressure
• palpitations and tachycardia
• chest pain
Most of these side effects are strongly associated with ergometrine so it is recommended that administration of intramuscular injection of syntocinon is used instead (NCCWCH, 2008). Also during the early puerperium, women may suffer side effects from pharmacological methods of pain relief administered during labour. Pethidine may induce drowsiness, fatigue and nausea within the mother and reduce the suckling instinct of the infant, thus interfering with feeding. The effects of an epidural anaesthetic may take several hours to wear off, which affects maternal mobility and the ability to void urine.
Women in the postpartum period have increased vulnerability to affective disorders which are classified on the basis of severity, such as postpartum ‘blues’, postpartum depression and postpartum psychosis. It is estimated that as many as 80% of women may experience some fluctuations in mood, mostly transient emotional disorders at about day 3 described as ‘the blues’ (Steiner, 1998). Ten to twenty percent of puerperal women develop true depressive illness, which may have a later onset (or referral) and delayed recovery. A few women (0.1–0.2%) develop severe prolonged psychotic illness following childbirth. Although many of these cases may be recognized in the early postnatal period, some become evident much later and depression is frequently under-reported and not always recognized. Certain symptoms are recognized to be important in the diagnosis of postnatal depression (Box 14.5). Overall, these figures mean that postnatal depression is the most common disorder of the puerperium.
Classic signs of postnatal depression
• Depressed mood
• Sleep disturbance not related to discomfort and infant wakening
• Unable to cope—guilt
• Thoughts of harming self or baby
• Rejection of baby
• Altered libido
The aetiology of these depressive disorders is not fully understood. Immediately after delivery, the infant may feed often and this may be increased at night adding to maternal fatigue. Initially, the mother's fatigue is overcome by intense feelings of relief and excitement at the birth of her baby. By day 3, however, the woman may become emotional, tearful and tired and need a lot of support and comfort during this period. This low ebb of hormonal withdrawal is physiologically marked by the commencement of full lactogenesis following the initial production of small volumes of colostrum (see Chapter 16). The ‘blues’ coincide with lactation, breast engorgement, perineal pain and wound discomfort.
As the withdrawal of steroid hormones has been postulated to have a role in the aetiology of postnatal depression, clinical trials have investigated whether either progesterone or oestrogen supplementation might be of prophylactic or therapeutic value in postnatal depression. Some uncontrolled studies (e.g. Dalton, 1980) reported the benefit of progesterone in preventing postnatal depression. However, use of synthetic progesterone is positively associated with depression in the postnatal period and should be used with caution (Karuppaswamy and Vlies, 2003).
Oestrogen has also been associated with psychological well-being (Brace and McCauley, 1997); sudden changes in oestrogen levels such as those experienced in the puerperium may result in effects on neurotransmitter release. Oestrogen therapy may be of modest value in severe postnatal depression but more research is needed.
Other authors suggest that levels of cortisol or β-endorphin have a stronger association with postnatal depression (Harris et al., 1996). The hypothalamic–pituitary–adrenal (HPA) axis is very active in the third trimester as placental corticotrophin-releasing hormone (CRH) production increases and CRH-binding protein (CRH-BP) levels fall. Suppression of hypothalamic CRH secretion is implicated in the aetiology of postnatal depression (Magiakou et al., 1996). The relationship between breastfeeding and postnatal depression is controversial. However, hormones involved in lactation affect cortisol levels (Amico et al., 1994). Lactation may also predispose the breastfeeding mother to depression by isolating her and increasing levels of fatigue. Women who develop postnatal depression make a good recovery with the right treatment and support. Exercise programmes have been found to decrease anxiety and depression in the puerperium significantly (Koltyn and Schultes, 1997). The recurrence of postnatal depression is high, which allows identification of women at increased risk. It has been suggested that women who have a low intake of fish (and omega-3 fatty acids) are more likely to suffer from postnatal depression (Hibbeln, 2002). Certainly, the high docosahexaenoic acid (DHA) requirements of the fetus and for breast milk may deplete women. Although a number of studies have investigated possible relationships between dietary factors, including omega-3 fatty acids and various micronutrients, and the aetiology and treatment of postnatal depression, the results are generally inconsistent and inconclusive (Derbyshire and Costarelli, 2008).
Case study 14.4 describes an example of a hormonal complication of the puerperium.
Case study 14.4
At delivery, Sarah suffered a large haemorrhage that was difficult to control; she finally underwent a hysterectomy following a total blood loss of over 4 L. Her recovery was uneventful but within 6 months she was diagnosed as suffering from Sheehan's syndrome—necrosis of the pituitary gland.
• What would her symptoms be?
• What endocrine function would be disrupted as a result of this condition?
• Maternal physiology and anatomy adapt rapidly to the withdrawal of steroid hormones, following the delivery of the placenta. These dramatic physiological changes increase the risk of infection, haemorrhage and psychological and emotional changes.
• The uterus rapidly involutes after delivery; normal involution can be monitored by assessment of fundal height and characteristics of the lochia.
• After delivery, there is a dramatic and rapid decrease in circulating blood volume followed by a return to normal cardiovascular parameters. As stroke volume initially remains high, bradycardia is usual, particularly in the first 2 weeks.
• The postpartum physiological changes allow the woman to tolerate considerable blood loss at delivery, but alteration in clotting factor concentration and venous stasis predispose the woman to thromboembolic disorders; the risk is enhanced by immobility and sepsis.
• Marked diuresis is normal in the puerperium but overdistension, or decreased sensitivity, of the bladder can predispose the woman to urinary problems.
• Ovulation occurs before menstruation and is delayed by breastfeeding; lactational amenorrhoea is useful in birth spacing rather than being a reliable method of contraception.
Application to practice
In comparison to pregnancy, when the changes induced by endocrine effects are at a relatively slow pace, the reversal of this in the puerperium is much more dramatic. These rapid changes occur at the same time as another endocrine-induced change resulting in the initiation of lactation.
Fatigue from labour, perineal pain from trauma and the demands of a newborn infant can also complicate the situation.
The midwife needs to use her knowledge of the puerperium to support women through this often difficult period of adaptation.
Knowledge of mental health issues in the postnatal period is essential in differentiating between mild depressive states and recognizing severe psychotic disorders.
Annotated further reading
Lynch, C.; Keith, L.G.; Loonde, A.; et al., In: A textbook of postpartum haemorrhage: a comprehensive guide to evaluation, management and surgical intervention (2006) Sapiens Publishing.
This book provides an in-depth guide to the management of postpartum haemorrhage in relation to the possible causes and factors that contribute to excess bleeding post delivery. Midwives will find the detail of this obstetric text very useful in developing their understanding and ability to deal with this often complex situation.
Barlow, J.; Svanberg, P.O., In: Keeping the baby in mind (2009) Routledge, London.
An interesting book which covers the transition to parenthood from the infant's mental health and development perspective.
Baston, H.; Hall, J., In: Midwifery essentials: postnatal, vol. 4 (2009) Churchill Livingstone.
The fourth title in the Midwifery Essentials series which includes the postnatal examination of the woman and neonate, hospital postnatal care and caesarean section, emotional wellbeing, postnatal fertility issues and lactational support.
Byrom, S.; Edwards, G.; Bick, D., In: Essential midwifery practice: postnatal care (2009) Wiley-Blackwell.
An edited textbook written by midwifery experts which covers postnatal clinical care in hospital and community settings, transition into parenthood, empowering parents and supporting vulnerable women and their families.
Hanley, V., In: Perinatal mental health: a guide for health professionals and users (2009) Wiley-Blackwell.
A comprehensive reference book health professionals which focuses on perinatal mood and mental health disorders and includes topics on the antenatal period, postnatal depression, bipolar disorder, psychosis, personality disorders, eating disorders, sexual issues, self harm and suicide.
Hughes, H., Postpartum contraception, J Fam Health Care 19 (12) (2009) 9–10.
A review covering the advantages and disadvantages of commonly used methods of postpartum contraception including lactational amenorrhoea, combined oral contraception, the progesterone-only pill, injectable methods, implants, intrauterine devices and systems, barrier methods and sterilization, and emergency contraception.
Moore, L.J.; Jones, S.L.; Kreiner, L.A.; et al., Validation of a screening tool for the early identification of sepsis, J Trauma 66 (2009) 1539–1546.
Practitioners may find this tool and guidelines useful in assessing women for signs of sepsis throughout the pregnancy continuum.
National Collaborating Centre for Mental Health, Antenatal and postnatal mental health: the NICE guideline on clinical management and service guidance. (2007) British Psychological Society/RCPsych Publications, (NICE guideline) .
This is a very comprehensive guide to a wide range of mental health issues in relation to pregnancy, childbirth and the postnatal period.
Royal College of Obstetricians and Gynaecologists, In: Thromboembolic disease in pregnancy and the puerperium: acute management green top guideline (2007) RCOG, London, p. 28.
Clinical guidance and management for the treatment of venous thromboembolism.
Royal College of Obstetricians and Gynaecologists, Reducing the risk of thrombosis and embolism during pregnancy and the puerperium Green-top Guideline. (2009) RCOG, London ; NO. 37.
Clinical guidance and management for the prevention of venous thromboembolism.
van Dillen, J.; Zwart, J.; Schutte, J.; et al., Maternal sepsis: epidemiology, etiology and outcome, Curr Opin Infect Dis 23 (2010) 249–254.
This review focuses on focus on new findings concerning epidemiology, etiology and outcome of maternal sepsis in low-income as well as high-income countries.
Amico, J.A.; Johnston, J.M.; Vagnucci, A.H., Suckling-induced attenuation of plasma cortisol concentrations in postpartum lactating women, Endocrinol Res 20 (1994) 79–87.
Blackburn, S.T., Maternal, fetal, and neonatal physiology: a clinical perspective. ed 3 (2007) Saunders, Philadelphia .
Bourjeily, G.; Paidas, M.; Khalil, H.; et al., Pulmonary embolism in pregnancy, Lancet 375 (2010) 500–512.
Brace, M.; McCauley, E., Oestrogens and psychological well-being, Ann Med 29 (1997) 283–290.
Clapp, J.F.; Capeless, E., Cardiovascular function before, during, and after the first and subsequent pregnancies, Am J Cardio. 80 (1997) 1469–1473.
Colman-Brochu, S., Deep vein thrombosis in pregnancy, MCN Am J Matern Child Nurs 29 (3) (2004) 186–192.
Cosner, K.R.; Dougherty, M.C.; Bishop, K.R., Dynamic characteristics of the circumvaginal muscles during pregnancy and the postpartum, J Nurse Midwifery 36 (1991) 221–225.
Dalton, K., Depression after childbirth. (1980) OUP, Oxford .
Dellinger, R.P.; Levy, M.M.; Carlet, J.M.; et al., Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008, Crit Care Med 36 (2008) 296–327.
Derbyshire, E.; Costarelli, V., Dietary factors in the aetiology of postnatal depression, Nutr Bull 33 (2008) 162–168.
Harris, B.; Lovett, L.; Smith, J.; et al., Cardiff puerperal mood and hormone study III: postnatal depression at 5 to 6 weeks postpartum, and its hormonal correlates across the peripartum period, Br J Psychol168 (1996) 739–744.
Hibbeln, J.R., Seafood consumption, the DHA content of mothers' milk and prevalence rates of postpartum depression: a cross-national, ecological analysis, J Affect Disord 69 (1–3) (2002) 15–29.
Howie, P.W., The physiology of the puerperium and lactation, In: (Editor: Chamberlain, G.) Turnbull's obstetrics ed 2 (1995) Churchill Livingstone, New York.
Hytten, F., The clinical physiology of the puerperium. (1995) Farand Press .
James, A.H., Venous thromboembolism in pregnancy, Arterioscler Thromb Vasc Biol 29 (2009) 326–331.
Karuppaswamy, J.; Vlies, R., The benefit of oestrogens and progestogens in postnatal depression, J Obstet Gynaecol 23 (4) (2003) 341–346.
Koltyn, K.F.; Schultes, S.S., Psychological effects of an aerobic exercise session and rest session following pregnancy, J Sports Med Phys Fitness 37 (1997) 287–291.
Lanir, N.; Aharon, A.; Brenner, B., Haemostatic mechanisms in human placenta, Best Pract Res Clin Haematol 16 (2) (2003) 183–195.
Letsky, E., The haematological system, In: (Editors: Chamberlain, G.; Broughton Pipkin, F.) Clinical physiology in obstetrics ed 3 (1998) Blackwell, Oxford, pp. 71–110.
Lewis, P.R.; Brown, J.B.; Renfree, M.B.; et al., The resumption of ovulation and menstruation in a well-nourished population of women breastfeeding for an extended period of time, Fertil Steril 55 (1991) 529–536.
Macklon, N.S.; Greer, I.A., The deep venous system in the puerperium: an ultrasound study, Br J Obstet Gynaecol 104 (1997) 198–200.
Magiakou, M.A.; Mastorakos, G.; Rabin, D.; et al., Hypothalamic corticotrophin-releasing hormone suppression during the postpartum period: implications for the increase in psychiatric manifestations at this time, J Clin Endocrinol Metab 81 (5) (1996) 1912–1917.
Mahmoodi, B.K.; Brouwer, J.L.; Ten Kate, M.K.; et al., A prospective cohort study on the absolute risks of venous thromboembolism and predictive value of screening asymptomatic relatives of patients with hereditary deficiencies of protein S, protein C or antithrombin, J Thromb Haemost 8 (6) (2010) 1193–1200.
Miller, A.W.F.; Hanretty, K.P., In: Obstetrics illustrated ed 5 (1998) Churchill Livingstone, New York, p. 336.
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Quillin, S.L., Infant and mother sleep patterns during the 4th postpartum week, Issues Compr Pediatr Nurs 20 (1997) 115–123.
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Swain, A.M.; O'Hara, M.W.; Starr, K.R.; et al., A prospective study of sleep, mood, and cognitive function in postpartum and nonpostpartum women, Obstet Gynecol 90 (1997) 381–386.
Sweet, B.; Tiran, D., In: Mayes' midwifery ed 12 (1996) Baillière Tindall, London, p. 405, 406.
Tekay, A.; Jouppila, P., A longitudinal Doppler ultrasonographic assessment of the alterations in peripheral vascular resistance of uterine arteries and ultrasonographic findings of the involuting uterus during the puerperium, Am J Obstet Gynecol 168 (1993) 190–198.
Thranov, I.; Kringelbachh, A.M.; Melchior, E.; et al., Postpartum symptoms: episiotomy or tear at vaginal delivery, Acta Obstet Gynecol Scand 69 (1990) 11–15.
Wang, I.Y.; Fraser, I.S., Reproductive function and contraception in the postpartum period, Obstet Gynecol Surv 49 (1994) 56–63.
Weetman, A.P., Immunity, thyroid function and pregnancy: molecular mechanisms, Nat Rev Endocrinol 6 (2010) 311–318.