Definition1. It is the period of adjustment after pregnancy and delivery when anatomical and

physiological changes of pregnancy are reversed and the body returns to the normal non pregnant state.. (reproductive tract returns to its normal, non-pregnancy state)

2. 6 weeks in duration. (periods after birth ). Early puerperal period lasts 2 hours.

PHYSIOLOGIC CHANGES OF THE POSTPARTUM PERIODGenitourinary ChangesThe most obvious postpartum change is involution of the uterus from a 1-kg structure with a 5- to 10-L volume to a 60-g structure holding 3 to 5 mL. This involution begins during the third stage of labor, accelerates after expulsion of the placenta, and continues over the next 5 to 6 weeks. Typically, the uterus is at the umbilicus after delivery of the placenta, and it decreases in height by about a centimeter a day until it again becomes a pelvic organ at about 12 days postpartum. Slower involution continues over the next several weeks until prepregnant size is attained. Restoration of the normal endometrial lining occurs by the 16th day postpartum. The cervix closes to about 1 cm over the 1st week postpartum, but may take several months to attain prepregnant firmness and length. The postpartum cervix often has a transverse or “smiling” appearance, as opposed to the nulliparous pinpoint appearance. This persists indefinitely.

SONOGRAPHY.Because the normal pattern of uterine involution varies significantly, it is sometimes difficult to identify an abnormal pattern of subinvolution. Although a patient’s complaints of persistent heavy bleeding should always be taken seriously, some patients do not verbalize these concerns or have a sense of what constitutes heavy bleeding. For this reason, postpartum daily rounds should always include some attempt to quantify bleeding. The fundus should be palpated each time the patient is evaluated, and any increase in fundal height should be further evaluated. Several groups have characterized the sonographic appearance of the postpartum uterus during various stages of involution. These references may assist in distinguishing pathology from normal variation.

RESUMPTION OF MENSES.Resumption of menses after delivery is highly variable. For most non-breastfeeding mothers, the first postpartum menses occurs at approximately 55 to 60 days (range 20 to 120) post delivery. Breastfeeding may delay return of menses by several months, especially if the child is getting no other supplemental source of nutrition. Although the first several cycles may be anovulatory, ovulation has been demonstrated in 52% of women whose menses resumed less than 60 days following delivery. It is therefore of primary importance that women be provided adequate birth control very early in the postpartum period.

PELVIC FLOOR SUPPORT.Some changes to the genitourinary system are much longer in resolving, and some may never fully revert to the prepregnant state. A burgeoning volume of literature on pelvic floor support implicates childbirth as the initiation of a whole host of conditions including

stress urinary incontinence, incontinence of flatus or feces, uterine prolapse, cystocele, and rectocele. Many variables affect the duration and severity of these conditions, including the patient’s intrinsic collagen support, the size of the infant, the route of delivery, and the degree of perineal trauma occurring either naturally (lacerations) or iatrogenically (episiotomy). Even when full recovery of pelvic floor integrity appears to be the case, menopause may elicit a return of many of these problems as the collagen support of estrogen is withdrawn. Although surgical intervention should not be considered until 6 months postpartum (the length of time for complete restoration of connective tissue support), an aggressive program of pelvic floor exercises may be prescribed at any time during the antenatal or postpartum course and has been shown to be of benefit in some series.

Cardiovascular ChangesCardiovascular changes in the puerperium are dramatic. Blood volume increases by about 50% at the time of delivery. There is an average 500-mL blood loss at vaginal delivery, and a gradual replacement of this with an “autotransfusion” of 500 to 750 mL as the uterus contracts. This massive volume shift, as well as hormonal vascular effects and compression-decompression of the great vessels, all result in measurable and significant changes in every cardiac function parameter—mean arterial pressure, cardiac output, stroke volume, and systemic vascular resistance are all affected. This makes delivery and the few days following it extremely risky for patients with pre-existing cardiac conditions that limit adaptability to the rapid changes taking place. Most of the hemodynamic recovery occurs in the first 2 weeks postpartum, with more gradual shifts continuing over the next 4 or 5 months.

Renal ChangesRenal anatomic changes of pregnancy (particularly dilated ureters) persist for at least 5 days postpartum. Renal function (plasma flow and glomerular filtration rate) are at prepregnant levels by 6 weeks postpartum.

Metabolic/Hormonal ChangesMetabolic and hormonal changes postpartum are poorly understood and probably of much greater importance than the paucity of literature would suggest. The plummeting of estrogen and progesterone levels may play a role in the mood changes associated with the postpartum period, and there is an interesting association of testosterone level with mood as well. Changes in blood volume, vascular bed area, all of the cardiac parameters mentioned previously, as well as activity level, sleep pattern, and emotional stressors are all profound during the first 2 to 6 weeks postpartum, and the ability of the body to metabolically compensate is astounding but imperfect. It is not surprising that many women with seemingly completely normal findings nonetheless complain of periods of profound exhaustion or mood lability during this period.

Breast ChangesChanges in the breast begin well before delivery but become most dramatic postpartum. Several hormones interact to allow smooth production and excretion of milk, including the

withdrawal of estrogen and progesterone, along with prolactin, glucocorticoid, insulin, and thyroid hormone activity. For approximately 3 days postpartum, the breast secretes colostrum, distinct from milk in having higher amounts of immunoglobulins and white blood cells and lower amounts of fat and lactose. Over 2 weeks, the milk assumes its typical nutritional properties.

Breast milk excretion requires oxytocin release, which usually occurs through a reflex initiated by suckling. Oxytocin causes contraction of the myoepithelial cells surrounding the alveoli and leads to milk ejection. Whereas the mechanics of breastfeeding seem quite straightforward, many women have substantial difficulty in establishing a comfortable breastfeeding capability. The practicalities are such that a lactation consultant is an essential resource of any postpartum service.

Bone DensityBone density decreases somewhat during normal pregnancy, probably due to calcium mobilization from maternal skeleton to fetal. The effect of breastfeeding on the restoration of bone mineral density is controversial, with some studies showing a continued loss of bone during breastfeeding and others showing stabilization at delivery levels. The exact time course of maternal bone remineralization is unclear, but it would appear that there is no long-term loss of bone mineral density associated with pregnancy.

Hematologic Changes of the PuerperiumPrimary changes of the puerperium include the acute loss and gradual recovery of red blood cells and iron, and a sharp leukocytosis in the 1st postpartum day. Although this leukocytosis may change the parameters whereby a postpartum infection is diagnosed, a white blood cell count can nonetheless be useful in the assessment of febrile morbidity. The physiologic leukocytosis is probably due to demargination and resolves within a few days of delivery.

MANAGEMENT OF THE NORMAL PUERPERIUMPerineal CarePerineal care used to be one of the central facets of the hospitalized postpartum course. With the decrease in use of routine episiotomy, inspection of the perineum is no longer a well-ingrained ritual in the habits of obstetric caregivers. Nonetheless, if a significant laceration or episiotomy has been sustained, the perineum should be inspected at least once prior to discharging the patient to home. Although perineal complications are uncommon, they are invariably highly consequential when they do occur. Sitz baths can provide substantial comfort as well as cleansing, and a simple squirt bottle with tap water can be used for perineal cleansing after bladder or bowel evacuation. If lacerations have occurred in the anterior compartment (upper labia or clitoris), voiding function should be monitored carefully. Occasionally, catheterization is required because of swelling and/or discomfort. This can normally be discontinued after 24 hours. Stool softeners are often prescribed if there has been a third- or fourth-degree laceration, in hopes of preventing undue pressure on the repair site.

LACTATION.Breast care is one of the patient’s primary interests postpartum. For the non-breastfeeding patient, engorgement is an extremely uncomfortable condition and can account for substantial morbidity. For the breastfeeding woman, issues such as nipple care and maintenance of good milk flow are of concern. Health care professionals are unfortunately often poorly trained to address these concerns, with little practical experience to supplement training.

MEDICATION USE IN LACTATION.One of the most commonly asked questions in the postpartum period regards medication use and breastfeeding. Each medication should be reviewed in a current publication prior to approval of its use because intuition does not always suffice with regard to concentration in milk and effects on the infant. One of the most common “medications” used by patients who are breastfeeding is ethanol. This is because there is a substantial mythology that alcohol stimulates breast milk production and is nutritious for the infant. In fact, alcohol slightly decreases milk production, and crosses easily into breast milk, where it has the same effects on the infant as on an adult. There is no established or theoretical benefit to its use, and this should be explicitly discussed with the patient, as she may not bring it up herself. Depot medroxyprogesterone acetate, on the other hand, does appear to increase milk production and carries no known deleterious effect on the infant, making it an excellent choice for contraception in the breastfeeding patient.

CARE OF THE BREASTFEEDING BREASTS.Breasts should be emptied whenever they become uncomfortably full, to avoid engorgement and mastitis. If the infant is not interested in feeding, milk can be expressed and frozen for later use. Use of a breast cream to help protect the nipples against cracking has been helpful. Any signs of skin breakdown should be treated promptly, and a high index of suspicion should be maintained for the possibility of yeast infection, especially if the infant has any sign of thrush.

CARE OF THE NON-BREASTFEEDING BREASTS.Women who are not breastfeeding should be instructed to wear a tightly fitting bra continuously except while in the shower (including while sleeping). Stimulation should be avoided, even to the extent of not allowing a direct stream of water from the shower to hit the breasts. Often this is sufficient to prevent engorgement, but in the event the breasts do fill despite these measures, ice packs and nonsteroidal anti-inflammatories have been very effective at providing relief. Medication should be used only if conservative measures fail. Early pharmaceutical attempts at lactation suppression included high doses of estrogens or androgens, but large doses of estrogen have been associated with a 4-fold to 10-fold increase in the risk of thromboembolic disease, and elevated testosterone levels have been associated with depression and anger. Bromocriptine has been widely used and is highly effective at suppressing lactation, but it has also been associated with postural hypotension, paradoxical hypertension, and there are case reports of stroke and myocardial infarction. Although these grave side effects are extremely uncommon, the fact that most

women who choose not to breastfeed will never become engorged is reason enough not to prescribe lactation suppression as a routine postpartum order.

Rh FactorIf the parturient is Rh-negative, the infant’s Rh status should be evaluated via cord blood. If the infant is Rh-positive and there was no evidence of an unusual fetal-maternal transfusion, the standard dose of 300 μg of Rh-immune globulin may be administered. This will provide passive immunity for up to 30 mL of fetal blood in the maternal circulation. If the infant is Rh-positive and concerns exist regarding a greater red cell exchange (abruption, previa, abdominal trauma, severe neonatal anemia, bloody or wine-colored amniotic fluid at rupture of membranes), then a quantitative method such as the Kleihauer-Bettke test should be used to determine an approximate volume of fetal blood in the maternal circulation, and the dose of Rh-immune globulin should be calculated based on this estimate.

ContraceptionWhereas patients are often not considering contraception in the immediate postpartum period, providers should be. As indicated previously, couples often resume intercourse prior to a 6-week postpartum check, and ovulation may occur quite soon after delivery in the nonlactating woman. Ideally, options for birth control should have been discussed prior to labor, but no woman should be discharged from the postpartum ward without documentation of contraception planning. Other excellent postpartum contraceptive choices include intrauterine devices (copper or levonorgestrel), depot medroxyprogesterone, and in some cases, combination or progestin-only oral contraceptives. Intrauterine devices should not be placed until 6 weeks postpartum to allow for optimal uterine involution, so some parturients choose a single injection of depot medroxyprogesterone at time of hospital discharge to allow near-perfect coverage. One of the primary advantages of depot medroxyprogesterone is its extended action. A single injection will provide reliable contraception for up to 3 months, allowing some flexibility in postpartum follow-up. This is particularly useful when patient compliance is suspect and there is a special need to space pregnancies (such as in adolescents or profoundly anemic women). As noted previously, depot medroxyprogesterone may also actually increase milk production in lactating women. Progestin-only oral contraceptives have been highly studied and found to be safe in breastfeeding women, but are associated with elevated levels of maternal milk triglycerides compared with nonhormonal methods. They also have a somewhat higher failure rate than other methods. This is compensated for in the exclusively breastfeeding patient by the ovulation suppression associated with lactation. As soon as supplementation occurs, however, the ovulation-suppressing benefits of breastfeeding sharply diminish, and risk of unexpected pregnancy increases. Use of combination estrogen-progesterone contraceptives remains controversial. If administered immediately postpartum, they may diminish or entirely prevent milk production. In addition, there is a distinct increase in thromboembolic risk associated with immediate postpartum estrogen use. If use is deferred 2 weeks, however, they may suppress the quantity of milk only very slightly, and there is no evidence of any deleterious effect on infants of breastfeeding mothers who use combination contraceptives. The risk of

thromboembolism also decreases as vascular responsiveness returns, activity is increased, and uterine involution allows improved blood return from the pelvis and lower extremities. Thus, if combination contraceptives are used, it is recommended that low-dose formulations be prescribed and that they not be initiated prior to 2 weeks postpartum. Although there are no data with regard to combination contraceptive patches or vaginal rings, they should theoretically have the same limitations and outcomes as oral preparations because they function in much the same way.

ExerciseExercise during the postpartum period should be in proportion to the patient’s previous fitness and current energy level. Whereas most healthy women are capable of beginning a formal exercise program within days of delivery, the physical stressors of late pregnancy, labor and delivery, and caring for a newborn all take their toll in both exercise intensity and endurance. In general, it can be assumed that the level of exercise a patient was undertaking prior to pregnancy should be achievable by about 4 to 6 weeks postpartum if resumed in gradual increments. Complications such as postpartum hemorrhage, hypertensive disease, or postpartum depression may all delay the normal return of good physical condition, and the notion of “No pain, No gain” should be discouraged in favor of a more gradual physical conditioning program. Concerns about exercise diminishing milk production or infant acceptance of breast milk appear unfounded.

SYSTEMIC PATHOLOGY OF SPECIAL INTEREST IN THE POSTPARTUM PERIODSeveral conditions, although far from unique to the postpartum period, pose special risk or concern during this time. These include thyroiditis, connective tissue disease, thromboembolic disease, and domestic violence. Postpartum depression should by all rights also go in this category because the primary predisposing factor is a past history of depression. Nonetheless, because of its unique features in the postpartum period, it is addressed in the next section.

Connective Tissue DiseaseMany connective tissue diseases show significant regression during pregnancy, followed by postpartum flares. Of particular interest, however, is the new onset of disease in the postpartum period. Several series have suggested that, in women who eventually develop diseases such as rheumatoid arthritis, there is an uneven distribution of disease onset, with 12% to 20% developing initial signs and symptoms during the 1st year postpartum or postabortion. The immunology of the postpartum period is poorly understood, but the unexpectedly high new onset of connective tissue diseases as well as thyroiditis suggests a susceptibility to autoimmune phenomena not present at other times in a woman’s life.

Thromboembolic DiseaseThromboembolic disease is overrepresented in parturients because of a particular propensity for Virchow’s triad of risk factors—stasis due to poor return from the lower extremities (partly a compression phenomenon from the uterus against the inferior vena cava, and partly a progesterone effect of smooth muscle relaxation leading to decreased

vascular tone), hypercoagulability due to high endogenous estrogen levels, and trauma associated with prolonged labor or cesarean delivery. Special risk factors include hypertensive disorders, multiple-order gestation, smoking, and operative delivery, but these risk factors do not account for the majority of the pregnancy-related risk, at least of pulmonary embolism and stroke.33 Thus, no parturient may truly be considered at low risk for thromboembolic phenomena until the resolution of her hormonal and anatomic risks—in other words, until she has successfully traversed the postpartum period.

PATHOLOGY DISTINCTIVE TO THE POSTPARTUM PERIODMastitisMastitis is arguably the most easily recognized complication of the postpartum period next to hemorrhage. It occurs in 5% of breastfeeding women and is associated with fevers that can be quite high, erythema of a portion of a breast, induration, exquisite tenderness, and systemic findings such as chills and malaise. Ninety-five percent of these infections are from single-organism gram-positive sources, and 50% are due to Staphylococcus aureus. The organism is commonly transferred from the infant’s mouth during breastfeeding. Treatment includes thorough and frequent expression of milk (there is no risk to the infant of continuing to breastfeed, if the patient’s pain threshold will allow it; otherwise she should be instructed to manually express her breasts at frequent intervals) to prevent stasis, analgesics such as aspirin or acetominophen, local comfort measures such as a well-supporting bra and local heat, and a semisynthetic penicillin (erythromycin or cephalosporins are acceptable alternatives). Failure of the process to respond promptly suggests an abscess, and consideration must be given to incision and drainage.

Epidural Back PainBack pain is a common complaint of pregnancy, but new-onset postpartum back pain has often been associated with use of epidural analgesia. It appears to be more common with a dense motor block, presumably because this allows for nonphysiologic labor positions to be maintained for prolonged periods. It is also more common when epinephrine is used in the anesthetic, or when chloroprocaine is used rather than bupivacaine. Attention must be paid to this complaint because it is occasionally related to an epidural hematoma or abscess. Careful imaging studies are required to identify these complications. In general, new-onset postpartum backache related to epidural anesthesia is not severe, although it may persist for many months.

Postpartum Renal FailureSeveral extremely serious and sometimes lethal conditions may occur in the puerperium. Hypertensive crises such as eclampsia are certainly in this group, but are common in pregnancy as well as postpartum, and are thus dealt with extensively in other chapters.Postpartum renal failure is an idiopathic condition that is uncommon but devastating. It is similar to hemolytic uremic syndrome, and is manifested by renal failure, microangiopathic hemolytic anemia, thrombocytopenia, and hypertension. It can occur anywhere from 72 hours to 10 weeks following delivery. It can be extremely difficult to distinguish idiopathic postpartum renal failure from severe preeclampsia, acute tubular necrosis from hemorrhage, and sepsis. Once other diagnoses are excluded, the treatment

for postpartum renal failure is supportive, with dialysis as the primary intervention. It is usually reversible.

Sheehan’s SyndromePostpartum pituitary necrosis, commonly known as Sheehan’s syndrome, may occur following profound hemorrhage or eclampsia. The mechanism of injury is thought to be hypoxic because the anterior pituitary is the area of the brain most sensitive to hypoperfusion. The posterior pituitary is generally spared. Clinical signs include absence of lactation, amenorrhea, loss of axillary and pubic hair, genital and breast atrophy, “superinvolution” of the uterus, infertility, hypothyroidism (fatigue, cold intolerance, edema), and adrenocortical insufficiency (fatigue, anorexia, weight loss, decreased skin pigmentation, abnormal stress response). Many of these symptoms overlap common postpartum findings, so the diagnosis may be elusive, especially if necrosis is incomplete and areas of the anterior pituitary are spared. Any prolonged amenorrhea in the face of inability to lactate should lead the clinician to consider this diagnosis in the differential. Pituitary function is not generally retrieved, so replacement of anterior pituitary hormones must be lifelong.

Primary post-partum haemorrhage is the loss of >500 ml of blood per-vagina within 24 hours of delivery. It can be classified into two main types:

Minor PPH – 500-1000ml of blood loss Major PPH – >1000ml of blood loss

It is a major cause of obstetric morbidity and mortality worldwide.In this article, we shall examine the risk factors, clinical features and management of a primary post-partum haemorrhage.

Etiology and Risk Factors:The causes for primary post-partum haemorrhage can be broadly categorised by the 4 T’s – tone, tissue, trauma and thrombin.Tone‘Tone’ refers to uterine atony, which is the most common cause of primary post-partum haemorrhage. This is where the uterus fails to contract adequately following delivery, due to a lack of tone in the uterine muscle.The risk factors for uterine atony include:

Maternal profile: Age >40, BMI > 35, Asian ethnicity. Uterine over-distension – multiple pregnancy, polyhydramnios, fetal macrosomia. Labour – induction, prolonged (>12 hours). Placental problems – placenta praevia, placental abruption, previous PPH.

Tissue ‘Tissue’ refers to retention of placental tissue – which prevents the uterus from contracting. It is the second most common cause of 1° PPHTraumaThis refers to damage sustained to the reproductive tract during delivery (e.g. vaginal tears, cervical tears). Risk factors include:

Instrumental vaginal deliveries (forceps or ventouse)

Episiotomy C-section

Thrombin‘Thrombin’ refers to coagulopathies and vascular abnormalities which increase the risk of primary post-partum haemorrhage:

Vascular – Placental abruption, hypertension, pre-eclampsia. Coagulopathies – von Willebrand’s disease, haemophilia A/B, ITP or acquired

coagulopathy i.e. DIC, HELLP.

Fig 1 – Placenta praevia, where the placenta is inserted into the lower uterine segment. It is an important risk factor for post-partum haemorrhage.

Clinical FeaturesThe main feature of a post-partum haemorrhage is bleeding from the vagina.If there is substantial blood loss, the patient may complain of dizziness, palpitations, and shortness of breath.On Examination:

General examination may reveal haemodynamic instability with tachypnoea, prolonged capillary refill time, tachycardia, and hypotension.

Abdominal examination may show signs of uterine rupture i.e. palpation of fetal parts as it moves into the abdomen from the uterus.

Speculum examination may reveal sites of local trauma causing bleeding. Examine the placenta to ensure that the placenta is complete (a missing cotyledon

or ragged membranes could both cause a PPH).

Fig 2 – A complete placenta. In the assessment of post-partum haemorrhage, the placenta should be examined.InvestigationsThe initial laboratory tests in primary post-partum haemorrhage include:

Full blood count Cross match 4-6 units of blood Coagulation profile Urea and Electrolytes Liver function tests

ManagementThe management of primary post-partum haemorrhage should include the simultaneous delivery of TRIM:

Teamwork (Immediate Management) Resuscitation (Immediate Management) Investigations and Monitoring (Immediate Management) Measures to arrest bleeding (Definitive Management)

Immediate Management Teamwork – Involve appropriate colleagues for minor and major PPH, including

the midwife in charge and midwives, obstetricians, anaesthetists, blood bank, clinical haematologist and porters. Communication between the team, and diligent documentation is vital.

Investigations and Monitoring – Investigations as above. Monitoring should include RR, O2 sats, HR, BP, temperature every 15 mins. Consider catheterisation and insertion of a central venous line.

ResuscitationResuscitate the patient via an A-E approach:

Airway o Protect airway (may lose it with reduced levels of consciousness).

Breathing o 15L of 100% oxygen through non-rebreathe mask. 

Circulation: o Assess circulatory compromise (Cap refill, HR, BP, ECG)

o Insert two large bore (14G) cannulas and take blood samples (see below) Start circulatory resuscitation. Give cross-matched blood as soon as it

is available, until then give up to 2L of warmed crystalloid and 1-2L of warmed colloids, then transfuse O negative or uncross matched group specific blood.

o Additional blood productions i.e. factor VIIa in Haemophilia A, and if major haemorrhage protocol activated may need to supplement fresh frozen plasma, platelets, fibrinogen. (Discussion with blood bank)

Disability o Monitor patient’s Glasgow coma score (GCS).

Exposure o Expose patient to identify bleeding sources.

Definitive ManagementThe definitive treatment for primary post-partum haemorrhage is largely dependent on the underlying cause:Uterine Atony

Bimanual compression to stimulate uterine contraction – insert a gloved hand into the vagina, then form a fist insider the anterior fornix to compress the anterior uterine wall and the other hand applies pressure on the abdomen at the posterior aspect of the uterus (ensure the bladder is emptied by catheterisation).

Pharmacological measures (Table 1) – act to increase uterine myometrial contraction.

Surgical measures – intrauterine balloon tamponade, haemostatic suture around uterus (e.g. B-lynch), bilateral uterine or internal iliac artery ligation, hysterectomy (as a last resort).

Fig 3 – Management of PPH; (a) Bimanual compression, (b) Balloon tamponade.

TraumaPrimary repair of laceration, if uterine rupture: laparotomy and repair or hysterectomy.TissueAdminister IV Oxytocin, manual removal of placenta with regional or general anaesthetic, and prophylactic antibiotics in theatre. Start IV Oxytocin infusion after removal.ThrombinCorrect any coagulation abnormalities with blood products under the advice of the haematology team.

Table 1 – Drugs used in Primary Post-Partum Haemorrhage

Drug Mechanism of Action Side Effects Contraindications

Syntocinon

Synthetic oxytocin, act on oxytocin receptors in the myometrium

Nausea, vomiting, headache, rapid infusion à hypotension

Hypertonic uterus, severe CVS disease

Ergometrine Multiple receptor sites action

Hypertension, nausea, bradycardia

Hypertension, eclampsia, vascular disease

Carboprost Prostaglandin analogue

Bronchospasm, pulmonary oedema, HTN, cardiovascular collapse

Cardiac disease, pulmonary disease i.e. asthma, untreated PID

Misoprostol Prostaglandin analogue Diarrhoea

PreventionActive management of the 3rd stage of labour routinely reduces PPH risk by 60%:

Women delivering vaginally should be administered 5-10 units of IM Oxytocin prophylactically.

Women delivering via C-section should be administered 5 units of IV OxytocinSecondary postpartum haemorrhage is defined as excessive vaginal bleeding in the period from 24 hours after delivery to six weeks postpartum.The overall incidence of secondary postpartum haemorrhage in the developed world has been reported as 0.47% – 1.44%.In this article, we shall look at the risk factors, clinical features and management of secondary post-partum haemorrhage.Aetiology & Risk FactorsThe main causes of secondary post-partum haemorrhage are:

Uterine infection – (known as endometritis). o Risk factors include Caesarean section, premature rupture of membranes and

long labour. Retained placental fragments or tissue Abnormal involution of the placental site (inadequate closure and sloughing of

the spiral arteries at the placental attachment site).

Trophoblastic disease (very rare).A personal history of secondary PPH is a strong predictive factor; it has a recurrence rate of 20–25%.

Fig 1 – Placental site involution; the physiological occlusion and shedding of the spiral arteries. If this process is defective, secondary PPH can result.

Clinical FeaturesThe main symptom of secondary post-partum haemorrhage is excessive vaginal bleeding. In contrast to primary PPH (an acute condition requiring immediate management), the bleeding in secondary post-partum haemorrhage is usually not as severe.The patient may complain of spotting on-and-off for days after her delivery, with an occasional gush of fresh blood. However, approximately 10% of cases will present with massive haemorrhage – and this can quickly lead to hypovolemic shock.Additional clinical features will depend on the underlying cause. For example, women with endometritis may also present with fever/rigors, lower abdominal pain or foul smelling lochia (the normal discharge from the uterus following childbirth).On abdominal examination, the patient may complain of lower abdominal tenderness (usually a sign of endometritis), or the uterus may still be high (sign of retained placenta). Speculum examination is important in order to assess the amount of bleeding, and a high vaginal swab should be taken at the same time.InvestigationsIf the patient is haemodynamically unstable or is bleeding heavily, then call for help and follow the resuscitation algorithm. Resuscitation should be commenced prior to establishing a cause, and senior staff should be involved at the earliest opportunity.

Laboratory TestsThe appropriate laboratory tests include:

Full Blood Count Urea and Electrolytes C-Reactive Protein Coagulation profile Group and Save sample Blood cultures (if the patient is pyrexial)

Imaging TestsA pelvic ultrasound scan can assist in the diagnosis of retained placental tissue.Note: The over-diagnosis of retained placental tissue on ultrasound can lead to unnecessary surgical intervention. However, ultrasound does have a good negative predictive value, and is therefore particularly helpful in excluding a diagnosis of retained placental tissue.

Fig 2 – Pelvic ultrasound scan. Retained products are demonstrated by the yellow arrows.ManagementThe mainstay of treatment in secondary PPH is with antibiotics and uterotonics:

Antibiotics – usually a combination of ampicillin (clindamycin if penicillin allergic) and metronidazole.

o Gentamicin should be added to the above combination in cases of endomyometritis (tender uterus) or overt sepsis.

Uterotonics – examples include syntocinon (oxytocin), syntometrine (oxytocin+ergometrine), carboprost (prostaglandin F2) and misoprostol (Prostaglandin E1).

Surgical measures should be undertaken if there is excessive or continuing bleeding (irrespective of ultrasound findings). In continuing haemorrhage, insertion of a balloon catheter into the uterus may be effective.In the case of massive secondary PPH, management includes four components, which should be undertaken simultaneously. These are: (i) communication, (ii) resuscitation, (iii) monitoring and investigation (as described in the investigation section) and (iv) arresting the bleeding (with uterotonics/surgical measures, depending on the suspected cause).

Note: Any surgical evacuation of retained products of conception carries a high risk of uterine perforation (as the uterus is softer and thinner post-partum). It should involve a senior obstetrician in the planning and delivery of surgery.

Fig 3 – Balloon Tamponade, a surgical intervention of severe bleeding in secondary post-partum haemorrhage.Summary

Secondary PPH may occur between 24hrs up to six weeks postpartum. It may be associated with infection, retained placental tissue or abnormal involution

of the placental site. A pelvic USS should be arranged in order to rule out the possibility of retained

placental tissue. However, it is often difficult to differentiate between blood clots and retained tissue.

The mainstay of management is antibiotics and uterotonics. Surgical measures should be undertaken if there is excessive or continuing bleeding,

irrespective of ultrasound findings.