Acquired Bleeding Disorders in Pregnancy: Obstetric Hemorrhage


Maternal age over 40 years

Multiparity

Previous Cesarean section

Uterine scarring (previous myomectomy, uterine curettage)

Previous spontaneous or induced miscarriage

Cigarette smoking and use of drugs such

as cocaine

Multiple pregnancies

Previous placenta previa



Approximately 10% of women with placenta previa will develop placenta accreta; the diagnosis of placenta accreta is virtually excluded in the absence of placenta previa, with an incidence of only 0.005 % [12]. Previous Cesarean section (CS) and increased maternal age are independent risk factors for developing placenta accreta [12]. The incidence of placenta accreta and the risk of peripartum hysterectomy rises with the number of previous CS [14]. With the rising incidence of CS as well as steadily increasing average maternal age, the incidence of placenta previa/accreta and the associated complications are expected to rise.



14.2.2.2 Diagnosis


Current practice involves screening for low-lying placentas at the routine second trimester anatomy scan in order to predict the likelihood of placenta previa at delivery. If the placenta remains low lying in the third trimester, a transvaginal scan should be performed to confirm the diagnosis. Transvaginal sonography is deemed safe and more accurate in the diagnosis of placenta previa [1518].

The majority of women in whom the placental edge reaches or overlaps the internal os in mid-pregnancy will not have placenta previa at term. ‘Placental migration’ is believed to occur in the second and third trimesters as the lower segment of the uterus develops. It is less likely to occur in cases where the placenta is posterior, in women who have had previous Cesarean section(s) and when the placenta completely or substantially overlaps the internal os [1927].

Regardless of previous scan results, placenta previa should be suspected in any pregnant woman who presents with painless vaginal bleeding, particularly with a high presenting part or an abnormal fetal lie (because the placenta prevents the fetal presenting part, usually the head, from engaging into its mother’s pelvis).

Women who have had a previous CS and have an anterior placenta or placenta previa are at significantly increased risk of placenta accreta. Clinical suspicion of placenta accreta may be confirmed by ultrasonography; when ultrasonography is equivocal, magnetic resonance imaging (MRI) may clarify the situation. Two recent meta-analyses suggest that ultrasound has a sensitivity of 80–90 % in the diagnosis of placenta accreta, with specificity of 95–97 % [28, 29]. One of these meta-analyses [29] also looked at MRI diagnosis; sensitivity for placenta accreta was 82 % with a specificity of 88 %. Definitive diagnosis, however, can be made only at the time of CS and by histopathological examination.


14.2.2.3 Presentation and Management


Women with placenta previa and/or accreta may be asymptomatic (i.e. with no history of APH) or symptomatic (i.e. present with vaginal bleeding).

Elective CS is recommended for women with placenta previa persisting at term. CS is usually performed at 38 weeks’ gestation in cases with placenta previa and at 36–37 weeks in cases of placenta accreta, in order to minimise the risk of labour leading to bleeding prior to the booked CS date. Of course, if there is major APH prior to this, urgent delivery may be required, regardless of the gestation [20]. Evidence around the mode of delivery for women who have minor placenta previa is less clear. Women with a placental edge which lies less than 2 cm from the cervical os are likely to require delivery by CS. If the fetal head is engaged closer to term (as the lower segment continues to develop beyond 36 weeks), a transvaginal ultrasound scan is performed. If the leading placental edge is more than 2 cm from the internal os, the likelihood of achieving a vaginal delivery is at least 63 % [30]. The risk of postpartum hemorrhage (PPH) remains higher in this group of women, so should be anticipated and managed accordingly.

The management of women who present with bleeding depends on the extent of bleeding and fetal maturity. All women should have a full blood count (FBC) and ‘group and save’ on admission. Corticosteroids should be administered in women less than 35 weeks’ gestation to improve fetal lung maturity in the event of threatened preterm delivery [31]. All RhD (Rhesus) negative women should have estimation of fetal maternal hemorrhage by the Kleihauer-Betke test or flow cytometry, and receive prophylactic anti-D immunoglobulin intramuscularly (IM) [32]. Women who present with massive ongoing bleeding will require urgent surgical intervention following hemodynamic stabilisation. Women that are stable at presentation (i.e. no maternal or fetal compromise) with a self-limiting episode of painless unprovoked bleeding can be managed conservatively. However, they are thought to be at high risk of further sudden unprovoked bleeding, so are routinely admitted for 24–48 h following cessation of bleeding.

The use of tocolytics [3337] or cervical cerclage [38, 39] to treat women who bleed with placenta previa has been investigated; their use remains controversial and is not recommended for routine clinical use.

In the past it was recommended that women with major previa who had previously bled should receive in-patient care from approximately 34 weeks of gestation [40]. There is, however, no clear evidence to suggest an association between the extent of placenta previa and the likelihood of bleeding or the requirement for urgent delivery [22, 25]; the risk of bleeding and need for in-patient management should be assessed on an individual basis. All women with a risk of major APH should be advised to remain close to the recommended hospital for delivery for the duration of the third trimester.

As a minimum requirement, a consultant obstetrician and consultant anaesthetist should be present on site when women with a placenta previa undergo CS. All women should have a baseline FBC and four units of red cells cross-matched. The Royal College of Obstetricians & Gynaecologists’ (RCOG) guideline [25] suggests that prophylactic steroids for fetal lung maturation should be given prior to any elective CS performed up to 38 + 6 weeks’ gestation. Prior to delivery a consultant led discussion regarding the delivery, risk of significant hemorrhage, indications for transfusion and the possibility of peripartum hysterectomy should be held and documented clearly.

In cases of confirmed or suspected placenta accreta a consultant obstetrician and anaesthetist should be present and directly supervising delivery. The procedure is ideally planned ahead, involving a multidisciplinary team (including haematologist, interventional radiologist, intensive care staff, and blood transfusion laboratory staff), with blood and blood components available on standby. Discussion regarding the significant risk of peripartum hemorrhage, anticipated skin and uterine incisions and possible interventions including conservative management, use of cell salvage, interventional radiology and the possibility of hysterectomy should be discussed with the woman and documented clearly in both the notes and consent form.

When placenta accreta is suspected antenatally, the surgical avoidance of the placental site and non-separation of the placenta is thought to be associated with reduced maternal mortality by reducing the risk of bleeding [25, 41]. Data from observational studies support avoiding the placenta and leaving it attached, or proceeding with peripartum hysterectomy [4143] in cases of placenta percreta.

The risk of massive PPH is 12 times greater in women with placenta previa [40]. This is mainly because the lower segment of the uterus (where the placenta was implanted) contracts less efficiently than the upper segment (the usual site of placental implantation), leading to continued bleeding from the placental bed vessels. The rate of peripartum hysterectomy is also increased, particularly if the woman has had a previous CS.

Leaving the placenta adherent may reduce intra-operative bleeding but is associated with an increased risk of postpartum bleeding and infection. Prophylactic antibiotics may be considered postpartum. Prophylactic arterial embolisation or methotrexate have not been shown to reduce the risk of these complications and are therefore not routinely recommended [25].

If the placenta separates, it should be delivered. Subsequent hemorrhage must be anticipated and managed appropriately. Partial separation of the placenta is also possible and adherent portions may be left attached. Massive hemorrhage is highly likely in this situation and timely and appropriate management is essential [12, 44].



14.2.3 Placental Abruption


Placental abruption is defined as the partial or complete separation of the placenta prior to the delivery of the fetus [45].


14.2.3.1 Incidence and Risk Factors


Fewer than 1 in 100 pregnancies are complicated by placental abruption at term [46]. The occurrence is significantly higher in preterm pregnancies, affecting around 5 % of preterm deliveries [47]. Risk factors for placental abruption are summarised in Table 14.2 [4756].


Table 14.2
Risk factors for placental abruption [5058]





























Prior history of abruption (15–20 fold increase in risk) [53, 59]

Advanced maternal age

Multiparity

Cigarette smoking

Recreational drug use

Multiple pregnancy

Pre-eclampsia

Chronic hypertension

Gestational hypertension

Premature rupture of membranes

Oligohydramnios

Chorioamnionitis

Placental abruption is also associated with trauma [57], CS for first birth (compared to vaginal first birth) [56, 57], vaginal bleeding in early pregnancy [58, 59], thrombophilias [60, 61] and raised second trimester alpha-fetoprotein [62].


14.2.3.2 Diagnosis


The diagnosis of placental abruption is made clinically. The classic symptoms are abdominal pain and vaginal bleeding. In practice, there is a wide spectrum of clinical presentations ranging from asymptomatic or minor bleeding to massive abruption leading to fetal demise and/or severe maternal morbidity. Placental abruption may also present as idiopathic preterm labour. On examination, the uterus is often tender and may be hard (‘woody’) on palpation. There may be evidence of acute fetal hypoxia on fetal monitoring. In cases of concealed abruption women may present with hypovolemic shock or abnormal bleeding secondary to disseminated intravascular coagulation (DIC) as a result of concealed hemorrhage.

A range of ultrasonographic appearances of placental abruption have been described [6366]. The diagnosis of abruption is highly likely when the possibility of placental abruption is suggested by ultrasound. A seemingly normal ultrasound scan does not, however, exclude the diagnosis of placental abruption; by the time an abruption is apparent on ultrasound scan, it is usually clinically obvious.


14.2.3.3 Management


The management of placental abruption depends on the gestation, the presentation and degree of fetal and/or maternal compromise. All women who present with suspected placental abruption should have an FBC, coagulation studies and group and save on admission. Blood should be crossmatched when there is evidence of significant bleeding. Corticosteroids should be administered to women less than 35 weeks’ gestation in view of the increased risk of preterm delivery [31] and all RhD negative women should have estimation of fetal maternal hemorrhage by the Kleihauer-Betke test or flow cytometry, and receive prophylactic anti-D immunoglobulin IM [32].

Prompt delivery is indicated in women who present with placental abruption at or near term with a live fetus. If there is no evidence of fetal or maternal compromise, conservative management with the aim of vaginal delivery is appropriate and these women often labour and deliver quickly. Both the fetus and mother should be monitored closely during labour and, should there be any evidence of fetal or maternal compromise, delivery should be expedited.

Conservative management is appropriate in those who present with partial abruption in preterm pregnancies (between 20 and 34 weeks’ gestation) when the status of both the mother and fetus is reassuring. This is appropriate given that preterm birth is the leading cause of perinatal mortality in cases of placental abruption. If there is evidence of fetal or maternal compromise in pregnancies greater than 24 weeks’ gestation; delivery is indicated.

In women who present with severe abruption with fetal demise at any gestation, it is reasonable to aim for a vaginal delivery, as long as the mother is stable and there are no contraindications to vaginal delivery. If the labour fails to progress as expected, if the mother is unstable or there is clinical evidence of significantly worsening coagulopathy, Cesarean delivery is indicated. Fetal compromise alone is not an indication to expedite delivery if the fetus is not viable (i.e. less than 24 weeks’ gestation) and conservative management may be considered in these cases if the mother’s condition allows.

When placental abruption is discovered incidentally on ultrasound scan, a thorough history and examination should be sought including identification of predisposing factors. Management should be individually tailored, taking into account the gestational age as well as fetal and maternal well-being.

Significant PPH is 13 times more common in women with placental abruption [40]. This is because they may have already developed coagulopathy by the time the baby is delivered. Furthermore, they may have a Couvelaire uterus; this is when blood tracks into the myometrium, making it ‘woody’ so that it contracts poorly after delivery, leading to prolonged bleeding from the placental bed. These women are also at significant risk of developing hypovolemic shock and renal failure.

All women who are admitted with placental abruption associated with major hemorrhage should be managed as detailed below. Principles of management include careful clinical monitoring with regular assessment including fluid balance and blood tests to check FBC, renal function, and coagulation screen plus fibrinogen. Blood and blood volume should be appropriately replaced, and coagulopathy and thrombocytopenia corrected. Management should involve a multidisciplinary team including a haematologist, interventional radiologist, intensive care staff, laboratory staff, and blood bank.


14.2.4 Vasa Previa


Vasa previa is a condition in which the fetal blood vessels traverse the fetal membranes of the lower segment of the uterus below the presenting part, unsupported by the umbilical cord or placental tissue [67]. Vasa previa has an estimated incidence of 1 in 2,000–5,000 deliveries [67, 68]. Associated risk factors are summarised in Table 14.3 [6774].


Table 14.3
Risk factors for vasa previa [10, 7075]















A low-lying placenta in the second trimester

Accessory placental lobes

Multiple pregnancy

Pregnancies resulting from in vitro fertilization

Velamentous cord insertion


14.2.4.1 Diagnosis


In the absence of any signs or symptoms, vasa previa may be found incidentally on digital vaginal examination [75] or at a routine antenatal ultrasound scan. More often the diagnosis is confirmed following delivery of placenta.

The possibility of vasa previa, though rare, should always be borne in mind when a woman presents with vaginal bleeding, particularly if associated with rupture of the membranes and there is evidence of of fetal compromise. Immediate delivery should be arranged without delaying management to confirm the diagnosis.

Several tests may differentiate between fetal and maternal blood [7679]. These include the Kleihauer-Bekte test, the Apt test and hemoglobin electrophoresis. Their use is not usually practical in this situation given the invariable urgency for delivery. A bedside test using sodium hydroxide has been described by Lindqvist and Glen which may be useful in the setting of vasa previa but it needs further evaluation [80].

Vasa previa can be diagnosed antenatally with expert ultrasonography. Although specificity is good, the sensitivity cannot be determined owing to the low prevalence of this condition [8188]. Several groups advocate screening with Doppler ultrasound for those at increased risk of developing vasa previa [10, 8991], but this approach is not universally accepted as the test does not fulfil the requirements of a screening test; there remains insufficient information on the case definition, natural history and epidemiology of the condition. Moreover, if vasa previa is diagnosed, there is no consensus on appropriate management.


14.2.4.2 Management


There is currently no agreed management pathway for those with vasa previa diagnosed antenatally [87, 92]. If a woman presents with bleeding with a confirmed diagnosis of vasa previa, an urgent CS should be performed. In women who have confirmed vasa previa at term, an elective CS should be carried out at 39 weeks’ gestation, though some recommend earlier delivery [93]. In utero laser ablation of aberrant vessels has been reported in a few case reports [94].



14.3 Postpartum Haemorrhage


Postpartum hemorrhage is the commonest form of obstetric hemorrhage. There is currently no single globally agreed definition for PPH, hence various definitions exist [95]. Traditionally, PPH is defined as blood loss from the genital tract more than 500 mL occurring after delivery until 12 weeks after birth [96]. At CS, PPH has traditionally been defined as blood loss greater than 1,000 mL [97]. Primary PPH is that occurring within the first 24 h of delivery, though usually occurs shortly after birth. Secondary PPH is hemorrhage which occurs more than 24 h but before 12 weeks after delivery [95]. PPH can be minor (500–1,000 mL) or major (more than 1,000 mL). Major PPH may be further sub-classified into moderate (1,000–2,000 mL) or severe (more than 2,000 mL) [40].


14.3.1 Incidence and Risk Factors


Varying incidences of PPH are described in the literature, partly as a result of the lack of a universal definition and partly due to inaccuracy in estimates of blood loss [98]. Although an incidence of between 3 and 6 % has been reported based on hospital discharge data in the United States, Canada and Australia [99101], up to 15 % women are reported to suffer from excessive bleeding following delivery [102]. There were 5 deaths as a direct result of PPH reported in the 2006–2008 triennium in the UK [3]. Although mortality rates as a result of PPH may be declining in the UK (there were 9 deaths related to PPH in the previous (2003–2005) triennium), the incidence of PPH is increasing in the western world in general [4].

PPH results from abnormalities in four processes – uterine contraction, retained products of conception, genital tract trauma and coagulation abnormalities. These are often referred to as the “four T’s”- Tone, Tissue, Trauma and Thrombin [102]. Of these, the most common cause of PPH is uterine atony, accounting for over 70 % of PPH [98]. The risk factors for PPH can be antenatal or intrapartum and are summarised in Table 14.4 [103107].


Table 14.4
Risk factors for postpartum haemorrhage (PPH) [106110]

















































Antenatal

Previous PPH

Asian ethnicity

Obesity (BMI > 35 kg/m2)

Pre-eclampsia/gestational hypertension

Anaemia (<9 g/dL)

Multiple pregnancy

Polyhydramnios

Placenta previa

Known or suspected placenta abruption

Age over 40 years

Grand multiparity (≥5 deliveries)

Underlying bleeding disorders

Intrapartum

Induction of labor

Cesarean delivery (elective or emergency)

Retained placenta

Mediolateral episiotomy

Assisted vaginal delivery

Intrapartum pyrexia

Prolonged labor > 12 h

Large for gestational age infant > 4kg


14.3.2 Prevention


Although women with risk factors are more likely to experience PPH, unfortunately most cases of PPH occur in women who do not have any identifiable risk factors. Prevention begins with assessment and identification of risk factors, and women at high risk should be advised to deliver at a centre with adequate obstetric and hematological facilities.

Modifiable risk factors such as anemia should be addressed antenatally. Women at significantly increased risk of major PPH, such as those with placenta accreta or with a history of bleeding disorders, should ideally have a planned delivery at a centre where specialised obstetric, hematology and anesthetic services, as well as intensive care, blood transfusion laboratory, and pharmacy services are available. In cases where significant hemorrhage is expected an individualised management plan for delivery and blood component replacement should be drawn up prior to delivery.

Active management of the third stage of labour includes the use of a uterotonic drug, early clamping of the umbilical cord and controlled traction for the delivery of the placenta [108], and has been shown to reduce blood loss as well as the incidence of moderate and severe PPH [108, 109] compared to allowing a physiological third stage of labour.

The uterotonic of choice for routine prophylaxis in women with no risk factors for PPH is oxytocin (5 or 10 units by IM injection) [40]. Five units of slow intravenous injection is recommended in women who deliver by CS [110]. Syntometrine (oxytocin-ergometrine) may be used in the absence of hypertension or severe cardiac disease, as it has been shown to further reduce minor PPH when compared with oxytocin alone; however, there is a fivefold increase in side-effects of nausea, vomiting and increased blood pressure when ergometrine is used [111]. Oral misoprostol may also be used for active management of the third stage; however, it is not as effective as oxytocin and may be of benefit in community or resource poor settings where there is not ready access to the injectable oxytocics (oxytocin and ergometrine) [112, 113].


14.3.3 Management of Primary Postpartum Haemorrhage



14.3.3.1 General Measures


Analysis by CMACE shows that the management of fatal cases was often suboptimal with underestimation of the degree of hemorrhage and poor team working, and the CMACE team emphasise the need for the following: (a) clear local policies; (b) training of front-line staff; (c) multidisciplinary team working; (d) regular ‘fire drills’; and (e) excellent communication with the blood transfusion laboratory [3].

The RCOG has identified four components to be initiated and simultaneously progressed in the management of PPH. These include communication, resuscitation, monitoring and intervention [40].

A rapid clinical response with an appropriate multi-disciplinary approach is essential in order to reduce the morbidity and prevent mortality associated with PPH. For minor PPH (500–1,000 mL with no clinical evidence of shock) the charge midwife and first-line obstetric and anesthetic staff should be informed. In cases of major bleeding (blood loss >1 L, with ongoing bleeding and/or clinical shock) the on-call consultant obstetrician and anesthetist should be called and the consultant hematologist, blood transfusion laboratory and porters (for delivery of blood samples and components/products) should be alerted and involved early in the management.

Initial resuscitation should be tailored to the degree of clinical shock. Resuscitation in the management of all PPH should begin with the simple ‘ABC’ (‘airway, breathing, circulation’) approach. Administration of high flow oxygen is recommended regardless of oxygen saturation [40]. At least one large bore (14G) intravenous cannula should be inserted and a crystalloid infusion commenced in the first instance when dealing with what appears to be minor PPH.

In cases where a minor bleed progresses to meet the definition of major PPH (blood loss of >1 L, ongoing bleeding and/or clinical signs of shock), the woman should have two 14G intravenous cannulae and should be repositioned to remain supine. Fluid resuscitation should begin immediately and transfusion should be sought as soon as possible. Up to 3.5 L of rapid warmed clear fluids may be infused until red cells are available. If crossmatched red cells are unavailable by the time 3.5 L of clear fluids have been infused, ABO and Rh group specific or, if the group is unknown, O RhD negative red cells may be given.

The trigger for activating a massive obstetric haemorrhage (MOH) protocol must be clearly defined in all institutions, and in most is an estimated blood loss of 1,000–1,500 mL [113]. Key principles of an MOH are: first, that the blood transfusion laboratory staff and a senior hematologist should be contacted immediately when the MOH protocol is activated; and secondly, locally agreed protocols should enable red cells, FFP, cryoprecipitate and platelets to be issued at the earliest possible opportunity, without the initial approval of a hematologist.

The goals in the management of massive hemorrhage are to maintain a haemoglobin above 80 g/L, a platelet count of >50 g × 109/L (with a platelet transfusion trigger of 75 to provide a margin of safety), prothrombin time (PT) and activated partial thromboplastin time (APTT) less than 1.5 times the mean control level, and fibrinogen greater than 1 g/L [114, 115].

The following general principles should be observed:



  • Inadequate volume replacement, acidosis and hypothermia increase the risk of DIC. The woman should be kept warm and blood components transfused using a validated blood warmer; hypothermia will exacerbate coagulopathy.


  • Hypothermia adversely affects hemostasis on several levels: platelet function, the coagulation cascade and fibrinolytic system.


  • Rapid infusion of blood components/products, particularly fresh frozen plasma (FFP) and platelets which contain citrate as the anticoagulant, will lower ionised calcium and reduce cardiac contractility/lower blood pressure; the calcium should be corrected if indicated. Hypocalcemia is unlikely to occur when less than 1.5 × blood volume is replaced. Citrate toxicity is more likely in the hypothermic patient due to impaired citrate metabolism.


  • Hyperkalemia is possible in massive transfusion due to the concentration of potassium in stored red cells as they near expiry; this is usually a problem only if the woman has coexisting renal or hepatic disease but may be exacerbated by hypothermia [115117].

An FBC and group and screen must be obtained in all women with even a minor PPH. A coagulation screen, fibrinogen and baseline liver and renal function tests should be obtained if massive hemorrhage is anticipated, and the pulse and blood pressure monitored every 15 min until stabilised. In cases of massive hemorrhage, continuous pulse, blood pressure and respiratory rate monitoring should be commenced. An indwelling catheter should be inserted to monitor hourly urine output.


14.3.4 Obstetric Management


In tandem with resuscitation efforts, the cause of the PPH must be sought (considering the four T’s); extra-genital bleeding (such as splenic rupture or sub-capsular liver rupture) is rare but should be borne in mind.

Uterine atony is the commonest cause of primary PPH and it is best to administer further uterotonics (see below) while other possible causes for the PPH are being sought. Non-pharmacological measures are traditionally used as the first line management while these further uterotonics are being prepared. These include fundal massage, bimanual uterine compression and the emptying of the bladder in order to stimulate uterine contractions.

The pharmacological means of managing uterine atony are as follows [40]:

1.

5 Units of oxytocin by slow intravenous injection (IVI)

 

2.

Ergometrine 0.5 mg by IM injection (contraindicated in hypertension or severe cardiac disease)

 

3.

Oxytocin infusion (40 units in 500 mL Hartmann’s solution at 125 mL/h)

 

4.

Carboprost [0.25 mg = 250 mcg, IM or intramyometrially (easier to achieve at the time of CS), repeated at 15 min intervals to a maximum of 6 doses]. Contraindicated in women with asthma as it may cause severe bronchospasm.

 

5.

Misoprostol 800 micrograms rectally.

 

If bleeding persists in spite of these initial measures, the woman should be transferred to the operating theatre for examination under anesthesia so that a more thorough, controlled assessment for retained products and genital tract trauma can be made, and treatment carried out, if indicated. If bleeding continues despite pharmacological therapy, surgical therapy is warranted. There is limited evidence with regards to the most effective techniques in this situation: surgical techniques, radiological interventions or other hemostatic medical therapies. The available guidelines and recommendations are based on observational data and consensus only.

If the bleeding is perceived to be mainly or only from uterine atony, the first line surgical therapy is balloon tamponade. This technique has superseded the more traditional uterine packing. Several types of balloon catheters have been described such as the urological Rusch balloon [118], Foley catheter [119], Bakri balloon [120], Sengstaken–Blakemore esophageal catheter [121] and a condom catheter [122]. An 87 % success rate (defined as avoidance of hysterectomy) has been described in a series of 53 women who underwent balloon tamponade for the management of PPH [123].

Uterine hemostatic brace suturing is the next line of surgical management for atonic bleeding. Data from observational studies have shown that hemostatic brace suturing can successfully prevent hysterectomy in up to 81 % of cases [123]. Several variations of compression sutures have been described, the best known of which was described by B-Lynch in 1997 [124]. In the absence of comparative data, no particular method is thought to be superior.

Selective arterial embolisation may also be utilised to manage PPH, if onsite interventional radiology services are available; success rates of 75–100 % have been reported [123, 125, 126].

Step-wise ligation of uterine or internal iliac arteries has also been utilised [127]. The available evidence suggests that balloon tamponade and hemostatic suturing may be more effective. Lack of comparative studies means that one surgical technique cannot be strongly recommended above another. The appropriate surgical management will depend at least in part on the expertise and experience of the available staff.

Aortic compression may be used as a temporary means of hemostasis while awaiting surgical support or to allow resuscitation. The decision for hysterectomy as a life saving measure in the treatment of PPH should be made by a consultant and ideally discussed with and performed with a second consultant.


14.3.5 Causes and Management of Secondary Postpartum Hemorrhage


Secondary PPH typically occurs 10–14 days after the birth, and causes include retained products of conception and infection (endometritis). Endometritis may be managed with antibiotics. In case of excessive or ongoing bleeding, surgical management is warranted regardless of ultrasound findings. The decision for surgical management should involve a consultant, given the high risk of uterine perforation in this situation (because the uterine cavity is still large and the myometrium very soft).


14.3.6 Hematological Management of Postpartum Hemorrhage


During massive obstetric hemorrhage, blood loss >40 % of the patient’s estimated blood volume (EBV) is immediately life threatening. Clear communication, cooperation & effective team working by all members of the multidisciplinary team are a priority and essential for optimal clinical management of the patient. Early recognition of the deteriorating patient and the activation of a locally agreed ‘massive obstetric hemorrhage protocol’ at the appropriate point are essential.

The priorities from a haematological perspective are [114, 115]:



  • To maintain tissue/organ perfusion and oxygenation by restoration of blood volume and hemoglobin, through rapid provision of red cells.


  • To maintain hemostasis through the appropriate use of additional blood components, to correct resultant coagulopathy and thrombocytopenia.


  • To control ongoing bleeding ensuing from obstetric, surgical origins and/or abnormal systemic hemostasis.

Initial assessment is a combination of clinical signs and estimation of blood loss, with reference to baseline and ongoing hematology results (when available); non-visible blood loss (for example intra-peritoneal bleeding from a uterine rupture or bleeding into the broad ligament from cervical or uterine trauma) may be difficult to quantify. Empiric use of blood components may be required whilst awaiting coagulation results.


14.4 Massive Obstetric Hemorrhage (MOH) Protocols


Massive blood loss is normally defined as the loss of one blood volume in 24 h. An alternative definition which may be more useful in an acute situation is loss of 50 % of total blood volume in 3 h or >150 mL/min [40, 114, 115].

Estimated blood volume: pregnant women at term have an approx EBV of 100 mL/kg, when allowing for physiological increase. A pregnant woman weighing 70 kg at delivery would have an EBV of 7,000 mL; a loss of 20 % blood volume would be approximately 1,500 mL and a loss of 40 %, approximately 2,800 mL, and will require rapid access to red cell transfusion [40].

Many women will be able to tolerate an estimated blood loss between 500 and 1,500 mL without requiring blood component transfusion, provided they have had adequate fluid resuscitation. Consideration should be given to the patient’s underlying condition (e.g. respiratory/cardiac status), body weight & baseline hemoglobin. Reliable estimation of blood loss is extremely difficult and blood loss is frequently underestimated; if a woman is showing clinical signs of shock during massive obstetric haemorrhage (MOH), with ongoing blood loss, the MOH protocol should be activated to mobilise additional resources. Many institutions define the trigger for activation of an MOH protocol as an estimated blood loss of between 1,000 and 1,500 mL [113].

Successful management of PPH will require the involvement of clinicians, departments and personnel not present at the site of hemorrhage:



  • Robust systems must be in place to improve outcomes for women: effective local protocols must be developed in consultation with all the departments and people involved in the care of women during an MOH [127].


  • There must be an explicit and well understood phrase used for the activation of an MOH protocol, for example ‘massive obstetric hemorrhage’ ‘location and contact number’[128].


  • During an MOH a nominated clinician should be responsible for coordinating communications with laboratory staff, hematologists and personnel transporting blood components/products, for the duration of the emergency. The rapid provision of red cells and other blood components is critical and the importance of effective communication cannot be over-emphasised.


  • Blood transfusion laboratory staff and a senior hematologist should be contacted immediately when the MOH protocol is activated.


  • Locally agreed protocols should enable red cells, FFP, cryoprecipitate and platelets to be issued at the earliest possible opportunity, without the initial approval of a hematologist.


  • Protocols may define a ‘hemorrhage pack’ containing red cells and blood components that can be requested on the activation of the MOH procedure to facilitate rapid access to appropriate components.


  • All members of the multidisciplinary team who may be involved in an MOH should be familiar with the agreed protocol and know where to locate it; this should be supported by regular training, education and drills to practice and test the effectiveness of the procedure [127, 128].


  • Straightforward algorithms describing the key steps within the local protocol and system for communication during PPH should be available in all relevant clinical areas.


14.4.1 Blood Transfusion: Laboratory Testing and General Principles


Blood transfusion:

Oct 31, 2016 | Posted by in HEMATOLOGY | Comments Off on Acquired Bleeding Disorders in Pregnancy: Obstetric Hemorrhage

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