Placental abruption

Placental abruption can be defined as the partial or complete detachment of the placenta before delivery of the fetus, with dissection and bleeding at the interface between the decidua, that is the modified mucosal lining of the uterine endometrium, and the placenta. It is a major cause of perinatal haemorrhage, maternal morbidity and mortality, and fetal compromise and demise.

Classification

The clinical presentation can be revealed, that is with vaginal bleeding, or concealed, with blood encapsulated between the uterine wall and placenta. The Sher classification describes the following stages: Stage I is mild and involves the retrospective diagnosis of a small postpartum haematoma; Stage II is intermediate in severity and associated with a hypertonic uterus and the delivery of a live fetus; and Stage III is severe and involves an intrauterine fetal death, without (IIIa) or with (IIIb) the presence of coagulopathy.¹

Incidence and risk factors

Between 0.4 and 1% of pregnancies may be affected by placental abruption and 70% of cases occur in patients who are at low risk, leading to challenges in its prediction.2, 3, 4, 5 The risk factors for placental abruption are detailed in Table 1.

Table 1.

Risk factors for placental abruption.2, 3, 4, 5

Risk factor	Odds ratio/relative risk	Comments
Medical and social history
Amphetamine or cocaine use	5–10	Placental abruption occurs in 10% of active cocaine users
Chronic hypertension	1.8–5.1
Thrombophilia	1.8–2	Risk associated with heterozygous factor V Leiden and heterozygous prothrombin 20210A
Cigarette smoking	1.4–2.5	Correlation with number of cigarettes smoked
Maternal age ≥35 yrs	1.3–2.6
Maternal age ≤20 yrs	1.1–1.5
Obstetric history
Uterine abnormalities	5.0–8
Previous Caesarean delivery	1.3–2.4
Uterine leiomyoma	Up to 2
Parity ≥3	1.1–1.4
Ischaemic placental disease history
Previous placental abruption	8–12	Recurrence in 4.4%
Previous placental abruptions ≥2	—	Recurrence in 19–25%
Previous pre-eclampsia	1.5
Previous intrauterine growth restriction	1.4
Current pregnancy
Chronic hypertension with pre-eclampsia	Up to 7.8
Eclampsia	3–5.5
Pre-eclampsia	Up to 4.5
Chorioamnionitis	2–3.3
First trimester bleeding	2–3.1
Polyhydramnios	2–3
Multiple gestation pregnancy	2–2.9
Preterm rupture of membranes	1.8–5.9
Intrauterine growth restriction	1.3–4.1
Oligohydramnios	Up to 2.1
Trauma
Abdominal trauma	—	6% of all trauma cases 20–25% of major trauma

Pathophysiology

Placental abruption results from the rupture of maternal placental vessels in the decidua basalis; the underlying pathophysiology remains speculative. Ischaemic placental disease is the likely cause in chronic abruption and consequent decidual necrosis leads to maternal venous haemorrhage.⁴ Low-pressure venous haemorrhage, commonly at the periphery of the placenta in marginal placental abruption, is associated with the slower onset of clinical manifestations.⁴ Shearing of the inelastic placenta may occur from trauma or rapid uterine decompression, such as after the delivery of the first fetus in the context of multiple gestation pregnancy, or secondary to sudden loss of amniotic fluid, such as subsequent to delivery in the setting of polyhydramnios.^2,4 Acute vasospasm may be the precipitant in cocaine use, resulting in ischaemia followed by reflex vasodilation.^2,4 High-pressure and centrally located arterial haemorrhage is associated with the rapid onset of severe clinical manifestations.

Bleeding from fetal placental vessels is rare. Fetal compromise is caused by decreased oxygen and nutrient transfer across the placenta, and placental abruption involving >45% of the placental area has been related to very poor neonatal outcomes. Fetal mortality increases from 0.6% in deliveries without placental abruption to 3–12% in deliveries with placental abruption.⁴

Thrombin concentrations increase secondary to the release of decidual tissue factor (i.e. thromboplastin) and vascular endothelial growth factor in response to decidual hypoxia. Thrombin itself is a trigger of uterine hypertonus and disseminated intravascular coagulation (DIC).⁴

Clinical presentation

The clinical presentation depends on the site and severity of placental abruption. Chronic placental abruption can be asymptomatic or present with intermittent vaginal bleeding, oligohydramnios and poor fetal growth. The classic features of acute placental abruption include abdominal pain, back pain, or both, uterine contractions and vaginal bleeding.^2,4 Labour may progress rapidly with uterine hypertonus. Small and concealed placental abruption, however, can be asymptomatic.⁴ Reduced fetal movement, heart rate abnormalities or death may occur.⁴

It is important to note that the severity of placental abruption does not correlate well with the extent of vaginal bleeding, but the presence of severe abdominal pain, maternal hypotension and fetal heart rate abnormalities indicate clinically significant placental separation.⁴

Clinical management

Diagnosis

Diagnosis is primarily based on clinical features and must be considered in any patient in the context of trauma or with abdominal pain, vaginal bleeding, or both.⁴ Placental abruption is the cause of 10% of preterm labour and is often diagnosed at delivery.⁴ Differential diagnoses include labour, placenta praevia and uterine rupture.⁴ Concealed placental abruption and maternal haemodynamic compensation can lead to its underdiagnosis and underestimation of blood loss.

Laboratory tests must include full blood count, clotting studies and group type and screen with cross-matching of blood. Urea and electrolytes and liver function tests should also be measured. The concentration of haemoglobin in acute haemorrhage may be normal before resuscitation with fluids, leading to false reassurance. In major haemorrhage, the fibrinogen concentration and viscoelastic testing guide the correction of coagulopathy to a greater extent than the results of conventional clotting studies.

Ultrasound has a high specificity of 96% but poor sensitivity of 24% for detecting placental abruption owing to the isoechogenicity of concealed haemorrhage and placental tissue.⁶ The Kleihauer–Betke test identifies the presence of fetal cells in the maternal circulation and should be performed in all rhesus-negative patients who have an antepartum haemorrhage. However, it does have a poor correlation with the presence of placental abruption.^3,4

A cognitive aid diagram for the mangement of placental abruption is presented in Figure 1.

Fig 1.

Cognitive aid for the recommended management of placental abruption. HDU, high dependency unit; ICU, intensive care unit.^3,4,7, 8, 9

Mode and timing of delivery

Chronic placental abruption with reassuring maternal and fetal status can be managed expectantly with planned induction of labour or Caesarean delivery at ∼37 weeks of gestation.³ Delivery management for acute placental abruption depends on the maternal and fetal status and gestational age. Severe haemorrhage, maternal cardiovascular instability, or both mandates immediate fetal delivery regardless of gestational age or neonatal facilities. Viable fetuses with severe compromise require emergent Caesarean delivery unless vaginal delivery is imminent, while those with reassuring status may undergo non-urgent vaginal or caesarean delivery. If fetal death has occurred, vaginal delivery is recommended unless maternal status is compromised or vaginal delivery is contraindicated.³

Management of anaesthesia

Wide bore i.v. access must be secured and hypovolaemia corrected. Arterial cannulation for monitoring and repeated blood sampling can be needed. Major haemorrhage protocols, cell salvage and rapid infusion equipment should be used for major haemorrhage.

In order to facilitate obstetric management and fetal delivery, neuraxial techniques such as spinal anaesthesia are feasible in patients who are normovolaemic and in a stable cardiovascular state. However, the potential for earlier and more rapid coagulopathy associated with placental abruption should be considered before proceeding. Patients who have epidural catheters should have coagulation studies and coagulopathy corrected before catheter removal.

General anaesthesia is indicated in patients who are unstable and have major haemorrhage.³ It is recommended that rapid-sequence induction of anaesthesia is performed with the patient positioned with left lateral tilt to decrease aortocaval compression. Given its effect on haemodynamic stability, we suggest that ketamine may be the most appropriate anaesthetic agent in the setting of hypovolaemia. Target-controlled infusion in addition to volatile anaesthesia or total intravenous anaesthesia may be used to reduce the dose-dependent uterine relaxation associated with volatile anaesthetic agents. It is important to use depth of anaesthesia monitoring because changes in the physiological compartments in pregnancy and haemorrhage can potentially influence target infusion concentrations.

Management of haemorrhage

Placental abruption can be concealed, leading to an underestimation of blood loss, and, compared with other causes of antepartum haemorrhage, is associated with the earlier and more rapid development of coagulopathy and DIC.⁴ In view of this, major haemorrhage protocols must be activated early in suspected or confirmed placental abruption instead of relying on traditional thresholds of estimated blood loss.

The principles of major obstetric haemorrhage management include⁷:

• •replacing circulating volume and oxygen carrying capacity;
• •correcting coagulopathy;
• •preventing complications of blood transfusion.

Packed red cell and coagulation factor transfusion should be guided by clinical judgement and laboratory and point-of-care tests such as arterial or venous blood gases. Viscoelastometry tests, such as rotational thromboelastometry (ROTEM) or thromboelastography (TEG), have been found to decrease blood loss and blood product use in obstetrics.⁸ In major obstetric haemorrhage, haemostatic tests should be repeated every 30 min to identify rapid changes in coagulation and responses to recent transfusion. Frequent electrolyte level checks are also warranted during large-volume blood and blood product transfusion because of the risk of hypocalcaemia and potassium derangement.

Maternal fibrinogen concentration is normally 4–6 g L⁻¹ and greater than that in non-pregnant patients whose level is usually 2–4 g L⁻¹. It reduces more rapidly than platelets and other clotting factors in major obstetric haemorrhage and may be inadequate despite a normal prothrombin time and activated partial thromboplastin time. Fibrinogen concentrations <2 g L⁻¹ are insufficient to sustain effective coagulation and are predictive of severe haemorrhage.⁹ If the laboratory fibrinogen is ≤2 g L⁻¹ or the indices of viscoelastic tests suggest weak clot strength owing to inadequate fibrinogen alone, that is a ROTEM Fibtem A5 <12 mm or TEG CFF-MA ≤16 mm, then fibrinogen replacement is needed.8, 9, 10

Cryoprecipitate has a fibrinogen concentration of 15 g L⁻¹ and requires thawing, so may not be available immediately. Fibrinogen concentrate is stored at room temperature, prepared when needed and given at a typical dose of 2–6 g titrated to the degree of coagulopathy.⁹ Fresh frozen plasma (FFP) has a fibrinogen concentration of 2 g L⁻¹ and may dilute the maternal fibrinogen concentration with large volume transfusion, whilst also resulting in a risk of transfusion-related acute lung injury and transfusion-associated circulatory overload.^8,9 FFP and platelet transfusions, although often unnecessary, are more likely to be needed in placental abruption relative to other causes of obstetric haemorrhage.⁹

It is recommended that blood products be warmed and maternal hypothermia managed proactively to avoid the exacerbation of maternal coagulopathy. There is no evidence that the provision of fixed ratio blood product transfusion for obstetric haemorrhage leads to improved outcomes.⁸ When guided by haemostatic testing, many patients who have an obstetric haemorrhage do not require FFP.⁸

The antifibrinolytic, tranexamic acid, can be given at a dose of 1 g over 10 min i.v. as a supportive treatment in haemorrhage of >1000 ml.⁹ Of note, fibrinogen replacement is more effective when given after tranexamic acid. When blood loss is >1500 ml, a repeat dose of antibiotic must be given and a second dose of tranexamic acid should be considered once 30 min have passed in the presence of ongoing haemorrhage.

Postnatal management

Postnatal management includes monitoring for haemorrhage, coagulopathy and sequelae of major transfusion. Higher levels of care in a high dependency or intensive care unit may be required. Sensitive care of patients and their support persons must be provided. Debriefing in regard to the nature and sequence of events should occur, and arrangements for follow-up psychological support and counselling with respect to future pregnancies should be made.

Conclusions

Placental abruption is a primarily clinical diagnosis and is associated with increased rates of early coagulopathy and DIC relative to other causes of antepartum haemorrhage. Concealed placental abruption may result in underdiagnosis and underestimation of blood loss. Rapid recognition, intervention and management are vital to achieve the most favourable maternal and fetal outcomes.

Declaration of interests

AL is an editor and editorial board member of BJA Education. CDS declares that they have no conflict of interest.

Biographies

Craig D Smith BSc FRCA is a specialty registrar in anaesthesia in the East Midlands Deanery, England. His interests include obstetric anaesthesia and human factors.

Allison Lee MD MS is professor of anesthesiology and critical care and block chief for the Division of Obstetric Anesthesia at the University of Pennsylvania. She is an editor and editorial board member of BJA Education.

Matrix codes: 1A01, 1I03, 2A05, 2B02, 2B05, 2B06, 3B00