Postpartum haemorrhage (2024)

Postpartum haemorrhage (PPH) is an obstetrical emergency. It is a major cause of maternal morbidity, and one of the top three causes of maternal mortality the world over, although the absolute risk of death from PPH is much lower in “first world” nations.

PPH is a highly preventable cause of maternal mortality so long as there is timely diagnosis, appropriate resources, and appropriate management

Classification

Three major types of PPH are recognized:

1. Primary postpartum haemorrhage:

● This has been traditionally but somewhat unhelpfully, been defined as blood loss greater than or equal to 500 ml, within 24 hours of delivery.

It has been defined as ≥ 1000 ml after cesarean delivery, (though some define this as ≥ 700 ml).

Estimation of the true degree of blood loss however is difficult, and blood loss can be concealed.

Another classic definition is a 10% decline in postpartum hemoglobin concentration from antepartum levels. However, this is not a clinically useful definition as laboratory changes not correlated with acute events that endanger the patient should not be used to define a medical emergency.

An international expert panel defined PPH as “active bleeding >1000 mL within the 24 hours following birth that continues despite the use of initial measures, including first-line uterotonic agents and uterine massage”

Irrespective of all these arbitrary definitions, a critical part of the diagnosis should be a clinical assessment of the haemodynamic status of the patient.

2. Major PPH:

● This has been defined as continued bleeding and failure to respond to first line management and cases where blood loss is approaching or exceeding 1000 mls.

3. Secondary PPH:

● Thisis defined as a blood loss of more than 500mL after 24 hours and up to 6 weeks postpartum

Pathophysiology

Normal haemostasis:

The potential for massive hemorrhage after delivery is high because in late pregnancy uterine artery blood flow is 500 to 700 mL/min and accounts for about 15 percent of cardiac output.

Normally, hemostasis occurs upon placental separation because uterine bleeding is controlled by a combination of two principle mechanisms:

● Contraction of the myometrium:

♥ Which compresses the blood vessels supplying the placental bed resulting in mechanical hemostasis.

● Release of local decidual haemostatic factors:

♥ Such as tissue factor type-1 plasminogen activator inhibitor and systemic coagulation factors – such as platelets, circulating / clotting factors, which cause clotting.

Causes of Primary PPH:

The causes of a Primary PPH can be broadly thought of in terms of the 4 “T”s: Tone (or uterine atony), Tissue (retained placental tissue), Trauma (direct trauma to the uterus/ birth canal) and Thrombin (or coagulopathy).

1. Uterine atony (approximately 70 %):

The most common cause of primary PPH is uterine atony or lack of effective contraction of the uterus after delivery.

Blood loss can be much greater than observed because a boggy and dilated uterus may contain a significant amount of blood.

Conditions which predispose to uterine atony include:

● Prolonged labour

● Precipitate labour

● Dysfunctional labour

● Uterine overdistension:

♥ Multiple pregnancy

♥ Polyhydramnios

♥ Macrosomia (baby large for gestational age).

● Grand Multiparity

● Uterine abnormalities: fibroids

● Intrauterine infection

● Uterine relaxing agents:

♥ Magnesium sulphate / general anaesthetics/ tocolytic drugs.

2. Retained placental tissue (approximately 10%):

● Retained placental tissue

● Partial separation

Abnormal placental implantation:

● Placenta previa site

● Morbidly adherent:

♥ Placenta accreta (superficial), Placenta increta (into muscle), Placenta perceta (through muscle).

3. Trauma (approximately 20%):

● Lacerations of uterus, cervix or vagin*

● Uterine rupture

● At cesarean delivery, hemorrhage from the uterine incision is generally caused by an excessively lateral extension of the incision.

4. Coagulopathy (approximately 1%):

Coagulopathy is both a cause and result of PPH since persistent heavy bleeding, irrespective of the cause, leads to consumption of clotting factors and hemodilution of remaining clotting factors.

● DIC can be predisposed to by:

♥ PET/ eclampsia

♥ Abruptions

♥ FDIU (greater than 4 weeks)

♥ Amniotic fluid embolism.

♥ Sepsis

● HELLP Syndrome

● Bleeding disorders

● Drugs (aspirin / heparin)

Complications:

PPH is a major cause of maternal morbidity and mortality.

Complications of primary PPH include:

1. Hemorrhagic shock/ death

2. Hemorrhagic complications:

● Coagulopathy/ DIC

● Renal impairment

● Postpartum hypopituitarism (Sheehan’s syndrome)

♥ Sheehan syndrome (i.e, postpartum hypopituitarism) is a rare, but potentially life-threatening, complication.

The pituitary gland is enlarged in pregnancy and prone to infarction from hypovolemic shock.

Damage to the pituitary can be mild or severe, and can affect the secretion of one, several, or all of its hormones.

A common presentation is a combination of failure to lactate post delivery and amenorrhea or oligomenorrhea, but any of the manifestations of hypopituitarism (e.g. hypotension, hyponatremia, hypothyroidism) can occur anytime from the immediate postpartum period to years after delivery.

If the patient remains hypotensive after control of hemorrhage and volume replacement, she should be evaluated and treated for adrenal insufficiency immediately; evaluation of other hormonal deficiencies can be deferred until four to six weeks postpartum.

● Neurological deficits

● Postpartum anaemia.

3. Abdominal compartment syndrome (with compression of the IVC).

● This is rare but should be considered in patients with a tensely distended abdomen and progressive oliguria who are developing multiorgan failure.

4. Asherman syndrome:

● This is related to curettage (if performed for retained products of conception).

5. ARDS

6. Need for hysterectomy to control bleeding not controlled by other methods.

Risk assessment

Women with known risk factors for PPH should be identified where possible.

Antenatal diagnosis of placenta praevia acreta may be made using colour doppler and MRI.

Planning for these patients should involve ensuring the availability of resources that might be needed, including personnel, medication, equipment, and blood products.

Clinical assessment

The diagnosis of uterine atony is made if the uterus does not become firm after uterine massage and administration of uterotonic agents.

Biannual palpation of the uterus may reveal bogginess, or uterine enlargement, with a large amount of accumulated blood or retained placental tissue.

Note however that atony may be diffuse or localized to an area of uterine muscle. In the latter situation, the fundal region may be well contracted while the lower uterine segment is dilated and atonic, which is difficult to appreciate on physical examination.

During suctioning, careful visual inspection of the cervix and vagin* under good light may reveal the presence and extent of lacerations.

Examine the placenta for missing portions, which suggest the possibility of retained placental tissue.

Consider coagulopathy in cases of oozing from skin puncture sites or intravenous sites in patients with excessive bleeding.

Investigations

Blood tests:

1. FBE

2. U&Es and glucose

3. Cross match as clinically indicated.

● Activation of a massive transfusion protocol if required.

4. Coagulation profile:

● INR/APPT / platelets/ fibrinogen/ FDPs.

Importance of fibrinogen:

Fibrinogen as a predictor of worsening hemorrhage/coagulopathy.

Fibrinogen falls to critically low levels earlier than other coagulation factors during PPH, thus the fibrinogen level is a more sensitive indicator of ongoing major blood loss than the prothrombin time, activated partial thromboplastin time, or platelet count

The fibrinogen level at the time of diagnosis of PPH is predictive of severity and can be used to guide the aggressiveness of management.

The normal fibrinogen level in a term pregnancy is 350 to 650 mg/dL, which is nearly double that of nonpregnant adults (200 to 400 mg/dL).

In multiple studies of women with PPH, a low fibrinogen level (less than 200 mg/dL) was predictive of severe PPH defined as need for transfusion of multiple units of blood and blood products, need for angiographic embolization or surgical management of hemorrhage, or maternal death. ³

Management

In the non-coagulopathic setting, the empty, contracted and uninjured uterus does not bleed.

The routine prophylactic use of uterotonic drugs, such as oxytocin, reduces the risk of PPH by 50 percent in the overall obstetric population

1. Immediate attention to ABC issues:

● IV access and fluid resuscitation as clinically required.

● Blood products as required:

♥ O negative blood/ activate massive transfusion protocol if necessary.

● Correct any coagulopathy:

♥ Blood/ FFP/platelets:

Note that if the patient is coagulopathic with an extremely low fibrinogen level, cryoprecipitate or high concentration fibrinogen products (e.g., fibrinogen concentrate) are indicated since fresh frozen plasma alone may not increase the fibrinogen level to the normal range without requiring excessive volume infusion.

2. If the placenta has not been delivered then it will need to be delivered:

Empty the bladder with a urinary catheter, then:

● Brandt-Andrews maneuver:

♥ Controlled cord traction with one hand whilst pushing on the fundus rosterally with ulnar border of the other hand.

● Dublin maneuver:

♥ If above is not successful, the Dublin maneuver (fundal expulsion) may be tried. Give N₂O and push caudally on the fundus.

● Manual removal:

♥ If the placenta has not been delivered within 30 minutes then a manual removal under general anesthesia will be required.

Once the placenta has been delivered inspect for its completeness.

If the placenta has been delivered or there is ongoing bleeding:

3. “Rub up” the fundus:

● Fundal massage stimulates the atonic uterus to contract.

4. Uterotonic drugs:

Since uterine atony is the most common cause of PPH.

Uterotonic drugs are therefore administered for presumed atony until a therapeutic effect is observed or until it is obvious that these drugs are ineffective.

The important point is not so much the sequence of drugs, but the rather the prompt initiation of uterotonic therapy and the prompt assessment of its effect.

It should be possible to determine within 30 minutes whether pharmacologic treatment is reversing uterine atony.

If it does not then further measures should be initiated.

Options include:

Oxytocin:

● Oxytocin 10 units IV, or 10 units IM

● Oxytocin infusion; 40 units in 1 liter of Hartman’s solution over 4 hours.

Ergometrine:

● Ergometrine 0.25 mg IV and repeat up to 1 mg total as necessary, (including 3^rd stage)

Avoid ergometrine (or Syntometrine which is a combination of oxytocin and ergometrine) in situations of retained placenta because it causes tonic uterine contraction, which may delay expulsion.

Misoprostol:

● This is a synthetic prostaglandin E1 (PGE₁)

● Misoprostol: 800 – 1000 micrograms P.R. (i.e 4-5 x 200 microgram tablets).

Prostaglandin F2α (dinoprost):

As an alternative to misoprostol treatment of uterine atony may also be with intramyometrial PGF_2a

● Dilute the 5 mg in 1 ml ampoule into 10 mls saline, (to give 0.5mg per mL).

● Give an intramyometrial injection of 1mg of Prostaglandin F2α. This can be repeated up to a maximum dose of 3mg. ¹

● The transabdominal route is preferred

Toxic effects may include:

● Bronchospasm, (contraindicated in asthmatics)

● Hypertension

● Tachyarrhythmias

5. Inspect the birth canal for any obvious traumatic bleeding points.

● Packing or sutures to vagin*l wounds

● Cervical wounds may be clamped with sponge forceps.

6. Further manual compression methods:

● Bimanual compression:

♥ One hand is made into a fist and placed vagin*lly in the anterior fornix, while the other massages the fundus abdominally while firmly compressing it against the vagin*l hand.

Massage should be maintained while other interventions are being initiated, and continued until the uterus remains firm and bleeding has abated.

If the fundus is well contracted but bleeding continues unabated, then further massage is not likely to be effective and progression to other methods of hemorrhage control should occur promptly.

Maintain this compression for at least 30 minutes.

● Manual aortic compression:

♥ The aorta may be compressed against the vertebral column at the level of the umbilicus.

7. Intrauterine tamponade.

● Packing with sterile gauze. Do not leave in longer than 24 hours.

● Specific balloon tamponade devices:

An example is the Bakri balloon:

Thisis a balloon tamponade indicated for women not responding to uterotonics and uterine massage.

It is used to control haemorrhage due to uterine atony in the upper segment of the uterus and to control bleeding in the lower uterine segment secondary to placental implantation in the lower uterine segment.

The balloon catheter is inserted into the uterus under spinal, epidural or general anaesthesia in theatre.

Balloon tamponade is left in situ for 8 to 24 hours to allow time for blood transfusion and coagulopathy correction.

8. Radiographic embolization:

● This technique may be considered where timely expertise and resources are available.

Arterial embolization is an appropriate treatment option for persistent bleeding in a hemodynamically stable patient in whom the capacity for blood replacement exceeds that of the ongoing hemorrhage.

Generally, it should not be attempted in unstable patients who have to be transferred to a radiology suite for the procedure and it should not be considered an emergency procedure for managing uncontrolled PPH of indeterminate cause.

9. Surgery:

Ultimately surgical intervention may be necessary.

Options include:

● B-Lynch sutures:

These are uterine compression sutures running through the full thickness of both uterine walls (posterior as well as anterior) for surgical management of atonic PPH.

The B-Lynch suturing technique (brace suture) is useful because of its simplicity of application, life-saving potential, relative safety and capacity for preserving the uterus and subsequent fertility.

The adequacy of haemostasis can be assessed both before and immediately after application of the suture.

This technique is an alternative to major surgical procedures for controlling pelvic arterial pulse pressure or hysterectomy.

It has been shown, when applied correctly, to be successful with no problems and no apparent complications.

Only if it fails, need other more radical surgical methods be considered.

● Internal iliac artery ligation.

● Hysterectomy:

Early resort to hysterectomy is appropriate in women with severe bleeding due to diffuse placenta accreta/increta/percreta or a large uterine rupture.

In contrast, hysterectomy is generally a last resort in patients with atony, as these patients can often be managed successfully with medical therapy and less aggressive surgical interventions.

However, hysterectomy should not be delayed in those who have depleted their clotting factors and require prompt control of uterine hemorrhage to prevent death.

Secondary PPH

Introduction

Secondary post partum hemorrhage is vagin*l bleeding from 24 hours post partum to the end of the puerperium i.e first 6 weeks post partum, (though some definitions extend this period to 12 weeks post partum ¹).

Peak incidence is at one to two weeks postpartum.

Causes:

1. Infection, the vast majority of cases will be due to an endometriitis.

♥ Rare, but potentially lethal causes of endometritis include Clostridium perfringens and streptococcal or staphylococcal toxic shock syndrome.

2. Retained products of conception.

Rarely:

3. Trophoblastic disease, choriocarcinoma.

4. Bleeding disorders.

Sometimes definite cause cannot be determined.

Complications:

1. Life threatening hemorrhage is much less common than with primary PPH, however it may still occasionally occur.

• Sepsis

Clinical Assessment

Important points of History:

Pregnancy and labor predispositions to sepsis and retained placental products.

Important points of Examination:

1. ABC, evidence of blood loss / shock.

2. Evidence of sepsis, endometritis, septicemia

3. Uterus subinvolution, retained products.

Investigations

Blood tests:

1. FBE

2. CRP

3. U&Es and glucose

4. Group and save or cross match as clinically indicated.

5. Blood cultures if clinically indicated

6. Beta HCG:

● If choriocarcinoma is suspected, (or even a new pregnancy).

7. Coagulation profile as clinically indicated.

Microbiology

● Cervical cultures.

Ultrasound:

● To look for retained placental products.

Management

1. Immediate ABC issues

● IV access, fluid resuscitation as clinically indicated.

2. Antibiotics:

Empirical treatment should be given with:

● Amoxicillin/ clavulanic acid 875/125 mg bd orally for 5 – 7days.

● If systemically unwell, IV Ampicillin and metronidazole (to cover anaerobes) can be used.

Erythromycin is suitable for penicillin sensitive patients.

3. Retained placental products will require an EUA and curettage.

References

FOAMed

• Miers J, Beech A. Emergency Procedure: Postpartum haemorrhage LITFL

Publications

• Teede HJ, Misso ML, Boyle JA, Garad RM, McAllister V, Downes L, Gibson M, Hart RJ, Rombauts L, Moran L, Dokras A, Laven J, Piltonen T, Rodgers RJ, Thondan M, Costello MF, Norman RJ; International PCOS Network. Translation and implementation of the Australian-led PCOS guideline: clinical summary and translation resources from the International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. Med J Aust. 2018 Oct 1;209(S7):S3-S8.