Postpartum Hemorrhage

Pregnancy, Childbirth, & the Puerperium


Clinicals - History

Fact Explanation

Definition


Primary postpartum haemorrhage (PPH) is the excessive bleeding from the genital tract within 24 hours of childbirth, but most cases manifest immediately after birth. It is defined as total blood loss >500 mL after vaginal delivery and >1000 mL after delivery by a Caesarean section. Massive PPH refers to the loss of 30%–40% of the patient’s blood volume. Secondary PPH occurs between 24 hours and 12 weeks post-delivery.

Causes


The Four T's mnemonic is used to quickly identify and address the four most common causes of postpartum haemorrhage:

T – Tone for uterine atony;

T- Trauma for laceration, hematoma, inversion, rupture;

T – Tissue for retained tissue or invasive placenta; and

T– Thrombin for congenital or acquired coagulopathy.

Risk factors


Risk factors for PPH include: advanced maternal age, antepartum hemorrhage, augmented or prolonged labor, chorioamnionitis, fetal macrosomia, maternal anemia, multifetal gestation, preeclampsia, placenta praevia, placental abruption, invasive placentation, instrumental delivery, previous PPH or Caesarean section. 20% of PPH occurs in women with no risk factors.

Symptoms of hypovolemia


PPH can occur without obvious signs of external bleeding. It may present only with symptoms of hypovolemia including dizziness, nausea, restlessness, palpitations and excessive thirst. Loss of consciousness or maternal collapse, in the setting of vaginal bleeding after childbirth, indicate severe PPH complicated by hypovolemic shock.

Dyspnea


Shortness of breath and air hunger are decompensating features, suggesting significant PPH with more than 40% total blood volume loss.

Pain


Excessive or persistent pelvic pain after delivery may indicate hematoma formation. Abdominal pain is a feature of secondary PPH indicating endometritis.

History of clotting dysfunction


Coagulopathy can cause PPH or be the result of one. PPH can be anticipated in women with known congenital or acquired clotting disorders. Clotting defects should be suspected in women who have history of abnormal bleeding and bruising, or present with petechial, subconjunctival and mucosal haemorrhage.

Definition


Primary postpartum haemorrhage (PPH) is the excessive bleeding from the genital tract within 24 hours of childbirth, but most cases manifest immediately after birth. It is defined as total blood loss >500 mL after vaginal delivery and >1000 mL after delivery by a Caesarean section. Massive PPH refers to the loss of 30%–40% of the patient’s blood volume. Secondary PPH occurs between 24 hours and 12 weeks post-delivery.

Causes


The Four T's mnemonic is used to quickly identify and address the four most common causes of postpartum haemorrhage:

T – Tone for uterine atony;

T- Trauma for laceration, hematoma, inversion, rupture;

T – Tissue for retained tissue or invasive placenta; and

T– Thrombin for congenital or acquired coagulopathy.

Risk factors


Risk factors for PPH include: advanced maternal age, antepartum hemorrhage, augmented or prolonged labor, chorioamnionitis, fetal macrosomia, maternal anemia, multifetal gestation, preeclampsia, placenta praevia, placental abruption, invasive placentation, instrumental delivery, previous PPH or Caesarean section. 20% of PPH occurs in women with no risk factors.

Symptoms of hypovolemia


PPH can occur without obvious signs of external bleeding. It may present only with symptoms of hypovolemia including dizziness, nausea, restlessness, palpitations and excessive thirst. Loss of consciousness or maternal collapse, in the setting of vaginal bleeding after childbirth, indicate severe PPH complicated by hypovolemic shock.

Dyspnea


Shortness of breath and air hunger are decompensating features, suggesting significant PPH with more than 40% total blood volume loss.

Pain


Excessive or persistent pelvic pain after delivery may indicate hematoma formation. Abdominal pain is a feature of secondary PPH indicating endometritis.

History of clotting dysfunction


Coagulopathy can cause PPH or be the result of one. PPH can be anticipated in women with known congenital or acquired clotting disorders. Clotting defects should be suspected in women who have history of abnormal bleeding and bruising, or present with petechial, subconjunctival and mucosal haemorrhage.

Clinicals - Examination

Fact Explanation

Tachycardia


Raised heart rate may be the earliest sign of PPH, but due to plasma volume expansion in normal pregnancy, a healthy woman will typically tolerate 500-1,000 mL of blood loss before developing tachycardia. Tachycardia will occur earlier if a woman is of smaller stature, is dehydrated or has an underlying anemia or hypoproteinemia.

Hypotension


PPH is characterised by a decreasing blood pressure (BP) and narrowing pulse pressure. A systolic BP below 80 mmHg, associated with worsening tachycardia, tachypnea and altered mental state, usually indicates a PPH in excess of 1,500 mL. Hypotension out of proportion to the amount of blood loss should raise the suspicion for PPH with concealed bleeding.

Obstetric shock index


Calculating shock index (i.e. pulse rate divided by systolic blood pressure) is a simple way to assess the degree of blood loss after childbirth. The normal obstetric shock index (OSI) is 0.7-0.9, a range that is lower than non-pregnant adult population. OSI has been found to identify women at risk of adverse outcomes secondary to PPH.

Altered mental status


In the early stages of PPH the mental status will be unaltered or there may be slight anxiety. Mental state starts to deteriorate after more than 30% of total blood volume is lost. Decreased level of consciousness or loss of consciousness are signs of more than 40% total blood volume loss.

Skin changes


Skin changes occur in all stages of hypovolemic shock, with the skin initially being pale and then becoming progressively colder and clammier.

Capillary refill time (CRT)


CRT in the forehead, lips, and nail beds helps assess the level of tissue hypoperfusion due to PPH. CRT will be delayed at 15% total blood volume loss. It becomes absent at more than 40% total blood volume loss.

‘Rule of 30’


The ‘Rule of Thirty’ is a simple way to determine that 30% of blood volume has been lost. It implies that the patient is in moderate shock leading to severe shock if the systolic BP has fallen by 30 mmHg, the HR has risen by 30 beats per minute, the RR has increased by more than 30 breaths per minute, if urinary output is less than 30ml/h or if the hemoglobin or HCT has dropped by 30%.

Uterine tone and size


Following third stage of labour, the uterus should be examined to assess uterine contraction and tone. Uterine atony is diagnosed when there is continuing vaginal bleeding and the uterus feels relaxed, soft or ‘boggy’ on fundal palpation.

Genital tract inspection


When the uterus is contracted, but vaginal bleeding continues, systemic examination of the genital tract is required to exclude PPH due to trauma of the birth canal. Trauma to the periurethral, the clitoral region, the anal sphincter or the lower uterine segments can also occur. PPH associated with birth trauma may not be immediately visible, as large amounts of blood can accumulate in the paravaginal space.

Signs of placental separation


Sudden small gush of blood, lengthening of the umbilical cord and the uterus becoming more globular in shape, are the three classic signs of placental separation. They should occur within the first few minutes after fetal expulsion. Absent placental separation is suggestive of retained products of conception (RPOC) which prevents the uterus from contracting enough to achieve optimal tone. Retained placenta is diagnosed when the placenta is not spontaneously delivered within 30 min. after parturition.

Postpartum examination of the placenta


Quick postpartum examination of the placenta at the bedside allows for early detection of incomplete membranes or placenta shape abnormalities which are associated with PPH due to retained tissue.

Signs of clotting dysfunction


Clinical signs of clotting dysfunction include oozing from puncture or injection sites and failure of the blood to clot in bedside receptacles. A quick bedside test for coagulation defects can be performed with an empty full blood examination tube (“red top”) when filled with maternal blood and taped to the wall. With a normal clotting profile, it should form a clot within 5 to 10 minutes.

Tachycardia


Raised heart rate may be the earliest sign of PPH, but due to plasma volume expansion in normal pregnancy, a healthy woman will typically tolerate 500-1,000 mL of blood loss before developing tachycardia. Tachycardia will occur earlier if a woman is of smaller stature, is dehydrated or has an underlying anemia or hypoproteinemia.

Hypotension


PPH is characterised by a decreasing blood pressure (BP) and narrowing pulse pressure. A systolic BP below 80 mmHg, associated with worsening tachycardia, tachypnea and altered mental state, usually indicates a PPH in excess of 1,500 mL. Hypotension out of proportion to the amount of blood loss should raise the suspicion for PPH with concealed bleeding.

Obstetric shock index


Calculating shock index (i.e. pulse rate divided by systolic blood pressure) is a simple way to assess the degree of blood loss after childbirth. The normal obstetric shock index (OSI) is 0.7-0.9, a range that is lower than non-pregnant adult population. OSI has been found to identify women at risk of adverse outcomes secondary to PPH.

Altered mental status


In the early stages of PPH the mental status will be unaltered or there may be slight anxiety. Mental state starts to deteriorate after more than 30% of total blood volume is lost. Decreased level of consciousness or loss of consciousness are signs of more than 40% total blood volume loss.

Skin changes


Skin changes occur in all stages of hypovolemic shock, with the skin initially being pale and then becoming progressively colder and clammier.

Capillary refill time (CRT)


CRT in the forehead, lips, and nail beds helps assess the level of tissue hypoperfusion due to PPH. CRT will be delayed at 15% total blood volume loss. It becomes absent at more than 40% total blood volume loss.

‘Rule of 30’


The ‘Rule of Thirty’ is a simple way to determine that 30% of blood volume has been lost. It implies that the patient is in moderate shock leading to severe shock if the systolic BP has fallen by 30 mmHg, the HR has risen by 30 beats per minute, the RR has increased by more than 30 breaths per minute, if urinary output is less than 30ml/h or if the hemoglobin or HCT has dropped by 30%.

Uterine tone and size


Following third stage of labour, the uterus should be examined to assess uterine contraction and tone. Uterine atony is diagnosed when there is continuing vaginal bleeding and the uterus feels relaxed, soft or ‘boggy’ on fundal palpation.

Genital tract inspection


When the uterus is contracted, but vaginal bleeding continues, systemic examination of the genital tract is required to exclude PPH due to trauma of the birth canal. Trauma to the periurethral, the clitoral region, the anal sphincter or the lower uterine segments can also occur. PPH associated with birth trauma may not be immediately visible, as large amounts of blood can accumulate in the paravaginal space.

Signs of placental separation


Sudden small gush of blood, lengthening of the umbilical cord and the uterus becoming more globular in shape, are the three classic signs of placental separation. They should occur within the first few minutes after fetal expulsion. Absent placental separation is suggestive of retained products of conception (RPOC) which prevents the uterus from contracting enough to achieve optimal tone. Retained placenta is diagnosed when the placenta is not spontaneously delivered within 30 min. after parturition.

Postpartum examination of the placenta


Quick postpartum examination of the placenta at the bedside allows for early detection of incomplete membranes or placenta shape abnormalities which are associated with PPH due to retained tissue.

Signs of clotting dysfunction


Clinical signs of clotting dysfunction include oozing from puncture or injection sites and failure of the blood to clot in bedside receptacles. A quick bedside test for coagulation defects can be performed with an empty full blood examination tube (“red top”) when filled with maternal blood and taped to the wall. With a normal clotting profile, it should form a clot within 5 to 10 minutes.

Differential Diagnoses

Fact Explanation

Puerperal uterine inversion


Puerperal uterine inversion may be confused for atony-related PPH, because it can manifest as profuse vaginal bleeding and maternal shock after birth. Total uterine inversion can be recognized as a bluish-gray mass protruding from the vagina, but incomplete uterine inversion may be more subtle. If the uterus isn’t palpable on abdominal examination after birth, bimanual examination must be performed to confirm the location of the uterine fundus and reduce any potential uterine inversion.

Uterine rupture


Uterine rupture presenting after delivery can be similar to PPH, with signs of active bleeding, maternal tachycardia, hypotension, and/or uterine atony. Uterine rupture however, is more likely to develop during active labour and it is characterized with symptoms of abdominal pain and generalized peritonitis.

Puerperal sepsis


Similarly to PPH, maternal sepsis presents with signs of hypoperfusion or hypotension. Sepsis may or may not be associated with vaginal bleeding, but in contrast to PPH, women with puerperal sepsis are likely to develop fever.

Amniotic fluid embolus (AFE)


Amniotic fluid embolus is similar to PPH because it can cause hypotension, acute dyspnoea and maternal haemorrhage due to defects in coagulation. AFE differs from PPH by the symptoms and signs of pulmonary edema, bronchospasm and deoxygenation.

Puerperal uterine inversion


Puerperal uterine inversion may be confused for atony-related PPH, because it can manifest as profuse vaginal bleeding and maternal shock after birth. Total uterine inversion can be recognized as a bluish-gray mass protruding from the vagina, but incomplete uterine inversion may be more subtle. If the uterus isn’t palpable on abdominal examination after birth, bimanual examination must be performed to confirm the location of the uterine fundus and reduce any potential uterine inversion.

Uterine rupture


Uterine rupture presenting after delivery can be similar to PPH, with signs of active bleeding, maternal tachycardia, hypotension, and/or uterine atony. Uterine rupture however, is more likely to develop during active labour and it is characterized with symptoms of abdominal pain and generalized peritonitis.

Puerperal sepsis


Similarly to PPH, maternal sepsis presents with signs of hypoperfusion or hypotension. Sepsis may or may not be associated with vaginal bleeding, but in contrast to PPH, women with puerperal sepsis are likely to develop fever.

Amniotic fluid embolus (AFE)


Amniotic fluid embolus is similar to PPH because it can cause hypotension, acute dyspnoea and maternal haemorrhage due to defects in coagulation. AFE differs from PPH by the symptoms and signs of pulmonary edema, bronchospasm and deoxygenation.

Investigations - Diagnosis

Fact Explanation

Clinical diagnosis


The diagnosis of PPH is clinical. Laboratory values are quite useful at guiding management, but the diagnosis of PPH can be made by estimation of the degree of blood loss and assessing for parturient haemodynamic stability.

Blood loss evaluation


Visual estimation of blood loss has been shown to underestimate up to 50% of large volume blood loss. More accurate methods of blood loss evaluation include direct gravimetric measurement of blood-soaked material, periodic estimation of cumulative blood loss and calculation of the exact percentage of circulating blood volume loss based on a woman’s booking weight.

Non-invasive cardiovascular monitoring


Continuous non-invasive cardiovascular monitoring should occur in all women postpartum, to ensure rapid recognition of hypovolemia. In women with established PPH, monitoring should be intensified with BP measurements every 3–5 min, continuous HR, RR, peripheral oxygen saturation and electrocardiography (ECG).

Full blood count (FBC)


On serial measurement of hematocrit (HCT), a 10% drop of HCT establishes the diagnosis of PPH. Hemoglobin (Hb) is useful at prompting transfusion, but Hb should not be used to assess PPH severity. This is because the relative hemodilution and increased cardiac output in normal pregnancy allow for a significant amount of blood loss to occur, before a drop in Hb is demonstrated. Platelet count (PLT) can help detect any pre‐existing thrombocytopenia, but it is most likely going to be secondary to hemodilution. Serial PLT measurements are useful in defining consumptive coagulopathy.

Blood type and cross-match


Blood type should be identified and antibody screening should be performed in all women at the time of delivery. A patient’s blood should be fully cross-matched if transfusion is anticipated.

Venous blood gases (VBG)


Blood pH and lactate are sensitive measures of haemorrhage-related metabolic acidosis and shock. High lactate levels and low pH indicate hypoperfusion and tissue distress. A lactate higher than 72.0 mg/dL (4.0 mmol/L) in the setting of PPH, should prompt activation of MPHP.

Liver function tests (LFT)


LFTs are relevant in determining any PPH resulting from coagulopathy of liver dysfunction in pregnancy.

Clotting profile


Routine clotting profile may include prothrombin time (INR), partial thromboplastin time (aPTT) and fibrin split products (D-dimer). They can help guide clinicians in blood component therapy, but they are slow to obtain and often normal despite severe PPH. Fibrinogen concentration is high at the end of pregnancy and decreases rapidly in the setting of PPH. It can drop from its normal levels (4 - 6 g/L) to below 2 g/L before any change in PT or aPTT takes place. Early detection of hypofibrinogenemia is crucial in identifying women with PPH who may benefit from targeted haemostatic treatment.

Viscoelasticity tests


Point-of-care testing of coagulation using thromboelastography (TEG) or rotational thromboelastometry (ROTEM) provide in vivo monitoring of evolving clot strength and subsequent fibrinolysis. It can provide rapid feedback about key changes of maternal hemostatic mechanisms during PPH management and it can help in differentiation of the cause of bleeding.

Investigations of secondary PPH


The work-up in secondary PPH should include high and low vaginal swabs, full blood count, C-reactive protein and blood cultures if a woman is febrile. Transvaginal ultrasound is helpful in ruling out retained products of conception but it may be unreliable in the immediate postpartum period.

Clinical diagnosis


The diagnosis of PPH is clinical. Laboratory values are quite useful at guiding management, but the diagnosis of PPH can be made by estimation of the degree of blood loss and assessing for parturient haemodynamic stability.

Blood loss evaluation


Visual estimation of blood loss has been shown to underestimate up to 50% of large volume blood loss. More accurate methods of blood loss evaluation include direct gravimetric measurement of blood-soaked material, periodic estimation of cumulative blood loss and calculation of the exact percentage of circulating blood volume loss based on a woman’s booking weight.

Non-invasive cardiovascular monitoring


Continuous non-invasive cardiovascular monitoring should occur in all women postpartum, to ensure rapid recognition of hypovolemia. In women with established PPH, monitoring should be intensified with BP measurements every 3–5 min, continuous HR, RR, peripheral oxygen saturation and electrocardiography (ECG).

Full blood count (FBC)


On serial measurement of hematocrit (HCT), a 10% drop of HCT establishes the diagnosis of PPH. Hemoglobin (Hb) is useful at prompting transfusion, but Hb should not be used to assess PPH severity. This is because the relative hemodilution and increased cardiac output in normal pregnancy allow for a significant amount of blood loss to occur, before a drop in Hb is demonstrated. Platelet count (PLT) can help detect any pre‐existing thrombocytopenia, but it is most likely going to be secondary to hemodilution. Serial PLT measurements are useful in defining consumptive coagulopathy.

Blood type and cross-match


Blood type should be identified and antibody screening should be performed in all women at the time of delivery. A patient’s blood should be fully cross-matched if transfusion is anticipated.

Venous blood gases (VBG)


Blood pH and lactate are sensitive measures of haemorrhage-related metabolic acidosis and shock. High lactate levels and low pH indicate hypoperfusion and tissue distress. A lactate higher than 72.0 mg/dL (4.0 mmol/L) in the setting of PPH, should prompt activation of MPHP.

Liver function tests (LFT)


LFTs are relevant in determining any PPH resulting from coagulopathy of liver dysfunction in pregnancy.

Clotting profile


Routine clotting profile may include prothrombin time (INR), partial thromboplastin time (aPTT) and fibrin split products (D-dimer). They can help guide clinicians in blood component therapy, but they are slow to obtain and often normal despite severe PPH. Fibrinogen concentration is high at the end of pregnancy and decreases rapidly in the setting of PPH. It can drop from its normal levels (4 - 6 g/L) to below 2 g/L before any change in PT or aPTT takes place. Early detection of hypofibrinogenemia is crucial in identifying women with PPH who may benefit from targeted haemostatic treatment.

Viscoelasticity tests


Point-of-care testing of coagulation using thromboelastography (TEG) or rotational thromboelastometry (ROTEM) provide in vivo monitoring of evolving clot strength and subsequent fibrinolysis. It can provide rapid feedback about key changes of maternal hemostatic mechanisms during PPH management and it can help in differentiation of the cause of bleeding.

Investigations of secondary PPH


The work-up in secondary PPH should include high and low vaginal swabs, full blood count, C-reactive protein and blood cultures if a woman is febrile. Transvaginal ultrasound is helpful in ruling out retained products of conception but it may be unreliable in the immediate postpartum period.

Investigations - Management

Fact Explanation

Urinary output


Emptying the bladder to stimulate uterine contraction represents the first-line management of PPH. All women with established PPH require an indwelling catheter insertion in order to monitor output and maintain accurate fluid balance.

Lethal triad management


Uncontrolled PPH leads to the lethal triad of hypothermia, acidosis and coagulopathy. Each component of the triad exacerbates the other and require regular monitoring inwomen with PPH. Permissive hypotension during the bleeding phase, limiting the use of fluids and advocating the early use of blood products can help in avoid or manage the onset of the lethal triad.

Urinary output


Emptying the bladder to stimulate uterine contraction represents the first-line management of PPH. All women with established PPH require an indwelling catheter insertion in order to monitor output and maintain accurate fluid balance.

Lethal triad management


Uncontrolled PPH leads to the lethal triad of hypothermia, acidosis and coagulopathy. Each component of the triad exacerbates the other and require regular monitoring inwomen with PPH. Permissive hypotension during the bleeding phase, limiting the use of fluids and advocating the early use of blood products can help in avoid or manage the onset of the lethal triad.

Management - Supportive

Fact Explanation

Active management of the third stage of labor (AMTSL)


The most effective strategy in preventing PPH is AMTSL. It includes:

1. Administration of prophylactic uterotonics with or soon after the delivery of the anterior shoulder;

2. Controlled cord traction

3. Late cord clamping (performed 1-3 min after birth)

Intravenous fluid replacement


2 large bore cannulae should be placed and up to 2L of warmed intravenous fluid should be rapidly infused while awaiting compatible blood in women with severe PPH. Isotonic crystalloids are preferred to colloids. Greater than 3.5L of clear fluid replacement must be avoided because it causes dilutional coagulopathy.

Oxygen therapy


A high concentration of oxygen (10–15 L/min) should be administered in all women with PPH, regardless of maternal oxygen concentration. This will optimize oxygen transport and minimize the disruption of tissue metabolism.

Tranexamic acid (TXA)


TXA given alongside prophylactic oxytocin has been proven useful in preventing PPH after caesarean delivery. TXA has been found to be a life-saving intervention in PPH when uterotonics fail to stop bleeding or in trauma-associated uterine bleeding. It should be given intravenously, within three hours of giving birth.

Normothermia maintenance


Maintaining temperature > 35 °C with the help of warm fluids and external warming devices is imperative in women with PPH, especially those receiving transfusion. Hypothermia exacerbates coagulopathy and leads to impaired tissue oxygenation and myocardial dysfunction.

Correction of acidosis


Acidosis causes delay in clot formation and a reduction in clot strength and efforts to correct acidosis in severe PPH should be made with the help of bicarbonate supplementation. The efficacy of TXA and recombinant activated factor VII (rFVIIa) to restore pH in women with PPH is currently has been investigated.

Hypocalcemia management


Calcium has a crucial role in the normal process of coagulation and uterine muscle contraction, thus keeping an optimal calcium in a woman with PPH levels is very important. Hypocalcemia with ionised calcium < 1.1 mmol/L occurring during transfusion, should be corrected with IV 10% calcium gluconate.

Vasopressors


Vasopressors such as phenylephrine or norepinephrine can be used in PPH with unacceptable maternal hypotension, but aggressive treatment of hypovolaemia should always be prioritised.

Massive Postpartum Hemorrhage Protocol (MPHP)


Each maternity unit should have its own MPHP which involves th transfusion of large amount of blood products guided by checklists, PPH emergency kit and treatment algorithms. MPHP assists the multi-professional team in effective completion of tasks when responding to PPH, while decreasing the risk of dilutional coagulopathy and other PPH complications. As a rule, MPHP requires activation when a parturient is actively bleeding and has one or more of the following criteria:

1. Estimated blood loss > 1500mL

2. Actual or anticipated 4 RBC units in less than 4 hours with haemodynamic instability

3. Clinical or laboratory evidence of coagulopathy

Active management of the third stage of labor (AMTSL)


The most effective strategy in preventing PPH is AMTSL. It includes:

1. Administration of prophylactic uterotonics with or soon after the delivery of the anterior shoulder;

2. Controlled cord traction

3. Late cord clamping (performed 1-3 min after birth)

Intravenous fluid replacement


2 large bore cannulae should be placed and up to 2L of warmed intravenous fluid should be rapidly infused while awaiting compatible blood in women with severe PPH. Isotonic crystalloids are preferred to colloids. Greater than 3.5L of clear fluid replacement must be avoided because it causes dilutional coagulopathy.

Oxygen therapy


A high concentration of oxygen (10–15 L/min) should be administered in all women with PPH, regardless of maternal oxygen concentration. This will optimize oxygen transport and minimize the disruption of tissue metabolism.

Tranexamic acid (TXA)


TXA given alongside prophylactic oxytocin has been proven useful in preventing PPH after caesarean delivery. TXA has been found to be a life-saving intervention in PPH when uterotonics fail to stop bleeding or in trauma-associated uterine bleeding. It should be given intravenously, within three hours of giving birth.

Normothermia maintenance


Maintaining temperature > 35 °C with the help of warm fluids and external warming devices is imperative in women with PPH, especially those receiving transfusion. Hypothermia exacerbates coagulopathy and leads to impaired tissue oxygenation and myocardial dysfunction.

Correction of acidosis


Acidosis causes delay in clot formation and a reduction in clot strength and efforts to correct acidosis in severe PPH should be made with the help of bicarbonate supplementation. The efficacy of TXA and recombinant activated factor VII (rFVIIa) to restore pH in women with PPH is currently has been investigated.

Hypocalcemia management


Calcium has a crucial role in the normal process of coagulation and uterine muscle contraction, thus keeping an optimal calcium in a woman with PPH levels is very important. Hypocalcemia with ionised calcium < 1.1 mmol/L occurring during transfusion, should be corrected with IV 10% calcium gluconate.

Vasopressors


Vasopressors such as phenylephrine or norepinephrine can be used in PPH with unacceptable maternal hypotension, but aggressive treatment of hypovolaemia should always be prioritised.

Massive Postpartum Hemorrhage Protocol (MPHP)


Each maternity unit should have its own MPHP which involves th transfusion of large amount of blood products guided by checklists, PPH emergency kit and treatment algorithms. MPHP assists the multi-professional team in effective completion of tasks when responding to PPH, while decreasing the risk of dilutional coagulopathy and other PPH complications. As a rule, MPHP requires activation when a parturient is actively bleeding and has one or more of the following criteria:

1. Estimated blood loss > 1500mL

2. Actual or anticipated 4 RBC units in less than 4 hours with haemodynamic instability

3. Clinical or laboratory evidence of coagulopathy

Management - Specific

Fact Explanation

HAEMOSTASIS mnemonic


The HAEMOSTASIS mnemonic is used to help with systematic and stepwise management of PPH. It stands for:

H: Get Help and Hands on the uterus

A: Assess and resuscitate

E: Establish Etiology, Ensure availability of blood products and Ecbolics/uterotonics

M: Massage uterus

O: Oxytocics infusion/prostaglandins

S: Shift to theatre for bimanual compression

T: Tissue and Trauma – exclude/manage/proceed to balloon Tamponade

A: Apply B-Lynch/modified compression sutures

S: Systematic pelvic devascularization (uterine/ovarian/quadruple/internal iliac)

I: Interventional radiology – uterine artery embolization, if appropriate

S: Subtotal/total abdominal hysterectomy

Uterine massage


Transabdominal uterine massage is done after the delivery of the placenta if the uterus isn’t contracted well. With the woman’s leg bent, the uterine fundus is massaged in a circular motion until a contraction is felt, followed by expulsion of blood clots that reduces further bleeding.

Resuscitation goals


Resuscitation in PPH incorporates the standard structured approach of primary survey where vital signs and perfusion status are being assessed and simultaneously corrected. The goals of hemodynamic management in PPH are systolic blood pressure of 90–100 mmHg, MAP of 55–65 mmHg, HR <100 bpm, serum lactate <2 mmol/L and pH >7.20.

Transfusion goals


The goals of transfusion in a woman with PPH are as follows:

- Hemoglobin and hematocrit: 9–10 g/dL and 27–30%

- Platelets: >50,000

- Fibrinogen: 1.5–2 g/l

- Ionised calcium: Normocalcemia

- Temperature >35°C

Blood component therapy


The most commonly recommended method of improving hemostasis in severe PPH unresponsive to uterotonics, fluids and other resuscitation measures, is starting an early and rapid transfusion of packed RBC and FFP in 1-2:1 (RBC: FFP) ratio. Cryoprecipitate or human plasma-derived fibrinogen concentrate should be given to improve hypofibrinogenemia. Platelet transfusion is recommended in throbocytopenia or platelet dysfunction.

First line of uterotonic therapy: Oxytocin


Intravenous oxytocin is the first-line uterotonic indicated in all women with atonic uterus even if they have received oxytocin as PPH prophylaxis. Oxytocin causes rhythmic contraction of myometrium and decreases blood flow through the uterus. It has a very good safety profile if administered correctly.

Second line uterotonic therapy: Ergot alkaloid


The choice of a second-line uterotonic should be based on patient-specific factors and local maternity care practices. Ergot alkaloids such as methylergonovine and ergometrine are contraindicated in women with hypertensive disorders in pregnancy and in patients with HIV taking protease inhibitors.

Second line uterotonic therapy: Prostaglandins


Prostaglandins such as carboprost and misoprostol are strong uterotonics typically used as an intramyometrial injection during cesarean section or a postpartum surgical procedure to treat severe PPH. They need to be avoided in patients with asthma, hypertension, or significant cardiac or renal disease.

Birth trauma management


Up to 70% of vaginal deliveries require suturing of perineal trauma. Synthetic absorbable sutures are recommended as they are associated with decreased wound dehiscence and less postpartum perineal pain. Small tears (<2 cm), which do not bleed, can be managed conservatively.

Hematoma management


Small hematomas can be managed with ice packs, analgesia, and observation. Hematomas measuring >3-4 cm or enlarging hematomas, require incision and evacuation of the clot.

Bimanual uterine compression massage


Bimanual compression of the uterus is used to treat uterine atony refractory to uterotonics. Bimanual uterine compression massage is performed with one hand is placed internally in the vagina, pushing against the body of the uterus while the other hand is pushing against the fundus externally through the abdominal wall. The posterior aspect of the uterus is then massaged with the abdominal hand and the anterior aspect with the vaginal hand. Bimanual uterine compression massage may help stop bleeding entirely or be a temporary measure until alternative strategies of PPH management can be employed.

Manual removal of placenta


If oxytocin and controlled cord traction fail to aid with expulsion of the placenta, manual removal of the placenta should be performed. If blunt dissection with the edge of the proceduralit’s hand does not reveal the tissue plane between the uterine wall and placenta, invasive placenta should be considered. In some cases a blunt curette can be used often under ultrasound guidance to remove the placenta.

Manual exploration of uterine cavity


Manual exploration of uterine cavity is usually performed when symptoms of PPH persist even after uterine atony has been treated and no lacerations or hematomas have been recognized. It is indicated when the placenta appears incomplete after birth or in order to diagnose and treat retained placental fragments. It can also help detect ruptured or partial uterine inversion.

Non-pneumatic anti-shock garment (NASG)


NASG can buy time for women with haemorrhage-related hypovolemic shock regardless of the cause, by applying counter-pressure to the lower body and returning blood to the vital organs.

Aortic compression


Application of direct downward pressure over the aorta with a fist when the femoral pulse isn’t palpable is a life-saving intervention in the presence of severe PPH, whatever its aetiology. Aortic compression will cut off the blood supply to the pelvis, while preparing for other necessary intervention.

Intrauterine balloon tamponade


Intrauterine balloon tamponade is now considered a first-line treatment for PPH predominantly resulting from uterine atony. It is performed by inserting a balloon such as ‘Bakri SOS’ balloon or the Sengstaken–Blakemore oesophageal catheter, through the vagina and into the uterus. The balloon is then inflated to exert direct pressure against the uterine wall. This may stop the bleeding completely in over 50% of women or at least it will reduce persistent capillary and venous bleeding allowing the time to arrange for more permanent measures of PPH management.

Compression uterine sutures


When severe PPH due to atony is refractory to all conservative measures or minimally-invasive procedures, laparotomy with application of uterine hemostatic or compression sutures should be considered. Most commonly performed sutures are B-Lynch and Hayman sutures which work by enveloping the uterus with thick absorbable material that compresses the uterine anterior and posterior walls and can help avoid hysterectomy in up to 90% of cases.

Vessel ligation


In cases of continued bleeding after uterine packing and tamponade, systematic pelvic devascularization can be attempted. Uterine artery ligation (UAL) is the first step because the uterine arteries are responsible for about 90% of the uterine blood flow. UAL alone can be enough to treat PPH due to uterine atony. If UAL is ineffective, lower uterine segment vessels should be ligated next, followed by ovarian vessel ligation. The last step should be internal iliac artery ligation (IIAL) which is very effective at controlling bleeding from the uterine, cervical and vaginal vessels.

Uterine artery embolization


Uterine artery embolization can treat PPH as it blocks the blood supply to the uterus by injecting embolic material into the uterine arteries. It has a very high success rate, but it can only be considered in hemodynamically stable women with PPH.

Hysterectomy


If uterus-saving procedures have failed to treat PPH, hysterectomy is performed as a live-saving measure. If the upper segment of the uterus represents an isolated source of bleeding, then subtotal hysterectomy can be performed. In most other cases of unrelenting bleeding total hysterectomy is recommended. Hysterectomy may be considered a first choice of treatment in PPH due to placenta accreta or uterine rupture.

Triple P procedure


Triple P procedure involves perioperative placental localization and delivery of the fetus via transverse uterine incision above the upper border of the placenta. This is followed by pelvic devascularization, myometrial excision and reconstruction of the uterine wall. Triple P represents a conservative surgical alternative to peripartum hysterectomy for women with morbidly adherent placenta and is associated with a significant reduction in PPH, allowing preservation of reproductive health in young women.

Management of secondary PPH


Secondary PPH is often associated with endometritis and requires an antibiotic treatment with a beta-lactam combined with another agent with anaerobic coverage. If there is evidence of incomplete involution or retention of placental fragments, surgical evacuation of retained placental tissue should be performed by a senior obstetrician as these patients are at a high risk of uterine perforation. Uterotonics are also part of the treatment of secondary PPH.

HAEMOSTASIS mnemonic


The HAEMOSTASIS mnemonic is used to help with systematic and stepwise management of PPH. It stands for:

H: Get Help and Hands on the uterus

A: Assess and resuscitate

E: Establish Etiology, Ensure availability of blood products and Ecbolics/uterotonics

M: Massage uterus

O: Oxytocics infusion/prostaglandins

S: Shift to theatre for bimanual compression

T: Tissue and Trauma – exclude/manage/proceed to balloon Tamponade

A: Apply B-Lynch/modified compression sutures

S: Systematic pelvic devascularization (uterine/ovarian/quadruple/internal iliac)

I: Interventional radiology – uterine artery embolization, if appropriate

S: Subtotal/total abdominal hysterectomy

Uterine massage


Transabdominal uterine massage is done after the delivery of the placenta if the uterus isn’t contracted well. With the woman’s leg bent, the uterine fundus is massaged in a circular motion until a contraction is felt, followed by expulsion of blood clots that reduces further bleeding.

Resuscitation goals


Resuscitation in PPH incorporates the standard structured approach of primary survey where vital signs and perfusion status are being assessed and simultaneously corrected. The goals of hemodynamic management in PPH are systolic blood pressure of 90–100 mmHg, MAP of 55–65 mmHg, HR <100 bpm, serum lactate <2 mmol/L and pH >7.20.

Transfusion goals


The goals of transfusion in a woman with PPH are as follows:

- Hemoglobin and hematocrit: 9–10 g/dL and 27–30%

- Platelets: >50,000

- Fibrinogen: 1.5–2 g/l

- Ionised calcium: Normocalcemia

- Temperature >35°C

Blood component therapy


The most commonly recommended method of improving hemostasis in severe PPH unresponsive to uterotonics, fluids and other resuscitation measures, is starting an early and rapid transfusion of packed RBC and FFP in 1-2:1 (RBC: FFP) ratio. Cryoprecipitate or human plasma-derived fibrinogen concentrate should be given to improve hypofibrinogenemia. Platelet transfusion is recommended in throbocytopenia or platelet dysfunction.

First line of uterotonic therapy: Oxytocin


Intravenous oxytocin is the first-line uterotonic indicated in all women with atonic uterus even if they have received oxytocin as PPH prophylaxis. Oxytocin causes rhythmic contraction of myometrium and decreases blood flow through the uterus. It has a very good safety profile if administered correctly.

Second line uterotonic therapy: Ergot alkaloid


The choice of a second-line uterotonic should be based on patient-specific factors and local maternity care practices. Ergot alkaloids such as methylergonovine and ergometrine are contraindicated in women with hypertensive disorders in pregnancy and in patients with HIV taking protease inhibitors.

Second line uterotonic therapy: Prostaglandins


Prostaglandins such as carboprost and misoprostol are strong uterotonics typically used as an intramyometrial injection during cesarean section or a postpartum surgical procedure to treat severe PPH. They need to be avoided in patients with asthma, hypertension, or significant cardiac or renal disease.

Birth trauma management


Up to 70% of vaginal deliveries require suturing of perineal trauma. Synthetic absorbable sutures are recommended as they are associated with decreased wound dehiscence and less postpartum perineal pain. Small tears (<2 cm), which do not bleed, can be managed conservatively.

Hematoma management


Small hematomas can be managed with ice packs, analgesia, and observation. Hematomas measuring >3-4 cm or enlarging hematomas, require incision and evacuation of the clot.

Bimanual uterine compression massage


Bimanual compression of the uterus is used to treat uterine atony refractory to uterotonics. Bimanual uterine compression massage is performed with one hand is placed internally in the vagina, pushing against the body of the uterus while the other hand is pushing against the fundus externally through the abdominal wall. The posterior aspect of the uterus is then massaged with the abdominal hand and the anterior aspect with the vaginal hand. Bimanual uterine compression massage may help stop bleeding entirely or be a temporary measure until alternative strategies of PPH management can be employed.

Manual removal of placenta


If oxytocin and controlled cord traction fail to aid with expulsion of the placenta, manual removal of the placenta should be performed. If blunt dissection with the edge of the proceduralit’s hand does not reveal the tissue plane between the uterine wall and placenta, invasive placenta should be considered. In some cases a blunt curette can be used often under ultrasound guidance to remove the placenta.

Manual exploration of uterine cavity


Manual exploration of uterine cavity is usually performed when symptoms of PPH persist even after uterine atony has been treated and no lacerations or hematomas have been recognized. It is indicated when the placenta appears incomplete after birth or in order to diagnose and treat retained placental fragments. It can also help detect ruptured or partial uterine inversion.

Non-pneumatic anti-shock garment (NASG)


NASG can buy time for women with haemorrhage-related hypovolemic shock regardless of the cause, by applying counter-pressure to the lower body and returning blood to the vital organs.

Aortic compression


Application of direct downward pressure over the aorta with a fist when the femoral pulse isn’t palpable is a life-saving intervention in the presence of severe PPH, whatever its aetiology. Aortic compression will cut off the blood supply to the pelvis, while preparing for other necessary intervention.

Intrauterine balloon tamponade


Intrauterine balloon tamponade is now considered a first-line treatment for PPH predominantly resulting from uterine atony. It is performed by inserting a balloon such as ‘Bakri SOS’ balloon or the Sengstaken–Blakemore oesophageal catheter, through the vagina and into the uterus. The balloon is then inflated to exert direct pressure against the uterine wall. This may stop the bleeding completely in over 50% of women or at least it will reduce persistent capillary and venous bleeding allowing the time to arrange for more permanent measures of PPH management.

Compression uterine sutures


When severe PPH due to atony is refractory to all conservative measures or minimally-invasive procedures, laparotomy with application of uterine hemostatic or compression sutures should be considered. Most commonly performed sutures are B-Lynch and Hayman sutures which work by enveloping the uterus with thick absorbable material that compresses the uterine anterior and posterior walls and can help avoid hysterectomy in up to 90% of cases.

Vessel ligation


In cases of continued bleeding after uterine packing and tamponade, systematic pelvic devascularization can be attempted. Uterine artery ligation (UAL) is the first step because the uterine arteries are responsible for about 90% of the uterine blood flow. UAL alone can be enough to treat PPH due to uterine atony. If UAL is ineffective, lower uterine segment vessels should be ligated next, followed by ovarian vessel ligation. The last step should be internal iliac artery ligation (IIAL) which is very effective at controlling bleeding from the uterine, cervical and vaginal vessels.

Uterine artery embolization


Uterine artery embolization can treat PPH as it blocks the blood supply to the uterus by injecting embolic material into the uterine arteries. It has a very high success rate, but it can only be considered in hemodynamically stable women with PPH.

Hysterectomy


If uterus-saving procedures have failed to treat PPH, hysterectomy is performed as a live-saving measure. If the upper segment of the uterus represents an isolated source of bleeding, then subtotal hysterectomy can be performed. In most other cases of unrelenting bleeding total hysterectomy is recommended. Hysterectomy may be considered a first choice of treatment in PPH due to placenta accreta or uterine rupture.

Triple P procedure


Triple P procedure involves perioperative placental localization and delivery of the fetus via transverse uterine incision above the upper border of the placenta. This is followed by pelvic devascularization, myometrial excision and reconstruction of the uterine wall. Triple P represents a conservative surgical alternative to peripartum hysterectomy for women with morbidly adherent placenta and is associated with a significant reduction in PPH, allowing preservation of reproductive health in young women.

Management of secondary PPH


Secondary PPH is often associated with endometritis and requires an antibiotic treatment with a beta-lactam combined with another agent with anaerobic coverage. If there is evidence of incomplete involution or retention of placental fragments, surgical evacuation of retained placental tissue should be performed by a senior obstetrician as these patients are at a high risk of uterine perforation. Uterotonics are also part of the treatment of secondary PPH.

References

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