Postpartum Hemorrhage

Postpartum Hemorrhage (PPH) /Obstetrical Hemorrhage

1. What every clinician should know

Clinical features and incidence

Postpartum hemorrhage (PPH) is any excessive bleeding after delivery. It occurs in about 5% of all deliveries. Up to 25% of all pregnancy-related deaths are directly attributable to hemorrhage. It is the most common cause of maternal death worldwide.

PPH is traditionally defined as blood loss greater than 500mL for vaginal delivery or greater than 1000mL for cesarean delivery. However, as practitioners, we do a poor job at estimating blood loss, so we should maintain a heightened awareness of this serious complication for each delivery. Hemorrhage need not be a sudden massive quantity; even steady moderate bleeding can lead to serious hypovolemia. Quick recognition of PPH, along with identification of its cause and initiation of treatment, can avoid serious morbidity and mortality.

Risk factors

While many risk factors are associated with PPH, it often happens without warning. Therefore, hospitals providing obstetrical care should have in place PPH management protocols and a massive transfusion protocol.

Leading causes of early PPH:

Uterine atony (most common)

Risk factors: prolonged labor, overdistended uterus (multiple gestation, large baby or polyhydramnios), use of oxytocin, history of PPH, episiotomy, preeclampsia, operative delivery, chorioamnionitis, and Asian or Hispanic ethnicity.
Lacerations

Risk factors: operative vaginal delivery, malpresentation, fetal macrosomia, episiotomy, precipitous delivery, prior cerclage placement, Duhrssen’s incisions and shoulder dystocia.
Retained placenta

Risk factors: midtrimester delivery, chorioamnionitis and accessory placental lobes.
Other causes:

Uterine inversion

Risk factors: uterine overdistension, prolonged labor, fetal macrosomia, invasive implantation, short umbilical cord, oxytocin use.

Uterine rupture

Risk factors: prior uterine surgery (most commonly cesarean delivery), blunt trauma to abdomen, internal podalic version, breech extraction, difficult forceps delivery, use of utero-tonic agents in high parity patients.

Invasive implantation (placenta accreta, increta, percreta).

Risk factors: previous cesarean delivery or other uterine surgery, placenta previa, increasing parity, older maternal age.

2. Diagnosis and differential diagnosis

Early or primary PPH occurs in the first 24 hours after delivery, and the diagnosis is made clinically by identifying excessive bleeding after delivery. Physicians and nursing staff on labor and delivery should be skilled in accurately assessing blood loss and keenly aware that continued bleeding after delivery requires prompt evaluation and management. Once PPH is diagnosed, the cause should be identified. The differential diagnosis for the etiologies of early PPH include:

Uterine atony
Lacerations
Retained placenta
Uterine inversion
Uterine rupture

Examination is key to revealing the etiology. Bimanual pelvic exam will identify uterine atony. Manual uterine exploration can identify retained placental tissue. Careful inspection is needed to look for lacerations of the cervix and vagina. Uterine inversion is diagnosed by palpation of a mass within or through the cervix. Clinical suspicion and risk factors such as prior history of uterine surgery are important in diagnosing uterine rupture. One must quickly work through the differential causes and rapidly initiate treatment.

While a 10% drop in hemoglobin or hematocrit also has been used to define PPH, this does not always reflect the current status of the patient as bleeding continues. Also, the patient could seriously decompensate in the time it takes to get lab results. Other signs and symptoms such as dizziness, pallor, hypotension, tachycardia and oliguria add to the diagnosis, but these may not occur until late, when 15-20% or more of blood volume has been depleted.

Late or secondary PPH occurs between 24 hours and 6 weeks postpartum and occurs in about 1% of women postpartum. Bleeding most commonly occurs between 8 and 14 days after delivery. Common causes include: abnormal involution of the placental site, retained placental tissue, infection and inherited coagulation defects. When hemorrhage occurs between 2-5 days postpartum, von Willebrand’s disease is one of the most common causes.

Physical examination and ultrasound are helpful in identifying the cause. With placental subinvolution, on exam the uterus is usually larger and softer than would be expected. An empty uterine cavity on ultrasound will suggest placental site subinvolution that should be treated differently than retained products, which can be identified by identification of a thickened stripe or echogenic material within the uterine cavity on ultrasound.

However, at times it may be difficult to distinguish between blood clots and tissue on ultrasound. Examination is also helpful, as a dilated cervix leads one to suspect retained products of conception. Also, uterine tenderness along with fever points to infection as an etiology. Infection could be caused by retained products.

If the bleeding continues without one of the obvious common causes identified or if standard therapies are not effective, a coagulopathy should be considered. Disseminated intravascular coagulopathy (DIC) can rapidly ensue if PPH goes unrecognized, early management is unsuccessful or appropriate resuscitation is not initiated. Some women also may have an undiagnosed bleeding disorder such as von Willebrand’s disease. Usually these patients will have a history of menorrhagia.

3. Management

Prevention of postpartum hemorrhage

Active management of the third stage of labor is advocated to reduce the risk of PPH in all women. The preferred medication is Oxytocin 10 units intramuscularly given after delivery of the anterior shoulder. Alternatively, an intravenous infusion of oxytocin 20-40 units in 1000mL fluid running at 150mL/hour can be used.

Management of early PP

The goal is to control bleeding and achieve hemostasis. Least invasive methods are utilized first; however, at times immediate hysterectomy may be necessary to save the patient’s life. Management varies based on the cause of bleeding, available treatment options, and the patient’s status and her desire for future childbearing. A multidisciplinary approach is often essential.

Management of uterine atony

Given that atony is the most common cause, assessment and treatment for this should be quickly undertaken:

Drain the bladder.
Perform bimanual pelvic exam and uterine massage.
Perform manual uterine exploration for retained placenta.
If uterus is firm, look for lacerations and repair them.
If uterus is boggy and massage is unsuccessful start medical therapy with uterotonic agents.
Uterotonic therapy:

Oxytocin IV infusion:

Usually initiated as IV transfusion after delivery of the placenta.

Dose: 10-80 units in 1,000mL of crystalloid solution for IV infusion.

Route: 1st line: IV; second line: 10 units IM or IU(intrauterine).

Frequency: continuous IV infusion.

Side effects: nausea, emesis, hypotension if undiluted rapid IV infusion, water intoxication.

Contraindications: none.

Methyl ergonovine (Methergine)

Dose: 0.2 milligrams.

Route: 1st line: IM; second line: IU or PO.

Frequency: 2-4 hours.

Side effects: hypertension, hypotension, nausea, emesis.

Contraindications: hypertension, pre-eclampsia.

15-Methyl prostaglandin

Dose: 0.25 milligrams.

Route: 1st line: IM; second line: IU.

Frequency: 15-90 minutes.

Side effects: diarrhea, fever, chills, nausea, emesis, headache, flushing.

Contraindications: asthma, active cardiac, hepatic or renal disease.

Misoprostol (Cytotec)

Dose: 400-1000 micrograms.

Route: 1st line: Sublingual, buccal, or rectal; second line: PO.

Frequency: single dose

Side effects: fever, tachycardia

Contraindications: none

If heavy bleeding persists after initiation of basic management steps (bimanual uterine massage and uterotonic medications): CALL FOR HELP.

Mobilize additional nursing staff.
Obtain 2 large bore IVs.

Begin IV fluid resuscitation.
Monitor vital signs frequently.
Monitor urine output.
Get another physician for assistance OR Activate Hemorrhage Team (*see below)
Notify anesthesia for possible need for surgical intervention.
Draw baseline labs.
Type and cross patient for blood.

Transfuse based on blood loss or clinical signs and symptoms.

Do not wait for labs to initiate transfusion.

PPH management protocols and a massive transfusion protocol should be should be established on all labor and delivery units. Evidence supports use of standardized care bundles with an organized multidisciplinary team approach. An integrated *hemorrhage team consisting of obstetricians and surgeons skilled in medical and surgical techniques along with collaboration of nursing, anesthesiologists, transfusion medicine and critical care can reduce maternal morbidity and mortality from obstetrical hemorrhage. A dedicated hemorrhage cart allows easy access to equipment and medications necessary to control hemorrhage.

Next steps in management if medications fail

Tamponade

Tamponade of the uterus can be an effective method in treating hemorrhage due to uterine atony. By exerting pressure against the uterine wall, bleeding from the endometrium is stopped. It can be used to temporize bleeding while awaiting the transfusion of blood products or transfer to surgical location. Lacerations and retained placenta should be excluded.

Gauze

Use long continuous gauze (Kerlix) rather than multiple small sponges. If more than one roll is needed, the ends should be tied together.

Start at the fundus and move toward the os in a side-to side fashion avoiding dead space that could conceal bleeding.

Leave a tail of the gauze outside of the cervix.

Do not leave in place for more than 24 hours.

The use of broad spectrum antibiotics to prevent infection is recommended while the packing is in place.

Carefully monitor vital signs, urine output and hemocrit for sign of continued bleeding.

Balloons

Specifically developed as an alternative to uterine cavity packing for PPH. These balloon catheters are made of silicone and readily confirm to the shape of the uterus. They come presterilized and are easy to insert with minimal training. They have been show to be effective 92% of the time.

Bakri Balloon.

maximum fill volume: 500mL.

Ebb-Jetty system (has both a uterine and a vaginal balloon).

maximum fill volume for uterine balloon: 750mL (usually less than 500mL is required).

maximum fill volume for vaginal balloon: 300mL.

A Foley catheter or Sengstaken-Blakemore tube can be used as alternatives.

The balloon is placed in the uterine cavity and instilled with sterile saline to create tamponade in the uterine cavity; typically, about 300cc is effective at controlling bleeding.

Both manufacturers of the Bakri and Ebb-Jetty system recommend ultrasound to confirm placement.

Drainage tubing allows for the monitoring of persistent bleeding. Flushing the drainage port with sterile saline will allow clots to be removed and prevent occlusion of the tube with clotted blood.

Do not leave in place for more than 24 hours.

Administration of broad spectrum antibiotics to prevent infection is recommended while the balloon is in place.

Patients should be carefully monitored for continued hemorrhage with balloon in place.

Pressure from the balloon will cause pain so adequate analgesia is recommended.

Surgical Management

Utilized when uterine atony is unresponsive to conservative management.
Midline vertical skin incision recommended to optimize exposure.
Techniques:

Arterial ligation

Decrease uterine perfusion and bleeding.

Bilateral ligation can control hemorrhage about 85-90% of the time.

Use #0 chromic catgut or polyglycolic acid suture.

Use stepwise approach Uterine greater than utero-ovarian.

Uterine artery ligation (O’Leary sutures).

Utero-ovarian ligation.

Internal Iliac (hypogastric) artery ligation.

Technically difficult.

Not a first line technique.

Compression Sutures

B-Lynch

If done within 1 hour of onset of PPH decreases need for hysterectomy.

Effective for uterine atony, but not bleeding from placenta accreta.

Use large absorbable suture (#1 or #2 chromic catgut).

Anteriorly anchor the suture in the lateral lower uterine segment.

Pass it over the fundus of the uterus.

Anchor it on the posterior uterine wall going from same side as the anterior stitch to the other side.

Pass over the fundus again.

Anchor on opposite side of first stitch anteriorly.

Pull the ends of the suture tightly and tie down securely to compress uterus.

Other

Multiple square suturing

Eliminates space in the uterine cavity by suturing both anterior and posterior walls.

Other vertical and transverse techniques to compress the uterus have been described.

Hysterectomy

It can be life-saving and its use should not be delayed in cases of life-threatening hemorrhage.
Artery Embolization

ThThe patient must be hemodynamically stable.

Bleeding should not be excessive.

Mobilization of a radiology team and an angiography suite are necessary.

Can be used to avoid hysterectomy if above criteria are met or after hysterectomy to control further bleeding.
Recombinant Activated Factor VII (rFVIIa).

Successfully used off-label for treatment of intractable bleeding associated with PPH.

Dose variable: 50 to 100 mcg/kg every 2 hours until hemostasis achieved.

Usually controls bleeding in 10 to 40 minutes after first dose.

Fibrinogen must be >50 mg/dL for it to work (aggressive therapy with blood components should be started prior to use of rFVIIa).

Very expensive.

Management of lacerations

When bleeding persists despite adequate uterine tone, a laceration should be suspected.
Careful inspection should be done.

Use a systematic approach; start at the cervix and upper vagina and progress inferiorly to the lower vagina, introitus, perineum and vulva.

Adequate exposure, retraction and lighting are necessary.
Repair lacerations.

Relocation to the operating room may be necessary for better pain relief, exposure, visualization and pelvic relaxation.

Summon help for retraction if needed.

Management of retained placenta

Placental tissue and membranes can remain in the uterus and inhibit uterine contractions.
If atony persists, perform manual exploration of the uterus.

Wrap a moist gauze around your hand to facilitate removal of retained placental fragments and membranes.
If manual extraction is unsuccessful, uterine curettage must be undertaken.

Should be performed in an operating room.

Large blunt instrument such as a Banjo curette or ring forceps should be used.

Ultrasound guidance can facilitate removal of all tissue and decreases risk of perforation.

Management of uterine inversion

Refers to the collapse of the fundus into the uterine cavity.
Complete inversion occurs when the fundus comes through the cervical os into the vagina.
Causes:

Excessive traction on the cord of a placenta implanted in the fundus.

Fundal pressure on a relaxed uterus.
Risk factors:

Uterine overdistension.

Prolonged labor.

Fetal macrosomia.

Invasive implantation.

Short umbilical cord.

Oxytocin use.
Can occur before or after detachment of the placenta.
Diagnosis is made clinically:

Sudden onset of brisk bleeding.

Palpation of the uterine fundus in the lower uterine segment or in the vagina through the cervical os on bimanual exam.

Absence of the uterine fundus on palpation of abdomen.

Profound hemorrhage and maternal hemodynamic instability can occur rapidly.
Quick intervention is required, delay in treatment increases maternal mortality.
Management:

Immediately call for assistance.

Nursing staff, other physicians and anesthesia staff.

Obtain large-bore IV access and begin fluid resuscitation.

Give blood products as needed to treat hypovolemia.

If the placenta is detached, the fundus can be pushed with the fingers and palm of the hand in the direction of the long axis of the vagina to replace. If not easily accomplished a uterine relaxing agent may be needed.

If the placenta still attached, do not remove it until fluid resuscitation has begun and a uterine relaxing agent has been given. If the uterus has prolapsed outside the vagina, replace it within the vagina.

Uterine relaxing agents:

Halogenated anesthetic agent

Terbutaline

Magnesium sulfate

Nitroglycerin

After the placenta is removed, steady pressure with fist or rigid fingers is used to push the fundus through the cervix. Alternatively, the placenta can be left in place and removed after the uterus is returned to the normal position.

After replacement the relaxing agent is stopped and uterotonic medication is given.

Monitor the patient for subsequent inversion or continued bleeding.

If manual replacement is unsuccessful surgical intervention is required.

A dense constriction ring in the uterus usually inhibits manual replacement.

Two surgical procedures have been described:

The Huntington: using clamps, the fundus is grasped and using upward traction the fundus is replaced to its normal position.

A deep suture may be placed in the fundus to aid traction.

The fundus may simultaneously pushed up with a vaginal hand.

The Haultain: The constriction ring is incised posteriorly, exposing the fundus which is then digitally replaced.

A relaxing agent is used until the fundus is replaced.

Management of uterine rupture

Most commonly occurs as a result separation of a cesarean delivery scar.
Usually signs and symptoms occur prior to delivery.
Traumatic as well as spontaneous ruptures of previously unscarred uterus can occur (see risk factors in Section 2).
Diagnosis is suspected clinically, but made surgically.
Management:

Surgery

Choice of repairing the uterine separation or hysterectomy depends on the site of rupture, extent of damage, and the patient’s clinical condition and desire for future fertility.

Repair of uterine separation.

Freshen up edges of the scar followed by primary closure in layers with an absorbable suture.

Hysterectomy.

Management of late postpartum hemorrhage

Significant bleeding is typically treated with utero-tonic medications or curettage, and management depends on the cause. Of course, resuscitation with fluid and blood products should be carried out as deemed necessary by the clinical situation. Hysterectomy may be required.

Subinvolution of the placental site

A utero-tonic agent is given.

Methylergonovine 0.2 milligrams orally every 4 hours for 24-48 hours or intramuscularly if patient unable to tolerate PO.

Misoprostol 200 micrograms orally every 6 hours for 24-48 hours or 600-1000 micrograms vaginally or rectally if unable to tolerate PO.

Oxytocin 20-40 units in 1000mL lactated ringers as an IV infusion or 10 units intramuscularly.

An oral antibiotic is also given, since subinvolution can be caused by infection.

Doxycycline 100 milligrams twice daily for 7-10 days.

If large clots are seen on ultrasound, gentle curettage can be performed. If ultrasound reveals an empty cavity, curettage should be avoided since it could exacerbate bleeding by disrupting the placental implantation site.
Retained placental tissue

Suction evacuation and gentle curettage are indicated.

Care should be taken because the uterine wall is soft and easier to perforate.

Ultrasound guidance can be helpful.

Antibiotic administration can be considered if patient also has signs of infection.

4. Complications

A. Complications as a consequence of the condition

Excessive blood loss associated with postpartum hemorrhage can lead to hypovolemic shock. Due to the normal physiological changes of pregnancy (increased blood volume), most women can compensate for blood loss up to 10% of the circulatory volume. Women with severe pre-eclampsia present a unique challenge since their physiological adaptation is altered; they do not have the protective effect of intravascular volume expansion. Also, vasoconstriction may maintain blood pressure in the normal range, making estimation of blood loss more difficult.

When blood loss approaches 20% of volume, symptoms develop: tachycardia, tachypnea, narrowed pulse pressure and delayed capillary refill. If bleeding continues, tachycardia and hypotension worsen. As a protective effect to maintain cardiac output, peripheral vasoconstriction occurs, leading to decreased tissue perfusion. Cool extremities and ischemic injury to kidneys, liver, heart and brain can result. Urine output decreases and if intravascular volume is not adequately replaced cardiogenic shock ensues.

Treatment of PPH involves volume replacement with crystalloid solutions and packed red blood cells (prbc). While cross-matched blood is preferred, utilization of emergency release blood, either O negative or type specific, when type is known, can be life-saving. A dilutional coagulopathy (indistinguishable from disseminated intravascular coagulopathy) can result from the depletion of platelets and clotting factors. With impaired clotting, blood loss is further exacerbated. At times a true consumptive coagulopathy can be associated with PPH.

The treatment for both coagulopathies is the same: replacement of clotting factors and platelets. Clotting factors are replaced with fresh frozen plasma (FFP) and cryoprecipitate. FFP should also be used if fibrinogen is less than 100 mg/dL or if prothrombin and partial thromboplastin times are abnormal. In a bleeding patient, platelet transfusion should be given if levels fall below 50,000 mcL. Purified fibrinogen concentrates, such as RiaSTAP®, can be used to correct hypofibrinogenemia associated with PPH.

Institution of a massive transfusion protocol on labor and delivery units will decrease the morbidity and mortality associated with significant PPH.

Once activated, fresh frozen plasma and packed red blood cells are provided at a 1:1 or 1:2 ratio for transfusion. Platelets and cryoprecipitate are given with every 4-8 units of prbc or as indicated by lab results. This cycle continues until bleeding is stopped and the patient is stabilized.

Postpartum hypopituitarism (Sheehan syndrome)

PPH, especially that associated with prolonged hypotension and/or shock, can lead to pituitary ischemia and necrosis. This can result in loss of function of the pituitary gland. Failure of breast milk production is noted first. Other symptoms include: fatigue, amenorrhea, loss of pubic and axillary hair, and low blood pressure. Lack of adrenocorticotropic hormone (ACTH) can lead to adrenal failure, a life-threatening condition. Symptoms may not develop for years after delivery. Lifelong supplementation with hormones: estrogen, progesterone, thyroid and corticosteroids is the mainstay of therapy.

B. Complications as a consequence of management

Complications of blood transfusions include: infection, hemolytic transfusion reaction, transfusion-related acute lung injury (TRALI).

Infection: The risk of bacterial contamination occurs in less than 1 per millions units, but carries a morality rate of 60%. The risk of human immunodeficiency virus (HIV) and hepatitis C is less than 1 per 2 million units. Hepatitis B has the highest risk of transmission, with a rate of less than 1 per 100,000 units.
Hemolytic transfusion reaction: Transfusion of incompatible blood, usually a result of administrative error, can lead to acute hemolysis which can result in DIC, acute renal failure and death. Its risk is reported to be about 1 in 14,000 units transfused.
Transfusion-related acute lung injury (TRALI): It is a life-threatening complication characterized by severe dyspnea, hypoxia and noncardiogenic pulmonary edema. Onset is usually 6 hours after transfusion but can occur up to 72 hours later. Its risk is 1 in 5000 transfusions.

5. Prognosis and outcome

A. Maternal/fetal outcomes

PPH is still a leading cause of maternal morbidity in the United States. Institution of protocols for the treatment of postpartum hemorrhage can reduce mortality associated with hemorrhage.

B. Long term health

Women who have had a PPH at the time of delivery are at risk for another PPH in subsequent deliveries. Preparation at the next delivery can reduce morbidity and mortality. Utilization of preventive measures such as IM or IV oxytocin can decrease the risk for hemorrhage. Except for hysterectomy, other standard treatments for PPH do not adversely affect future fertility.

6. What is the evidence for specific management and treatment recommendations

“Clinical Management Guidelines for Obstetricians and Gynecologists Number 76. October 2006: Postpartum Hemorrhage”. Obstet Gynecol.. vol. 108. 2006. pp. 1039-47. (It outlines the ACOG clinical management guidelines for practicing Obstetrician-Gynecologists.)

Allams, MS, B-Lynch, C. “The B-Lynch and other uterine compression suture techniques”. Int J Gynaecol Obstet. vol. 89. 2005. pp. 236-41. (This article provides step-by-step instructions on the B-Lynch compression suture and discusses other techniques along with the importance of compression sutures in the treatment of postpartum hemorrhage.)

Adiel, Fleischer, Natalie, Meirowitz. “Care bundles for management of obstetrical hemorrhage, Seminars in Perinatology”. vol. 40. 2016. pp. 99-108. (Outlines care bundles including utilization of hemorrhage management and transfusion protocols, haemorrhage cart and dedicated multidisciplinary teams.)

Clark, SL. “Obstetric Hemorrhage”. Seminars in Perinatology. vol. 40. 2016. pp. 109-111. (Dr. Clark provides a protocol of treatment for postpartum hemorrhage which can improve care and possibly decrease morbidity and mortality associated with PPH.)

Cunningham, FG, Leveno, KJ, Bloom, SL. Williams Obstetrics. 2010. (This paper provides a systematic review of the causes and treatments for postpartum hemorrhage.)

Dildy, GA. “Postpartum Hemorrhage: New Management Options”. Clin Obstet Gynecol. vol. 45. 2002. pp. 330-44. (This article discusses adjunct measures such as pelvic packing, selective arterial embolization and cell saver.)

Doumouchtsis, SK, Papageorghiou, AT, Arulkumaran, S. “Systematic review of conservative management of postpartum hemorrhage: what to do when medical treatment fails”. Obstet Gynecol Surv. vol. 62. 2007. pp. 540-7. (This paper provides an in-depth review of balloon tamponade, compression sutures, arterial embolization and artery ligation sutures as methods in the treatment of PPH.)

Gabbe, SG, Niebyl, JR, Simpson, JL. Obstetrics: Normal and Problem Pregnancies. 2007. (This chapter provides a comprehensive information on the causes and treatments for PPH including treatment of disseminated intravascular coagulopathy and the use of blood components.)

Leduc, D, Denidas, V, Lalonde, AB, Ballerman, C. “Active management of the third stage of labour: prevention and treatment of postpartum hemorrhage”. J Obstet Gynaecol Can. vol. 31. 2009. pp. 980-93. (This article discusses active management of the third stage of labor which is one true preventive measure for PPH.)

Mousa, HA, Walkinshaw, S. “Major Postpartum Haemorrhage”. Curr Opin Obstet Gynecol. vol. 13. 2001. pp. 595-603. (This paper outlines a wide-range of medical and surgical interventions for the management for PPH and discusses volume replacement in detail.)

Sibai, BM. “10 practical, evidence-based recommendations for managing severe postpartum hemorrhage”. OBG Manag. vol. 23. 2011. pp. 44-48. (This commentary outlines evidence-based approaches to the treatment of PPH that can impact outcomes.)

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