Postpartum Complications

Postpartum Complications

Kathryn R. Alden

Providing safe and effective care of the woman and family experiencing postpartum physical or psychologic complications requires a collaborative effort from all members of the health care team. This chapter focuses on the postpartum complications of hemorrhage and infection; structural disorders of the uterus, vagina, and bladder that can result from childbearing; and psychologic complications.

Postpartum Hemorrhage

Definition and Incidence

Postpartum hemorrhage (PPH) is among the leading causes of maternal death in the United States and worldwide. It is a life-threatening event that can occur with little warning and is often unrecognized until the mother has profound symptoms. Postpartum hemorrhage occurs in approximately 3% of births (Callaghan, Kuklina, and Berg, 2010). It is preventable in more than half of the cases (Della Torre, Kilpatrick, Hibbard, et al., 2011).

PPH is defined as the loss of 500 mL or more of blood after vaginal birth and 1000 mL or more after cesarean birth. Either a 10% change in hematocrit between admission for labor and postpartum or the need for erythrocyte transfusion is used to define PPH (Francois and Foley, 2012). However, defining PPH clinically is not a clear-cut undertaking. Diagnosis is often based on subjective observations, with blood loss often being underestimated by as much as 50% (Cunningham, Leveno, Bloom, et al., 2010).

Postpartum hemorrhage is classified as early or late with respect to the birth. Early, acute, or primary PPH occurs within 24 hours of the birth. Late or secondary PPH occurs more than 24 hours but less than 6 weeks after the birth (Francois and Foley, 2012). Today’s health care environment encourages shortened hospital stays after birth, which increases the potential for acute episodes of PPH to occur outside the traditional hospital or birth center setting.

Etiology and Risk Factors

Excessive bleeding after birth can be considered with reference to the stages of labor. From birth of the fetus until separation of the placenta, the character and quantity of blood passed can suggest excessive bleeding. For example, dark blood is probably of venous origin, perhaps from varices or superficial lacerations of the birth canal. Bright blood is arterial and can indicate deep lacerations of the cervix. Spurts of blood with clots can indicate partial placental separation. Failure of blood to clot or remain clotted indicates a pathologic condition or coagulopathy such as disseminated intravascular coagulation (DIC) (see later discussion).

Excessive bleeding can occur during the period from the separation of the placenta to its expulsion or removal. Commonly, such bleeding is the result of incomplete placental separation, undue manipulation of the fundus, or excessive traction on the cord. After the placenta has been expelled or removed, persistent or excessive blood loss usually is a result of uterine atony (i.e., failure to contract well or maintain contraction) or prolapse of the uterus into the vagina. Late PPH usually is the result of infection, subinvolution of the placental site, retained placental tissue, or coagulopathy (Francois and Foley, 2012). Risk factors for and causes of PPH are listed in Box 21-1.

Uterine Atony

Uterine atony is marked hypotonia (relaxation) of the uterus. Normally, placental separation and expulsion are facilitated by contraction of the uterus, which also prevents hemorrhage from the placental site. The uterine corpus is in essence a basket weave of strong, interlacing smooth-muscle bundles through which many large maternal blood vessels pass (see Fig. 3-3). If the uterus is flaccid after detachment of all or part of the placenta, brisk venous bleeding occurs and normal coagulation of the open vasculature is impaired and continues until the uterine muscle is contracted.

Uterine atony is the leading cause of early PPH. It is associated with high parity, polyhydramnios, fetal macrosomia, and multifetal gestation. In such conditions, the uterus is “overstretched” and contracts poorly after birth. Other causes of atony include traumatic birth, use of halogenated anesthetic (e.g., halothane), magnesium sulfate, rapid or prolonged labor, chorioamnionitis, use of oxytocin for labor induction or augmentation, and uterine atony in a previous pregnancy (Francois and Foley, 2012).

Retained Placenta

When the placenta has not been delivered within 30 minutes after birth despite gentle traction on the umbilical cord and uterine massage, it is described as “retained.” Initial management of a retained placenta consists of manual separation and removal by the physician or nurse midwife. Supplementary anesthesia is usually not needed for women who have had regional anesthesia for birth. For other women, administration of light nitrous oxide and oxygen inhalation anesthesia or intravenous (IV) thiopental facilitates intrauterine exploration and placental separation. A tocolytic medication such as nitroglycerin IV may be given to promote uterine relaxation (Francois and Foley, 2012). After removal of a retained placenta, the woman is at continued risk for PPH and infection.

Fragments of the placenta can remain in the uterus after spontaneous separation of the placenta during the third stage of labor. In this case, the woman will have excessive bleeding and the uterus will feel boggy (soft) due to uterine atony. Ultrasonography can be used to detect placental fragments. The physician or midwife may attempt manual exploration to remove the fragments; uterine curettage (removal of uterine contents using a curette or vacuum suction) may be necessary.

In rare instances there is abnormal adherence of the placenta to the myometrium. It is unknown why this occurs, but it is thought to result from zygote implantation in an area of defective endometrium so that no zone of separation exists between the placenta and the decidua. Attempts to remove the placenta in the usual manner are unsuccessful, and laceration or perforation of the uterine wall can result, putting the woman at great risk for severe PPH and infection (Francois and Foley, 2012).

Unusual placental adherence can be partial or complete. The following degrees of attachment are recognized:

Placenta accreta is most common, with its incidence increasing in association with the rise in cesarean birth rates (Cunningham, Leveno, Bloom, et al., 2010). Other risk factors include placenta previa, prior uterine surgery, endometrial defects, submucosal fibroids, parity, and maternal age (Francois and Foley, 2012). Placenta accreta can be diagnosed before birth using ultrasound and MRI, but often it is not recognized until there is excessive bleeding after birth. Bleeding with complete or total placenta accreta may not occur unless separation of the placenta is attempted. With more extensive involvement, bleeding becomes profuse when delivery of the placenta is attempted. Less blood is lost if the diagnosis is made antenatally and no attempt is made to manually remove the placenta. Treatment includes blood component replacement therapy. Hysterectomy can be indicated if bleeding is uncontrolled (Cunningham, Leveno, Bloom, et al., 2010).

Lacerations of the Genital Tract

Lacerations of the cervix, vagina, and perineum can cause PPH. Hemorrhage related to lacerations should be suspected if bleeding continues despite a firm, contracted uterine fundus. This bleeding can be a slow trickle, an oozing, or frank hemorrhage. Factors that influence the causes and incidence of obstetric lacerations of the lower genital tract include operative birth, precipitous birth, congenital abnormalities of the maternal soft parts, and contracted pelvis. Size, abnormal presentation, and position of the fetus; relative size of the presenting part and the birth canal; previous scarring from infection, injury, or surgery; and vulvar, perineal, and vaginal varicosities can also increase the risk for lacerations. Extreme vascularity in the labia and periclitoral areas often results in profuse bleeding if laceration occurs. Hematomas can also be present.

Lacerations of the perineum are the most common of all injuries in the lower portion of the genital tract. These are classified as first, second, third, and fourth degree (see Chapter 16). An episiotomy can extend to become either a third- or fourth-degree laceration.

Prolonged pressure of the fetal head on the vaginal mucosa ultimately interferes with the circulation and can produce ischemic or pressure necrosis. The state of the tissues in combination with the type of birth can result in deep vaginal lacerations, with consequent predisposition to vaginal hematomas.

Cervical lacerations usually occur at the lateral angles of the external os. Most are shallow, and bleeding is minimal. More extensive lacerations can extend into the vaginal vault or the lower uterine segment.

Lacerations are usually identified and sutured immediately after birth. After the bleeding has been controlled, the care of the woman with lacerations of the perineum is similar to that for women with episiotomies (i.e., analgesia as needed for pain and hot or cold applications as necessary). The need for increased roughage in the diet and increased intake of fluids is emphasized. Stool softeners may be used to assist the woman in reestablishing bowel habits without straining and putting stress on the suture lines.


Pelvic hematomas (i.e., a collection of blood in the connective tissue) can be vulvar, vaginal, or retroperitoneal in origin. Vulvar hematomas are the most common. Pain is the most common symptom, and most vulvar hematomas are visible. Vaginal hematomas occur more commonly in association with a forceps-assisted birth, an episiotomy, or primigravidity (Francois and Foley, 2012).

Retroperitoneal hematomas are the least common but are life threatening. They are caused by laceration of one of the vessels attached to the hypogastric artery, usually associated with rupture of a cesarean scar during labor. During the postpartum period, if the woman reports persistent perineal or rectal pain or a feeling of pressure in the vagina, a careful examination is made. However, a retroperitoneal hematoma can cause minimal pain and the initial symptoms can be signs of shock (Francois and Foley, 2012).

Hematomas are usually surgically evacuated. Once the bleeding has been controlled, usual postpartum care is provided with paying attention to pain relief, monitoring the amount of bleeding, replacing fluids, and reviewing laboratory results (hemoglobin and hematocrit).

Inversion of the Uterus

Inversion (turning inside out) of the uterus after birth is a potentially life-threatening complication. The incidence of uterine inversion is approximately 1 in 3000 births (Cunningham, Leveno, Bloom, et al., 2010) and can recur with a subsequent birth. Uterine inversion can be incomplete, complete, or prolapsed. Incomplete inversion cannot be seen; a smooth mass can be palpated through the dilated cervix. In complete inversion, the lining of the fundus crosses through the cervical os and forms a mass in the vagina. Prolapsed inversion of the uterus is obvious—a large, red, rounded mass (perhaps with the placenta attached) protrudes 20 to 30 cm outside the introitus.

Contributing factors to uterine inversion include fundal implantation of the placenta, vigorous fundal pressure, excessive traction applied to the cord, fetal macrosomia, short umbilical cord, tocolysis, prolonged labor, uterine atony, nulliparity, and abnormally adherent placental tissue (Francois and Foley, 2012). The primary presenting signs of uterine inversion are sudden and include hemorrhage, shock, and pain. The uterus is not palpable abdominally. The uterus must be replaced into its proper position by the physician or nurse midwife.

Prevention—always the easiest, cheapest, and most effective therapy—is especially appropriate for uterine inversion. The umbilical cord should not be pulled unless the placenta has definitely separated.

Uterine inversion is an emergency situation requiring immediate interventions that include maternal fluid resuscitation, replacement of the uterus within the pelvic cavity, and correction of associated clinical conditions. Tocolytics or halogenated anesthetics may be given to relax the uterus before attempting replacement (Francois and Foley, 2012). Oxytocic agents are administered after the uterus is repositioned; broad-spectrum antibiotics are initiated. The woman’s response to treatment is observed closely to prevent shock or fluid overload. If the uterus has been repositioned manually, care must be taken to avoid aggressive fundal massage.

Subinvolution of the Uterus

Late postpartum bleeding can result from subinvolution of the uterus (delayed return of the enlarged uterus to normal size and function). Recognized causes of subinvolution include retained placental fragments and pelvic infection. Signs and symptoms include prolonged lochial discharge, irregular or excessive bleeding, and sometimes hemorrhage. A pelvic examination usually reveals a larger-than-normal uterus that can be boggy.

Treatment of subinvolution depends on the cause. Ergonovine (Ergotrate) or methylergonovine (Methergine), 0.2 mg every 3 to 4 hours for 24 to 48 hours, is often used. Dilation and curettage (D&C) may be performed to remove retained placental fragments or to debride the placental site. If the cause of subinvolution is infection, antibiotic therapy is needed (Cunningham, Leveno, Bloom, et al., 2010).

Care Management

Early recognition and treatment of PPH are critical to care management. The first step is to evaluate the contractility of the uterus. If the uterus is hypotonic, management is directed toward increasing contractility and minimizing blood loss.

If the uterus is firmly contracted and bleeding continues, the source of bleeding still must be identified and treated. Assessment may include visual or manual inspection of the perineum, the vagina, the uterus, the cervix, or the rectum and laboratory studies (e.g., hemoglobin, hematocrit, coagulation studies, platelet count). Treatment depends on the source of the bleeding.

The initial management of excessive postpartum bleeding due to uterine atony is firm massage of the uterine fundus. Expression of any clots in the uterus, elimination of bladder distention, and continuous IV infusion of 10 to 40 units of oxytocin added to 1000 mL of lactated Ringer’s or normal saline solution also are primary interventions. If the uterus fails to respond to oxytocin, other uterotonic medications are administered. Misoprostol (Cytotec), a synthetic prostaglandin E1 analog, is often used. An advantage is that it can be given by more than one route. Common dosages of misoprostol are 600 to 1000 mcg rectally or 400 mcg sublingually. A 0.2-mg dose of ergonovine (Ergotrate) or methylergonovine (Methergine) may be given intramuscularly to produce sustained uterine contractions; this can be repeated every 2 to 4 hours. A 0.25-mg dose of a derivative of prostaglandin F2α (carboprost tromethamine [Carboprost; Hemabate]) may be given intramuscularly. It can also be given intramyometrially at cesarean birth or intraabdominally after vaginal birth. Carboprost can be repeated in recurrent doses of 0.25 mg every 15 to 90 minutes, up to 8 doses. Women with a history of asthma should not receive this medication because it can cause bronchoconstriction (Francois and Foley, 2012). Prostaglandin E2 (Dinoprostone) 20-mg vaginal or rectal suppository can be used for postpartum hemorrhage (see the Medication Guide for a comparison of uterotonic drugs used to manage PPH). In addition to the medications used to contract the uterus, rapid administration of crystalloid solutions or blood or blood products or both will be needed to restore the woman’s intravascular volume (Francois and Foley, 2012). (See Evidence-Based Practice box.)

image Medication Guide

Uterotonic Drugs Used to Manage Postpartum Hemorrhage

Oxytocin (Pitocin) Contraction of uterus; decreases bleeding Infrequent: water intoxication, nausea and vomiting None for PPH 10 to 80 units/L diluted in lactated Ringer’s solution or normal saline at 125 to 200 milliunits/min IV; or 10 to 20 units IM Continue to monitor vaginal bleeding and uterine tone
Misoprostol (Cytotec) Contraction of uterus Headache, nausea, vomiting, diarrhea, fever, chills None 600 to 1000 mcg rectally once or 400 mcg sublingual or PO once Continue to monitor vaginal bleeding and uterine tone
Methylergonovine (Methergine) Contraction of uterus Hypertension, hypotension, nausea, vomiting, headache Hypertension, preeclampsia, cardiac disease 0.2 mg IM every 2 to 4 hr up to five doses; may also be given intrauterine or orally Check blood pressure before giving, and do not give if >140/90 mm Hg; continue monitoring vaginal bleeding and uterine tone
15-Methylprostaglandin F2α (Prostin/15 m; Carboprost, Hemabate) Contraction of uterus Headache, nausea, vomiting, diarrhea, fever, chills, tachycardia, hypertension Avoid with asthma or hypertension 0.25 mg IM or intrauterine every 15 to 90 min up to eight doses Continue to monitor vaginal bleeding and uterine tone
Dinoprostone (Prostin E2) Contraction of uterus Headache, nausea and vomiting, fever, chills, diarrhea Use with caution with history of asthma, hypertension, or hypotension 20 mg vaginal or rectal suppository every 2 hr Continue to monitor vaginal bleeding and uterine tone


IM, Intramuscular; IV, intravenous; PPH, postpartum hemorrhage.

Evidence-Based Practice

Active Third-Stage Labor Management for Preventing Postpartum Hemorrhage

Critically Analyze the Evidence

PPH is still a major cause of maternal death, especially in low- and middle-income countries.

• In third-stage labor, uterine contractions expel the placenta and constrict the blood vessels of the uterine wall. To prevent PPH, health care providers actively manage third-stage labor by clamping the cord before pulsations have stopped, administering uterotonics to increase uterine contractions, and providing steady traction on the cord and counterpressure on the fundus, causing earlier expulsion of the placenta.

• Maternal effects: When compared with expectant management, the active management protocol results in less maternal blood loss and less maternal anemia (Begley, Gyte, Devane, et al., 2011). Adverse effects of active management include side effects of the uterotonics and uterine pressure: higher maternal diastolic pressure, pain requiring analgesia, nausea and vomiting. Active management is also more likely to result in readmission for bleeding, for unknown reasons.

• Effects on the newborn: Birth weight is less when the cord was clamped before cessation of pulsing, because there is less transfer of blood volume to the newborn. However, there are no differences in the number of neonatal intensive care unit (NICU) admissions nor the occurrences of neonatal jaundice (Begley, Gyte, Devane, et al., 2011).

• Uterotonics stimulate smooth muscle contraction of the uterus. Intravenous carbetocin, when compared with oxytocin, results in less need for uterine massage and use of other uterotonics, but no difference in PPH. When compared with ergometrine-oxytocin, carbetocin is associated with less blood loss and fewer side effects of nausea, vomiting, and postpartum hypertension (Su, Chong, and Samuel, 2012).

• Prostaglandins are also uterotonic. Oral or sublingual misoprostol is better than placebo for preventing blood loss and need for blood transfusion but causes dose-related shivering, increased temperature, and diarrhea and is expensive.

• Conventional injectable uterotonics such as intramuscular (IM) ergot alkaloids are the drugs of choice for preventing PPH, but prostaglandins may be useful in low-resource areas (Tuncalp, Hofmeyr, and Gülmezoglu, 2012).

Apply the Evidence: Nursing Implications

• Active management of third-stage labor is beneficial and recommended. However, it may be possible to individualize the protocol. Women should be educated before labor on their options for third-stage management and the risks and benefits of uterotonics.

• Some women request that the cord clamping be delayed until pulsations have ceased. This may benefit the newborn without significantly increasing the woman’s risk for PPH.

• Nurses carefully assess the fundus and bleeding while recovering the immediate postpartum woman and are frequently the first to notice PPH.

• A protocol for PPH should be made clear to all staff. All staff should be able to identify when bleeding is too heavy and the correct steps of emptying the bladder, uterine massage, and whom to call immediately.

• Easily accessed kits of necessary medications should be available, along with training in their use.

*Adapted from QSEN at

Oxygen can be given by nonrebreather facemask to enhance oxygen delivery to the cells. An indwelling urinary catheter is usually inserted to monitor urine output as a measure of intravascular volume. Laboratory studies usually include a complete blood count with platelet count, fibrinogen, fibrin split products, prothrombin time, and partial thromboplastin time. Blood type and antibody screen are done if not previously performed (Cunningham, Leveno, Bloom, et al., 2010).

If bleeding persists, bimanual compression may be performed by the obstetrician or nurse-midwife. This procedure involves inserting a fist into the vagina and pressing the knuckles against the anterior side of the uterus and then placing the other hand on the abdomen and massaging the posterior uterus with it. If the uterus still does not become firm, the physician or midwife performs manual exploration of the uterine cavity for retained placental fragments. If the preceding procedures are ineffective, surgical management is needed. Surgical management options include uterine tamponade (uterine packing or an intrauterine tamponade balloon), bilateral uterine artery ligation, ligation of utero-ovarian arteries and infundibulopelvic vessels, and selective arterial embolization. Uterine compression suturing (using, for example, B-Lynch or Hayman vertical sutures) may be performed and is sometimes combined with a tamponade balloon. If other treatment measures are ineffective, hysterectomy will likely be needed (Cunningham, Leveno, Bloom, et al., 2010; Francois and Foley, 2012).

Nursing Interventions

The nurse must be alert to the symptoms of hemorrhage and hypovolemic shock and be prepared to act quickly to minimize blood loss (Fig. 21-1). Astute assessment of circulatory status can be done with noninvasive monitoring (Box 21-2). Interventions are based on the cause of PPH as previously discussed.

The woman and her family will be anxious about her condition. The nurse can intervene by calmly providing explanations about interventions being performed and the need to act quickly.

Once the woman’s condition is stabilized, preparations for discharge are made. Discharge instructions for the woman who experienced PPH are similar to those for any postpartum woman. In addition, the woman should be told that she will probably feel fatigue, even exhaustion, and will need to limit her physical activities to conserve her strength. She may need instructions in increasing her dietary iron and protein intake and iron supplementation to rebuild lost red blood cell (RBC) volume. She may need assistance with infant care and household activities until she has regained strength. Some women have problems with delayed lactation or insufficient milk production and postpartum depression (PPD). Referrals for home care follow-up or to community resources may be needed, such as to Postpartum Support International at (see Nursing Care Plan).

image Nursing Care Plan

Postpartum Hemorrhage

Deficient Fluid Volume related to postpartum hemorrhage Woman will demonstrate fluid balance as evidenced by stable vital signs, prompt capillary refill time, and balanced intake and output. Monitor vital signs, oxygen saturation, urine specific gravity, and capillary refill To provide baseline data and detect changes
Measure and record amount and type of bleeding by weighing and counting saturated pads; if woman is at home, teach her to count pads and save any clots or tissue; if woman is admitted to hospital, save any clots and tissue for further examination To estimate type and amount of blood loss for fluid replacement
Provide quiet environment To promote rest and decrease metabolic demands
Give explanation of all procedures To reduce anxiety
Begin intravenous (IV) access with 18-gauge or larger catheter for infusion of isotonic solution as ordered To provide fluid or blood replacement
Administer medications as ordered, such as oxytocin, misoprostol, methylergonovine, or prostaglandin F2α To increase contractility of uterus
Insert indwelling urinary catheter To provide most accurate assessment of renal function and hypovolemia
Prepare for surgical intervention as needed To stop source of bleeding
Ineffective Tissue Perfusion related to hypovolemia Woman will have stable vital signs, oxygen saturation, and arterial blood gases and adequate hematocrit and hemoglobin. Monitor vital signs, oxygen saturation, arterial blood gases, and hematocrit and hemoglobin To assess for hypovolemic shock and decreased tissue perfusion
Assess capillary refill, mucous membranes, and skin temperature To note indicators of vasoconstriction
Give supplementary oxygen as ordered To provide additional oxygenation to tissues
Suction as needed, and insert oral airway To maintain clear, open airway for oxygenation
Monitor arterial blood gases To provide information about acidosis or hypoxia
Administer sodium bicarbonate if ordered To reverse metabolic acidosis
Anxiety related to sudden change in health status Woman will verbalize that anxious feelings are diminished. Using therapeutic communication, evaluate woman’s understanding of events To provide clarification of any misconceptions
Provide calm, competent attitude and quiet environment To aid in decreasing anxiety
Explain all procedures To decrease anxiety about unknown
Allow woman to verbalize feelings To permit clarification of information and promote trust
Continue to assess vital signs or other clinical indicators of hypovolemic shock To evaluate if psychologic response of anxiety intensifies physiologic indicators
Risk for Infection related to blood loss and invasive procedures as result of postpartum hemorrhage Woman will verbalize understanding of risk factors. Woman will demonstrate no signs of infection. Maintain Standard Precautions and use proper hand hygiene technique when providing care To prevent introduction of or spread of infection
Teach woman to maintain proper hand hygiene (particularly before handling her newborn) and to maintain scrupulous perineal care with frequent change and careful disposal of perineal pads To avoid spread of microorganisms
Monitor vital signs To detect signs of systemic infection
Monitor level of fatigue and lethargy, evidence of chills, loss of appetite, nausea and vomiting, and abdominal pain To indicate extent of infection and serve as indicators of status of infection
Monitor lochia for foul smell To detect sign of infection
Assist with collection of intrauterine cultures or other specimens for laboratory analysis To identify specific causative organism
Monitor laboratory values (i.e., white blood cell [WBC] count, cultures) For indicators of type and status of infection
Ensure adequate fluid and nutritional intake To promote healthy recovery
Administer and monitor broad-spectrum antibiotics as ordered To prevent or treat infection
Administer antipyretics as ordered and necessary To reduce elevated temperature



Hemorrhagic (Hypovolemic) Shock

Hemorrhage can result in hemorrhagic (hypovolemic) shock. Shock is an emergency situation in which the perfusion of body organs can become severely compromised and death can occur. Physiologic compensatory mechanisms are activated in response to hemorrhage. The adrenal glands release catecholamines, causing arterioles and venules in the skin, lungs, gastrointestinal tract, liver, and kidneys to constrict. The available blood flow is diverted to the brain and heart and away from other organs, including the uterus. If shock is prolonged, the continued reduction in cellular oxygenation results in an accumulation of lactic acid and acidosis (from anaerobic glucose metabolism). Acidosis (lowered serum pH) causes arteriolar vasodilation; venule vasoconstriction persists. A circular pattern is established (i.e., decreased perfusion, increased tissue anoxia and acidosis, edema formation, and pooling of blood further decrease the perfusion). Cellular death occurs. See the Emergency box for assessments and interventions for hemorrhagic shock.

Medical Management

Vigorous treatment is necessary to prevent adverse outcomes. Management of hypovolemic shock involves restoring circulating blood volume and eliminating the cause of the hemorrhage (e.g., lacerations, uterine atony, or inversion). Critical to successful management of the woman with a hemorrhagic complication is establishment of venous access, preferably with a large-bore IV catheter. The establishment of two IV lines facilitates fluid resuscitation. Fluid resuscitation includes the administration of crystalloids (lactated Ringer’s, normal saline solution), colloids (albumin), blood, and blood components. To restore circulating blood volume, a rapid IV infusion of crystalloid solution is given at a rate of 3 mL infused for every 1 mL of estimated blood loss (e.g., 3000 mL infused for 1000 mL of blood loss). Packed red blood cells (RBCs) are usually infused if the woman is still actively bleeding and no improvement in her condition is noted after the initial crystalloid infusion. Infusion of fresh frozen plasma may be needed if clotting factors and platelet counts are below normal values (Cunningham, Leveno, Bloom, et al., 2010; Francois and Foley, 2012).

Nursing Interventions

Hemorrhagic shock can occur rapidly, but the classic signs of shock may not appear until the postpartum woman has lost 30% to 40% of blood volume. The nurse must continue to reassess the woman’s condition as evidenced by the degree of measurable and anticipated blood loss and mobilize appropriate resources.

Most interventions are instituted to improve or monitor tissue perfusion. Fluid resuscitation must be monitored carefully because fluid overload can occur. Intravascular fluid overload occurs most often with colloid therapy.

Transfusion reactions can follow administration of blood or blood components, including cryoprecipitates. Even in an emergency, each unit of blood or blood products should be carefully checked per hospital protocol. Complications of fluid or blood replacement therapy include hemolytic reactions, febrile reactions, allergic reactions, circulatory overloading, and air embolism.

The nurse continues to monitor the woman’s pulse and blood pressure. If invasive hemodynamic monitoring is ordered, the nurse may assist with placement of a central venous pressure (CVP) or pulmonary artery (Swan-Ganz) catheter. Subsequently, the nurse monitors CVP, pulmonary artery pressure, or pulmonary artery wedge pressure as ordered (Gilbert, 2011).

Additional assessments include evaluating skin temperature, color, and turgor; and mucous membranes. Breath sounds should be auscultated before fluid volume replacement to provide a baseline for future assessment. Inspection for oozing at the sites of incisions or injections and assessment for the presence of petechiae or ecchymosis in areas not associated with surgery or trauma are critical in evaluating for disseminated intravascular coagulation (DIC) (see later discussion).

Oxygen is administered, preferably by a nonrebreather facemask, at 10 to 12 L/min to maintain oxygen saturation. Oxygen saturation should be monitored with a pulse oximeter, although measurements are not always accurate in a patient with hypovolemia or decreased perfusion. Level of consciousness is assessed frequently and provides additional indications of blood volume and oxygen saturation (Gilbert, 2011). In early stages of decreased blood flow, the woman may report “seeing stars” or feeling dizzy or nauseated. She can become restless and orthopneic. As cerebral hypoxia increases, she can become confused and react slowly to stimuli or not at all. Some women complain of headaches. An improved sensorium is an indicator of improved perfusion.

Continuous electrocardiographic monitoring may be indicated for the woman who is hypotensive or tachycardic, continues to bleed profusely, or is in shock. A Foley catheter is inserted and a urometer is attached to allow hourly assessment of urine output. The most objective and least invasive assessment of adequate organ perfusion and oxygenation is a urine output of at least 30 mL/hr (Cunningham, Leveno, Bloom, et al., 2010). Hemoglobin and hematocrit levels, platelet count, and coagulation studies are closely monitored.


When bleeding is continuous and there is no identifiable source, a coagulopathy can be the cause. The woman’s coagulation status must be assessed quickly and continuously. Abnormal results depend on the cause and can include increased prothrombin time, increased partial thromboplastin time, decreased platelets, decreased fibrinogen level, increased fibrin degradation products, and prolonged bleeding time. Causes of coagulopathies can include pregnancy complications such as idiopathic or immune thrombocytopenic purpura (ITP), von Willebrand disease (vWD), or DIC.

Idiopathic Thrombocytopenic Purpura

Idiopathic or immune thrombocytopenic purpura (ITP) is an autoimmune disorder in which antiplatelet antibodies decrease the life span of the platelets. Thrombocytopenia, capillary fragility, and increased bleeding time are diagnostic findings. ITP can cause severe hemorrhage after cesarean birth or cervical or vaginal lacerations. The incidence of postpartum uterine bleeding and vaginal hematomas is also increased. Neonatal thrombocytopenia can result, but serious bleeding is unusual (Rozance and Rosenberg, 2012).

Medical management focuses on control of platelet stability. If ITP was diagnosed during pregnancy, the woman likely was treated with corticosteroids or IV immune globulin. Platelet transfusions are usually given when there is significant bleeding. A splenectomy may be needed if the ITP does not respond to medical management (Cunningham, Leveno, Bloom, et al., 2010).

von Willebrand Disease

von Willebrand disease (vWD), a type of hemophilia, is probably the most common of all hereditary bleeding disorders. Although von Willebrand disease is rare, it is among the most common congenital clotting defects in U.S. women of childbearing age. It results from a deficiency or defect in a blood clotting protein called von Willebrand factor (vWF). There are as many as 20 variations of vWD, most of which are inherited as autosomal dominant traits—types I and II are the most common (Cunningham, Leveno, Bloom, et al., 2010). Symptoms include recurrent bleeding episodes such as nosebleeds or after tooth extraction, bruising easily, prolonged bleeding time (the most important test), factor VIII deficiency (mild to moderate), and bleeding from mucous membranes. Although factor VIII increases during pregnancy, a risk for PPH still exists as levels of vWF begin to decrease (Cunningham, Leveno, Bloom, et al., 2010).

The woman can be at risk for bleeding for up to 4 weeks after birth. The treatment of choice is administration of desmopressin, which promotes the release of vWF and factor VIII. It can be given nasally, intravenously, or orally. Transfusion therapy with plasma products that have been treated for viruses and contain factor VIII and vWF also may be used. Concentrates of antihemophiliac factor (Humate-P or Alphanate) can be administered (Cunningham, Leveno, Bloom, et al., 2010).

Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC), also known as consumptive coagulopathy, is an imbalance between the body’s clotting and fibrinolytic systems. It is a pathologic form of clotting that is diffuse and consumes large amounts of clotting factors, including platelets, fibrinogen, prothrombin, and factors V and VII. Widespread external bleeding, internal bleeding, or both can result. DIC also causes vascular occlusion of small vessels resulting from small clots forming in the microcirculation. In the obstetric population, DIC can occur as a result of acute antepartum or postpartum hemorrhage, abruptio placentae, amniotic fluid embolism, dead fetus syndrome (i.e., fetus dies but is retained in utero for at least 6 weeks), severe preeclampsia, sepsis, saline abortion, and acute fatty liver of pregnancy (Francois and Foley, 2012).

The diagnosis of DIC is made according to clinical findings and laboratory markers. Physical examination reveals unusual bleeding; spontaneous bleeding from the woman’s gums or nose can occur. Petechiae can appear around a blood pressure cuff placed on the woman’s arm. Excessive bleeding can occur from the site of a slight trauma (e.g., venipuncture sites, intramuscular or subcutaneous injection sites, nicks from shaving of perineum or abdomen, and injury from insertion of a urinary catheter). Hypotension is out of proportion to the observed blood loss. Other symptoms include tachycardia and diaphoresis. Laboratory tests reveal decreased levels of platelets, fibrinogen, proaccelerin, antihemophiliac factor, and prothrombin (the factors consumed during coagulation). Fibrinolysis is increased at first but is later severely depressed. Degradation of fibrin leads to the accumulation of fibrin split products in the blood; these have anticoagulant properties and prolong the prothrombin time. Bleeding time is normal, coagulation time shows no clot, clot-retraction time shows no clot, and partial thromboplastin time is increased. DIC must be distinguished from other clotting disorders before therapy is initiated.

Primary medical management in all cases of DIC involves correction of the underlying cause (e.g., removal of the dead fetus, treatment of existing infection or of preeclampsia or eclampsia, or removal of a placental abruption). Volume replacement, blood component therapy, optimization of oxygenation and perfusion status, and continued reassessment of laboratory parameters are the usual forms of treatment. Resolution of DIC usually begins with the birth of the neonate (Francois and Foley, 2012).

Nursing interventions include assessing for signs of bleeding, administering fluid or blood replacement as ordered, observing for signs of complications from the administration of blood and blood products, and protecting from injury. Because renal failure is one consequence of DIC, urinary output is closely monitored, usually by insertion of an indwelling urinary catheter. Urinary output must be maintained at more than 30 mL/hr.

The woman and her family will be anxious and concerned about her condition and prognosis. The nurse offers explanations about care and provides emotional support to them through this critical time.

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Sep 16, 2016 | Posted by in NURSING | Comments Off on Postpartum Complications

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