Postpartum Emergencies

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123 Postpartum Emergencies

Epidemiology

Despite the fact that the first postpartum visit is generally scheduled at 6 weeks, most life-threatening complications arise within the first 3 weeks following delivery and are thus likely to be seen in the emergency department (ED). These complications are primarily related to infection, hemorrhage, pregnancy-induced hypertension, and embolic events.1,2 Infection is one of the top five causes of mortality, with approximately 13% of pregnancy-related deaths between 1991 and 1999 being due to infection.2 In the general population, the incidence of pregnancy-induced venous thromboembolism (VTE) is approximately 0.49 to 1.72 per 1000 deliveries.3 The risk for VTE is five times higher in a pregnant than in a nonpregnant patient. When compared with pregnancy, the risk for VTE is even higher postpartum: a postpartum woman’s risk for VTE is 20- to 80-fold higher in the first 6 weeks, and in the first postpartum week the risk is 100-fold higher.3,4 The majority of deaths from VTE occur during the first 2 weeks of the puerperium, but a significant number of nonfatal events occur 2 to 6 weeks after delivery.4 Approximately 75% of cases of pregnancy-associated VTE are deep vein thrombosis (DVT) and approximately 25% are pulmonary embolism (PE).3

Additionally, there is a high frequency of late maternal morbidity from a variety of causes; up to 87% of women note problems in the first 6 weeks postpartum, and as many as 76% of these patients continue to have these problems for as long as 18 months following delivery.

Pathophysiology: the Puerperium

Originally, the puerperium was defined as the period of confinement during and just after birth; it is now generally accepted to mean the 6 weeks after delivery. The puerperium has also been referred to as “the fourth trimester.” This period is marked by multiple physiologic changes (Table 123.1) as the woman returns to the prepregnant state, including healing physically from any trauma during delivery, and adjusts to the many physiologic and psychologic demands involved in caring for a newborn. Just as in pregnancy, when there are so many physiologic changes, the potential exists for the normal healing process to go awry and emergencies to occur.

Table 123.1 Physiologic Changes in the Puerperium

IMMEDIATELY FOLLOWING DELIVERY BY POSTPARTUM TIME*
Uterus palpable at the umbilicus By the 2nd wk, the uterus has shrunk back into the pelvis; complete involution takes 6-8 wk
Uterine blood flow via the uterine artery = 500-600 mL/min By the 2nd wk, uterine blood flow = 30-45 mL/min
Cardiac output and blood volume increased by 30% to 50% By the 2nd week, values are normalized to baseline
Breasts produce colostrum By day 5, mature breast milk produced
Thyroid size and function increase In 3 mo, the size of thyroid decreases; by the 4th wk, biochemical changes resolve (T3,T4, TSH are normalized)
Bladder has enlarged capacity and insensitivity to increased intravesicular pressure; renal pelvis and ureters dilated 2-3 mo to return to normal
GFR increased 8 wk to return to prepregnant GFR
Rectus abdominis muscles lengthened 3-4 wk minimum to shorten; may be altered by exercise and overall baseline tone of the mother
Leukocytosis 2 wk to return to baseline
Fibrinogen level elevated Increases on days 2-4; returns to normal levels by the end of the first week
Stretch marks 6-12 mo; depigmentation occurs but never fully resolves
Thicker and fuller hair 3-4 mo; delayed alopecia
Lower mean velocity of blood flow in the common femoral vein after cesarean section 6 wk to return to baseline

GFR, Glomerular filtration rate; T3, triiodothyronine; T4, thyroxine; TSH, thyroid-stimulating hormone;

* Approximate time.

Certain significant changes in the physiology of the coagulation system during pregnancy persist past delivery and into the puerperium, including major changes in the coagulation and fibrinolytic system, as well as a reduction in venous blood flow in the deep venous system. Combined, these alterations increase the thrombotic potential in near-term and immediate postpartum patients.

A pregnant patient around term and immediately postpartum has significant increases in factors I, V, VII, IX, X, and XII; von Willebrand factor antigen; and ristocetin cofactor activity. The endogenous anticoagulants protein C and antithrombin remain unchanged throughout pregnancy, but levels of protein S are reduced. Fibrinolytic activity is impaired during pregnancy as a result of placentally derived plasminogen activator inhibitor type II and pregnancy-induced increases (approximately threefold) in endothelial and hepatic-derived inhibitor of plasminogen activator type I. These changes rapidly return to normal following delivery.

During normal pregnancy there is a significant reduction in blood flow to the deep venous system, as well as an increase in diameter of the major leg veins. These changes do not occur evenly in both legs. Studies of patients in the puerperium have reported greater diameter and slower blood flow in the left common femoral vein than in the right. These differences are manifested clinically; in nonpregnant patients, the left leg was affected in 55% of cases of DVT, whereas in pregnancy the rate was 85%. The mode of delivery also affects the deep venous system. Women who delivered by cesarean section had a lower mean velocity of blood flow in the common femoral vein during the puerperium than did those who had delivered vaginally. These changes in flow velocity and diameter take approximately 6 weeks to return to baseline. Another significant clinical difference observed in pregnant and immediate postpartum patients is that the majority of DVT events seen during this time occur in the iliofemoral segments rather than in the calf veins and are therefore more likely to result in PE. Additional underlying risk factors that increase the likelihood for thrombotic complications are age older than 35 years, delivery by cesarean section, weight greater than 175 lb, and a family or personal history of thrombosis and thrombophilia (protein C or S deficiency, factor V Leiden).

Presenting Signs and Symptoms

The most common complaints in the postpartum period are fatigue (56%), breast problems (20%), backache (20%), depression (17%), hemorrhoids (15%), and headache (15%).5

The signs and symptoms of metritis are fever, uterine tenderness, abdominal pain, and either purulent lochia or a positive culture of endometrial fluid or tissue usually between the second and seventh days postpartum. Fever (>38° C [100.4° F]) is the most important criterion for the diagnosis of metritis. Lochia may be foul smelling or have no odor.

Peritonitis is manifested as severe abdominal pain but may be misdiagnosed because abdominal rigidity, guarding, or rebound tenderness are often not present on physical examination as a result of laxity of the rectus abdominus muscles. Commonly, an adynamic ileus is the first sign.

Symptoms of toxic shock syndrome (TSS) include fever with a temperature of 39° C (102.2° F) or higher; erythematous diffuse rash; headache, photophobia, myalgias, and altered sensorium; gastrointestinal complaints, including nausea, vomiting, and watery diarrhea; and rapid progression to renal failure, hepatic failure, disseminated intravascular coagulation, and circulatory collapse.

Clinical signs and symptoms associated with cardiopulmonary complications may include fatigue, dyspnea, cough, orthopnea, hemoptysis, chest pain, palpitations, abdominal pain, tachycardia, elevated blood pressure, pulmonary rales, third heart sound, mitral regurgitant murmur, and peripheral edema.

Symptoms of postpartum mood disturbance include mild depression, irritability, confusion, mood instability, anxiety, headache, fatigue, and forgetfulness. Usually, the postpartum blues appear in the first 2 weeks after delivery and last from a few hours to a few days. More severe symptoms may include delusions, hallucinations, rapid mood swings, sleep disturbances, and obsessive thoughts about the baby.

Differential Diagnosis and Medical Decision Making

Infections

Puerperal fever is defined as a temperature of 38° C (100.4° F) or higher that occurs on any 2 of the first 10 days postpartum, exclusive of the first 24 hours; the temperature should be taken orally by a standard technique at least four times daily.6 The usual cause is a genital tract infection, which can lead to significant morbidity and mortality.

In a small proportion of women, postpartum fever will develop as a result of breast engorgement, but the fever rarely exceeds 39° C (102.2° F) in the first few postpartum days and usually lasts less than 24 hours.

The most common infection in the postpartum period is a genital tract infection, but other sources must be eliminated, especially urinary tract infection and pneumonia. The puerperal bladder is prone to urine retention, especially after instrumental delivery and epidural analgesia; in addition, dilation of the ureters and renal pelvis makes them potential sites of infection.

Mild hypoventilation after delivery as a result of pain or limited ambulation, or both, predisposes some women to pneumonia. Additionally, minor elevations in temperature are occasionally caused by thrombosis of the superficial or deep veins of the lower extremities (Box 123.1).1,6

Genitourinary

Metritis and Pelvic Infections

In the past, uterine infections had different names based on the assumed location of the infection; however, the accepted terminology is now metritis or metritis with cellulitis because uterine infection often involves multiple tissue layers, usually the decidua and myometrial and parametrial tissue.

The single most significant risk factor for the development of metritis is the route of delivery. Women who deliver by cesarean section have a 6% to 18% incidence of metritis versus 0.9% to 3.9% with vaginal deliveries.7,8 Other recognized risk factors for the development of metritis are chorioamnionitis, anal sphincter laceration, prolonged rupture of membranes, and weight on admission of more than 200 lb. Rates of metritis are lower now than in the past 2 decades because of the routine use of prophylactic antibiotics for cesarean deliveries.6,7

Leukocytosis is often present but the white blood count is frequently elevated during the first 2 weeks postpartum. Chills may indicate bacteremia, which occurs in 10% to 20% of women with pelvic infection. Blood for culture is best obtained during the peak temperature elevations and chills that are associated with bacteremia.9 Complications of pelvic infections can be quite severe. If a patient with metritis does not respond to antibiotics after 48 to 72 hours, suspicion for complications should be high.

Wound infections are the most common cause of antimicrobial failure in women treated for metritis and are usually associated with fever around the fourth postoperative day in patients who deliver by cesarean section. Wound dehiscence, or separation of the fascial layer, is a complication of incisional infections and is associated with fascial infection and tissue necrosis.

One of the most severe complications of a pelvic infection is necrotizing fasciitis. It has a devastatingly high mortality of approximately 50%, even with appropriate treatment, and may be a complication of a cesarean incision, episiotomy, or perineal laceration. Risk factors for necrotizing fasciitis are diabetes, obesity, and hypertension.

Other complications include pelvic phlegmon, which is cellulitis that has extended to the broad ligament. These infections can extend into any blood collections that develop after a cesarean delivery, such as under the bladder flap, and cause an infected hematoma. If left untreated, a phlegmon can suppurate into an abscess. Pelvic abscesses can develop in the broad ligament, ovaries, rectovaginal septum, or psoas muscle.

Infections can extend into the veins and cause septic pelvic thrombosis, which usually involves one or both ovarian venous plexuses and occurs more predominantly on the right because of the slightly longer vein on the right and dextrotorsion of the puerperal enlarged uterus. In 25% of patients, these clots extend into the inferior vena cava and occasionally into the renal veins.

Urinary Tract Dysfunction

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