KEY QUESTIONS
What is the differential diagnosis of postpartum fever, and how is it managed?
What are common lower-extremity postpartum neuropathies, and how can they be prevented?
Why is exclusive breastfeeding important, and what is the role of the OB/GYN hospitalist in supporting this initiative?
How do you counsel a patient about postpartum contraception and the immediate placement of long-acting reversible contraceptives (LARCs)?
The postpartum period begins immediately after delivery and continues for 6 to 8 weeks. During this time, many changes occur to a woman’s physical, psychological and social state. The obstetrics and gynecology (OB/GYN) hospitalist plays a critical role in the evaluation and management of these patients. This chapter discusses the hospitalist’s role in managing common postpartum concerns, including postpartum fever, neuropathies, breastfeeding, and contraception. (Postpartum hemorrhage, another complication, is discussed separately in Chapter 41.)
CASE 44-1
A 24-y.o. gravida 1 para 1, 2 days postoperative from a primary C-section, is evaluated for a fever of 39°C. Her pregnancy had been uncomplicated, and she was GBS negative. She presented to the hospital at 38 6/7 weeks gestation with ruptured membranes and was given oxytocin to augment labor. She progressed slowly, and after more than 16 hours of labor, she was diagnosed with arrest of dilatation at 8 cm. A primary C-section was performed and was uncomplicated. She was given 2 g of cefazolin prior to skin incision.
The US Joint Commission on Maternal Welfare defines maternal postpartum febrile morbidity as an oral temperature of 38.0°C or more on any two of the first 10 days postpartum, exclusive of the first 24 hours. The first 24 hours are excluded because low-grade fever during this period is common and often resolves spontaneously, especially after vaginal birth.1
There are maternal, intrapartum, and perioperative factors that increase the risk of postpartum fever. Maternal factors include poor nutrition, diabetes mellitus, and anemia. Intrapartum factors consist of prolonged labor, prolonged rupture of membranes (>18 hours), use of intrauterine monitors, frequent cervical examinations, and intrauterine infection or inflammation. Perioperative factors include operative vaginal delivery and cesarean delivery.2–8
Because the differential diagnosis for postpartum fever is quite broad, a thorough physical exam should be performed, including pelvic, wound, and breast exams. In addition, a urinalysis should be sent to evaluate for a urinary tract infection (UTI) as well as a complete blood count (CBC) to evaluate for leukocytosis. Imaging is usually reserved for patients with clinical findings or when there is no response to empiric therapy. The goal is to identify the source of the fever and to direct therapy accordingly. The differential diagnosis includes endometritis, lactational mastitis, wound infection, UTI, pneumonia, atelectasis, drug reaction, Clostridium difficile–associated diarrhea, thromboembolic disease, septic pelvic thrombophlebitis (SPT), and anesthesia complications. Some important causes of postpartum fever are discussed next.
The most common cause of postpartum fever is endometritis, which usually occurs within 5 days of delivery. Endometritis is a polymicrobial infection involving both aerobes and anaerobes, for which the most important risk factor is nonelective cesarean delivery, especially when performed after the onset of labor.9–11 Women who undergo nonelective cesarean delivery are diagnosed with endometritis 11% of the time, whereas women who undergo elective cesarean deliveries and vaginal deliveries have postpartum endometritis incidences of 1.7% and 3%, respectively.9,12,13
Other important risk factors include intrapartum intrauterine infection or inflammation, prolonged labor and rupture of membranes, intrauterine monitoring, and bacterial vaginosis at the time of delivery.3,4,6,14,15 Postpartum endometritis may be reduced by treating symptomatic bacterial vaginosis late in pregnancy.16 However, we do not routinely screen asymptomatic women, as there is no data suggesting that this is a cost-effective approach.
Clinical findings include fundal tenderness, foul-smelling lochia, tachycardia, and leukocytosis. However, these findings are nonspecific. Therefore it is important to consider risk factors and the entire clinical picture as parts of the diagnosis.
Treatment of endometritis with broad-spectrum antibiotics is usually effective. Endometrial cultures rarely change the management and therefore should not be routinely performed. For similar reasons, blood cultures are not always obtained. However, bacteremia does occur in 5% to 20% of patients and blood cultures may be useful in guiding treatment if the patient fails to respond to empiric therapy or appears septic upon presentation (see the section entitled “Group A Streptococcal Infection and Sepsis,” later in this chapter).17
Standard antibiotic regimens include clindamycin [900 mg intravenously (IV) q8 hours] and gentamicin (1.5 mg/kg IV q8 hours or 5 mg/kg IV q24 hours). For patients with renal insufficiency, aztreonam (1–2 g IV q8 hours) can be substituted for gentamicin. If infection with enterococci or other Gram-positive organisms are identified, or if the patient does not have clinical improvement within 48 to 72 hours of initiation of therapy, ampicillin (2 g IV q6 hours) should be added. Treatment is continued until the patient has been afebrile for 24 to 48 hours. Generally, there is no need to continue oral antibiotics after discharge, unless the patient was bacteremic.18
Postpartum Group A streptococcal (GAS) infection is rare, occurring at an estimated rate of 0.06 per 1000 live births.19 Infection with GAS can lead to toxic shock syndrome (TSS) and other serious complications, such as necrotizing myometritis and necrotizing fasciitis.
Diagnosis of GAS infection is suggested by an early-onset (i.e. within 48 hours of delivery) high fever (>38.5°C), with hypotension and diminished function of other organ systems, including renal failure and acute respiratory distress syndrome. Patients with GAS infection often have a rash and pain that are out of proportion to clinical findings. If GAS infection is suspected, blood and urine cultures should be obtained, and postpartum women should have an endometrial aspiration for Gram stain and culture.
Treatment for GAS infection includes aggressive fluid resuscitation and antibiotic therapy with penicillin G and clindamycin for at least 14 days. In cases of sepsis, surgical debridement of the source of infection (vulvar debridement, hysterectomy, or a combination) could be life-saving, as the fatality rate of TSS is over 40%.19 Because GAS-produced toxins can lead to TSS, it is likely that antibiotics alone will not treat the infection. Therefore it is crucial that the source of GAS and its toxins be removed surgically.
Lactational mastitis is painful inflammation of the breast that occurs in breastfeeding women, typically in the setting of prolonged engorgement or poor drainage. It is estimated to occur in 2% to 10% of breastfeeding women.20 Breast abscesses can develop when mastitis is not treated or does not respond to antibiotic treatment (Figure 44-1).
FIGURE 44-1.
Puerperal mastitis with breast abscess. A. Indurated, erythematous skin overlying area of a right-sided breast infection. B. Sonographic picture of this 5-cm abscess. Reproduced with permission from Cunningham F, Leveno KJ, Bloom SL: Williams Obstetrics, 25th ed. New York, NY: McGraw-Hill Education; 2018. Photo contributor: Dr. Emily Adhikari.
The diagnosis of mastitis is typically made by history and physical exam. The affected area is often erythematous, indurated, and tender, and other symptoms include fever and malaise. The diagnosis of mastitis is an important differentiation from engorgement, which is breast fullness and tenderness occurring at the onset of lactation. Engorgement is often bilateral, usually occurs within the first 72 hours postpartum, and is typically not associated with systemic symptoms of fever and malaise. Prolonged or severe engorgement can ultimately result in progression to mastitis.
Treatment for mastitis includes symptomatic relief, complete emptying of the breast, and antibiotics. Lactation can and should continue during the treatment. Complete emptying of the breast via breastfeeding, pumping, or hand expression is encouraged. Symptomatic relief is primarily done with nonsteroidal anti-inflammatory drugs (NSAIDs) and ice packs to reduce local pain and swelling. Empiric antibiotic therapy for lactational mastitis should cover Staphylococcus aureus and continue for up to 14 days if necessary. Standard antibiotic regimens include dicloxacillin (500 mg orally, four times a day) or cephalexin (500 mg orally, four times a day). If a beta-lactam hypersensitivity is suspected, treatment with clindamycin (300 mg, orally three times a day) is usually effective. If there is no clinical improvement within 48 to 72 hours, ultrasound imaging is indicated to evaluate for an underlying breast abscess. If a breast abscess is present, ultrasound-guided aspiration or incision and drainage may be performed. Even in the setting of a breast abscess that has been treated surgically, breastfeeding should continue on both breasts when feasible.
Methicillin-resistant S. aureus (MRSA) has become an important pathogen in cases of lactational mastitis. The incidence of MRSA in all soft-tissue infections has been increasing over the past decade.21 A 2007 study found that 44% of postpartum mastitis cases were culture-positive for S. aureus, and the incidence today is estimated to be even higher.22
Risk factors for MRSA infection include recent hospitalization, an immunocompromised state, incarceration, and recent antibiotic use. When risk factors for MRSA infection are present, outpatient treatment with clindamycin may be initiated. Trimethoprim-sulfamethoxazole (1–2 tabs by mouth BID) is also acceptable for mothers not nursing, as there is an increased risk of neonatal kernicterus. In cases of severe infection with hemodynamic instability or progressively worsening erythema, empiric impatient therapy should be initiated with vancomycin (1 g IV q12 hours) and adjusted further according to culture and sensitivity results.
Surgical site infections can occur at skin incisions and episiotomy/perineal laceration sites. Perineal infections and the subsequent breakdown of repaired lacerations or episiotomies are usually localized to the skin and subcutaneous tissue. A case-control study of more than 104,000 deliveries reported an incidence of 0.1% perineal laceration breakdowns per delivery.23 Surgical site infections are diagnosed in 2.5% to 16% of patients after cesarean delivery.24
Treatment for wound infection consists of opening, draining, irrigating, and debriding the wound. Saline-soaked packing twice a day is appropriate to encourage the promotion of granulation tissue. Antibiotics are usually prescribed but are not always necessary unless there is accompanying cellulitis. Large defects may be resutured when granulation tissue is present.
Another cause of postpartum fever is SPT. Our understanding of this disease process has evolved significantly over the last century. The pathogenesis is thought to be a result of Virchow’s triad: hypercoagulability of pregnancy, venous stasis caused by dilated uterine and ovarian veins in the postpartum period, and endothelial injury caused by either infection or intrapartum trauma. The most recent documented incidence of SPT (from 1999) was 1 in 3000 deliveries overall. The incidence for vaginal deliveries was 1 in 9000, compared to 1 in 800 cesarean deliveries.25
Detecting SPT can be challenging, as it is often a diagnosis of exclusion. However, SPT can be presumed if patients defervesce within 48 hours of the appropriate treatment. SPT should be suspected in the postpartum period in a febrile patient who fails to respond to broad-spectrum antibiotic therapy. The physical exam may be significant for flank and/or lower abdominal tenderness to palpation; however, these patients usually do not appear toxic. Computed tomography (CT) and magnetic resonance imaging (MRI) are generally used to evaluate for SPT. These imaging studies may show enlargement of the vein involved, a low-density lumen within the vessel, and/or sharp enhancement of the vessel wall.26 It is important to note that a negative imaging study cannot exclude SPT, and there is no gold-standard imaging technique used for diagnosis.
The treatment of SPT includes antibiotics and anticoagulation. Because this is a diagnosis of exclusion, most postpartum patients have already been receiving broad-spectrum parenteral antibiotics. Antibiotic coverage should include Gram-negative and anaerobic organisms. The optimal duration of antibiotic therapy is unknown, but most clinicians favor discontinuing after clinical improvement, including the patient being afebrile for 48 hours and upon resolution of leukocytosis. The use of anticoagulation for management of SPT is controversial. Brown et al (1999) examined 14 cases at Parkland Hospital and found an equal duration of fever and hospital stay in SPT patients treated with antibiotics, with or without anticoagulation.25 However, most experts advocate using anticoagulation for the management of SPT, as this is thought to prevent further thrombosis and reduce the spread of septic emboli. Two options include unfractionated heparin, with a goal partial thromboplastin time (PTT) value of 1.5 to 2.0 times the patient’s baseline, or low-molecular-weight heparin (LMWH) at a dose of 1 mg/kg every 12 hours. There have been no studies to determine the optimal duration of anticoagulation therapy in SPT; however, it is reasonable to discontinue treatment after clinical improvement. If pelvic vein thromboses are documented radiographically, then at least 2 weeks of anticoagulation with LMWH is recommended. If the extent of the thromboses is severe, with septic pulmonary emboli or involvement of the ovarian vein, iliac veins, or vena cava (Figure 44-2), anticoagulation should be continued for at least 6 weeks, with follow-up imaging to guide subsequent management.
FIGURE 44-2.
SPT: Uterine and parametrial infection may extend to any pelvic vessel as well as the inferior vena cava. The clot in the right common iliac vein extends from the uterine and internal iliac veins and into the inferior vena cava. The ovarian vein septic thrombosis extends halfway to the vena cava. (Reproduced with permission from Cunningham FG, Leveno KJ, Bloom SL, et al: Williams Obstetrics, 25th ed. New York, NY: McGraw-Hill Education, Inc; 2018.)
PRACTICE POINTS
The differential diagnosis for postpartum fever is broad, and workup should include a thorough physical exam, urinalysis, and CBC.
Endometritis is the most common cause of postpartum fever. Diagnosis is clinical, and treatment is empiric. However, if GAS infection and sepsis are suspected, an endometrial sample should be obtained, and treatment should also include surgical debridement, as TSS has a high fatality rate.
Lactational mastitis is a common cause of postpartum fever and is treated empirically. Breast abscesses can be drained under ultrasound guidance or removed surgically if necessary. Clinicians should consider risk factors for MRSA infection when choosing the appropriate antibiotic regimen.
Wound infections should always be considered as a cause of postpartum fever in cases of both vaginal and cesarean delivery.
CASE 44-1 FOLLOW-UP
The patient was diagnosed with endometritis and started on IV gentamicin and clindamycin. She improved clinically and was discharged home after being afebrile for 48 hours.
CASE 44-2
A 28-y.o. gravida 2 para 2 complains of pain and numbness over her left anteromedial thigh and difficulty standing up from a sitting position 10 hours after a normal spontaneous vaginal delivery. She received neuraxial anesthesia for the delivery without complications.
The incidence of postpartum lower-extremity neuropathies is between 0.58% and 0.92% of births.1 Risk factors include nulliparity, short stature, instrumental delivery, and prolonged second stage of labor.27,28 Notably, cesarean section (C-section) is not a protective factor.28 The use of neuraxial anesthesia and maternal weight gain may be risk factors, although studies remain inconclusive.27–29 The most commonly involved nerves in postpartum lower-extremity neuropathies are the lateral femoral cutaneous, femoral, and peroneal nerves.27,28
Lower-extremity neuropathies typically result from nerves being stretched or compressed.29 In severe cases, this can compromise blood flow and cause nerve ischemia, which can lead to axonal damage and inhibited nerve conduction. Recovery may be prolonged in these cases, as it depends on the percentage of damaged axons in the nerve. However, in most postpartum cases of lower-extremity neuropathy, the injury is demyelination, which is less severe and has a favorable prognosis.28
Neuraxial anesthesia may contribute to the incidence of postpartum lower-extremity neuropathies, as women have less frequent position changes and can have an impaired ability to sense impending nerve injuries. As a result, patients receiving neuraxial anesthesia are less likely to change positions to prevent nerve compression than those without neuraxial anesthesia.29
The lateral femoral cutaneous and femoral nerves are often compressed at the inguinal ligament. Factors contributing to this compression include prolonged pushing in the semi-Fowler or lithotomy positions, instrumental vaginal delivery, edema, and abdominal distention due to a large fetus.27 In the case of cesarean delivery, nerve injury can occur from a wide Pfannenstiel incision or from stretching and pressure from retractors.28
In patients with preexisting neuropathies, such as diabetics, symptoms worsen 0.4% of the time after receiving regional anesthesia. This is thought to occur because the injured nerves are at increased risk of further compressive trauma due to sensory deficits and physical vulnerability.27 A preexisting neuropathy also may present in the lateral femoral cutaneous nerve, especially in the anatomical variant in which the nerve passes through, rather than under, the inguinal ligament. In this variant, the exacerbated lumbar lordosis of pregnancy can lead to nerve compression and injury prior to labor.28
The diagnosis of lower-extremity postpartum neuropathy is made based on clinical findings. Definitive diagnosis requires electromyography testing, but this is often not necessary, as some injuries require 3 weeks to be detectable and many have recovered in this period.28 Pudendal neuropathy can be confirmed with urodynamic testing and anorectal manometry.27
Women will generally complain of numbness, pain, and/or weakness in a peripheral nerve pattern distribution.27,28 Key details of the delivery history include patient positioning, duration of the second stage of labor, instrument assistance, perineal lacerations or trauma, and neuraxial anesthesia difficulties. It is important to obtain details on the timing and progression of pain and motor deficits and to ask about preexisting neuropathies.27 This information is key to determining the mechanism of injury, prognosis, and management.
A thorough back and lower-extremity exam should be conducted, including focal neurologic and musculoskeletal exams to determine distributions of sensory symptoms and muscle weakness. Look for bruising, edema, pain on palpation, and pain with movement as localization clues.27
Thoracic and lumbar imaging should be considered when back pain is present, especially in patients with immunosuppression, coagulopathies, unexplained fever, or worsening neurologic symptoms in a root or spinal cord pattern.27 For patients with motor deficits, consider having a physical therapist evaluate her condition prior to discharge.
Complications from neuraxial anesthesia must also be considered in the differential diagnosis of lower-extremity postpartum neuropathy, including subarachnoid bleeding, spinal/epidural hematoma, epidural abscess, cauda equine syndrome, and infection. The differential also includes lumbar and sacral plexopathies, nerve root radiculopathies, and lumbar disc herniation. The various peripheral neuropathies are differentiated with a detailed physical exam.27,29 See Table 44-1 for specific nerve details.27–29
| Nerve | Anatomy | Mechanism of Injury | Symptoms/Physical Exam | Differential Diagnosis |
| Lateral femoral cutaneous (most common) | L2–L3 origin Exits pelvis under or through inguinal ligament just medial to the anterior superior iliac spine | Compression at the inguinal ligament2 | – Sensory loss or pain over the anterolateral thigh, may be triggered by tapping on the inguinal ligament2 – No motor symptoms – Normal deep tendon reflexes | L2–3 radiculopathy |
| Femoral (second most common) | L2–L4 origin Travels retroperitoneally and exits the pelvis under the inguinal ligament2,4 | – Compression at the inguinal ligament2 – Stretch injury, as the intrapelvic portion has poor blood supply – Retroperitoneal compression from intrapelvic pathology or hemorrhage – Entrapment of the psoas/iliacus muscles due to variants splitting the nerve – Compression at the knee causes an isolated saphenous neuropathy | – Bilateral in 25% of cases27 – Sensory deficits over the anteromedial thigh/calf – Knee extensor weakness – Hip flexor weakness (climbing stairs, standing from sitting) if injured proximal to inguinal ligament – Absent patellar reflex | – L2–3 radiculopathy – Lumbar plexopathy |
| Obturator | L2–L4 origin Crosses the pelvic brim and travels through the obturator canal to the medial thigh. | – Compression at the pelvic brim by the fetal head, forceps, or position during delivery – Entrapment from a pudendal nerve block, causing a hematoma | – Sensory loss at the upper medial thigh – Thigh adductor weakness (wide-based circumduction gait) | |
| Sciatic and Peroneal | L4–S3 origin – Sciatic nerve splits to peroneal and tibial nerves just above the knee – Peroneal nerve is superficial at the fibular head. | – Proximal (sciatic): Stretch injury – Distal (peroneal): External compression at the fibular head from palmar pressure, lithotomy or knee-flexion positioning during pushing1,2 | – Foot drop – Proximal (sciatic): Back pain, absent ankle reflex, weak knee flexors, plantar flexors, and foot inverters – Distal (peroneal): Pain triggered by tapping over fibular head2 | – Lumbar or sacral nerve root injury – Lumbar or sacral plexopathies |
| Pudendal | S2–S4 origin Derived from the sacral plexus4 | Compression from fetal head or instrumental delivery | – Perineal numbness and pain – Pain gets worse with sitting2 – Prolonged urge urinary incontinence, overactive bladder, and/or fecal incontinence | – Local tissue injury, causing urinary retention or incontinence – Perineal trauma, causing fecal incontinence – Conus medullaris: Painless and has numbness over both buttocks |
| Lumbar plexopathy | L1–L4 roots Forms: Iliohypogastric, ilioinguinal, genitofemoral, femoral, lateral femoral cutaneous, and obturator nerves4 | Compression between the fetal head and bony pelvis | – Femoral distribution sensory loss – Hip and buttocks pain2 – Hip adductor weakness, foot drop | Radiculopathy |
| Sacral plexopathy | L4–5, S1–3 Forms: Sciatic and pudendal nerves | Compression at pelvic brim from a large fetus, instrumental delivery, or positioning | – Absence of back pain in most cases – No paraspinal involvement – Sciatic symptoms, pudendal symptoms, or both | Radiculopathy |
| Radiculopathy (nerve root injury) | L1–5 and S1 are among those injured | Herniated or ruptured intervertebral disk, spinal column lesions, muscle spasm, trauma, arachnoiditis, intradural or extradural tumors, inflammation, infection | – Positive reverse straight leg raise test (L2–4 involved) – Positive straight leg raise test (L4–S1 involved) – Back pain – Radicular distribution sensory symptoms – Motor deficits in innervated muscles | Peripheral nerve injury |
Preventive measures for lower-extremity postpartum neuropathy include frequent repositioning and protective padding during labor, especially in patients receiving neuraxial anesthesia and those with preexisting nerve injuries. Ensure that the legs are not pulled back too far while the patient pushes in lithotomy position, as those with neuraxial anesthesia may not sense impending nerve injury.
Treatment primarily consists of supportive measures, including pain treatment with NSAIDs, lidocaine patches, and peripheral nerve blocks in severe cases. Motor symptoms are treated with ongoing physical therapy. In the case of knee extensor weakness or foot drop, supportive braces are indicated. For pudendal neuropathies, exercises to stretch and strengthen the pelvic floor muscles are recommended.27 These include Kegel exercises, bringing the knees to the chest, and forward bends. Recovery for all the peripheral neuropathies takes 2 months on average, ranging from 1 week to over 18 months.28
PRACTICE POINTS
Postpartum neuropathy presents in about 1% of births and includes sensory deficits, motor deficits, or both.
Neuraxial anesthesia is potentially a risk factor due to infrequent repositioning and decreased ability to sense impending nerve damage.
A thorough musculoskeletal and neurological exam is necessary to differentiate the various nerve injuries.
Treatment is mainly supportive, including pain management and physical therapy if indicated.
Most patients will recover within 2 months.
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