Postpartum Emergencies



Postpartum Emergencies


David C. Jones



POSTPARTUM EMERGENCIES

Most pregnancies conclude successfully, and when postpartum complications arise, they usually arise prior to discharge from the hospital. However, occasionally, complications arise after discharge or are noted in women who have home births, and in the latter case, the emergency department physician may be faced with complications that are normally seen in labor and delivery suites (Table 15.1). Family members may become quite worried about relatively minimal complications or may dismiss signs and symptoms of significant disease as normal postpartum complaints. The emergency department physician may need to sort out the serious conditions from those that are self-limited. For that reason, this chapter will review some of the critical postpartum emergencies seen immediately postpartum as well as those normally seen in women discharged from the hospital following uncomplicated deliveries.


SEIZURES

Eclampsia is the most common etiology for postpartum or peripartum seizures. While most eclamptic seizures occur prior to or during labor, 20% occur postpartum. Most of those occur within the first 48 hours, but they may be seen as late as a week after birth and have even been reported 23 days after delivery. If there is no history of a prior seizure disorder, the diagnosis of eclampsia should be assumed until proven otherwise. The first priority in these cases is to stop the seizure, and the drug of choice for this is magnesium sulfate. There are several protocols for administration, but a reasonable choice with eclampsia is to load with 6 mg intravenously over 20 minutes and then begin an infusion of 2 mg per hour, aiming for a therapeutic level of 5 to 8 mg/dL. This infusion is continued for 24 to 48 hours, although this will most likely be managed by the admitting obstetrician. If the magnesium fails to control the seizure, secondary medications that may be used include thiopental 100 mg administered slowly intravenously or diazepam 2 to 10 mg intravenously.

Since eclampsia is usually accompanied by the standard signs of preeclampsia, the presence of hypertension and proteinuria as well as the symptoms of a severe headache, blurred vision, and scotoma would help support that diagnosis. The physical examination may also reveal right upper quadrant pain (due to swelling of the liver within the capsule), hyperreflexia, edema (particularly of the hands and face), and clonus. Laboratory studies may show an elevated uric acid, and possibly elevated liver functions, and elevated serum creatinine or thrombocytopenia. While eclampsia is the most likely diagnosis, once the seizure is controlled, other possible etiologies should be considered. A CT scan is indicated in the evaluation as the differential diagnosis includes cerebral venous thrombosis, hemorrhagic stroke, CNS tumors, and the syndrome of inappropriate antidiuretic hormone secretion. If associated symptoms such as hypertension are found, they should be controlled with relatively rapidly acting agents such as beta-blockers (e.g., labetalol) or calcium channel blockers (e.g., nifedipine). These patients are usually admitted to the labor and delivery suite or to a monitored floor where the magnesium infusion is continued for at least 24 hours and monitoring for further seizures is maintained.









TABLE 15.1 Primary Medical Problems of the Postpartum Patient seen at the Emergency Department






















































































Infection



Genital tract




Endometritis




Parametritis




Pelvic cellulitis (including infected vaginal lacerations and repaired < episiotomies)




Necrotizing fasciitis, toxic shock syndrome




Septic pelvic thrombophlebitis



Mastitis



Urinary tract




Cystitis




Pyelonephritis


Postpartum hemorrhage



Early



Late


Thrombosis and thrombophlebitis



Superficial thrombophlebitis



Deep venous thrombosis



Pulmonary embolism



Ovarian torsion


Postpartum seizures



Eclampsia



Other


Postpartum psychological reactions



Initial maternal indifference



Postpartum “blues”



Postpartum depression



Postpartum psychosis



POSTPARTUM HEMORRHAGE

Blood loss exceeding 500 mL at a vaginal delivery is generally considered a postpartum hemorrhage (PPH); however, studies have shown that the average blood loss at a delivery is about 600 mL. It is clear that blood loss is usually underestimated at uncomplicated deliveries. PPH is divided into two categories based on timing with “immediate” PPH occurring within 24 hours of delivery and “delayed” PPH occurring more than 24 hours of delivery. This distinction has a limited usefulness in terms of the differential diagnosis. The bleeding seen after delivery comes primarily from the placental implantation site and, to a lesser extent, from lacerations of the genital tract such as vaginal, introital, periurethral, and labial lacerations. The primary mechanism to control this bleeding from the placental implantation is the contraction of the myometrium. Normal hemostatic mechanisms are responsible for control of bleeding from lacerations and are the secondary means of controlling bleeding from the uterus.

Immediate PPH is usually due to uterine atony, but other etiologies must be considered including lacerations, retained placenta, uterine rupture (if the patient has a history of prior c-section), and coagulation abnormalities. When
a patient is seen emergently after a delivery outside the hospital, heavy bleeding can potentially lead to a state of shock, and fluid resuscitation must be pursued in parallel to the workup of the bleeding. Obstetric hemorrhage requiring a transfusion generally requires many units of blood, so getting units of packed cells typed and crossmatched should be done at the first thought a transfusion may be necessary. Late hemorrhage is more likely caused by retained placenta or membranes, infection, subinvolution of the placental site, coital trauma, or breakdown of genital tract laceration repairs.


Workup and Treatment

When a patient presents with bleeding, initial assessment must include vital signs, complete blood count, and obviously physical examination. The initial vital signs may suggest the need for fluid resuscitation, and placing one or two large-bore IVs is appropriate. The initial focus of the physical examination is the uterus. Palpation of the uterine fundus should suggest whether it is firm and well-contracted or boggy and soft, suggesting atony. Uterine atony is initially treated with an intravenous infusion of oxytocin (40 units of oxytocin/L of lactated ringers solution or normal saline). Examination of the uterus also has a secondary role. When the uterus is atonic, blood and clot build up in the uterine cavity, which by their presence can make uterine contraction difficult, causing more bleeding and clot. The atonic uterus should be massaged to squeeze out the clots, and occasionally, a manual sweep of the clots is necessary. If oxytocin alone is insufficient to maintain uterine contraction, a number of other options can be tried. The prostaglandin E1 analogue misoprostol has been successfully used to control PPH. The dosage has ranged widely and the route of administration has included rectal, oral, sublingual, and buccal (1,2,3). Reasonable dosing would include up to 1,000 µg rectally or 600 µg sublingual or buccally. This is an off-label use for misoprostol. Prostaglandin E2 is also available (20 mg given rectally), but it is more likely to cause fever, nausea, and diarrhea. Prostaglandin E2 is also not heat stable, so if it has not been stored properly, it will loose efficacy. Prostaglandin F2α (Hemabate) is also used (250 µg given intramuscularly, intracervically, or intramyometrially) but can cause bronchoconstriction in asthmatics, so a past medical history must be obtained that specifically asks about asthma and reactive airway disease. This dose may be repeated every 10 minutes up to a total of three doses. These prostaglandins have largely replaced the former second-line agent, the ergot alkaloid methylergonovine maleate (Methergine). Methylergonovine maleate is usually given as 0.2 mg intramuscularly, but it may be administered at the same dose orally. If the atony persists despite these treatments, other etiologies must be considered, particularly retained placenta or membranes. In the setting of delayed PPH, ultrasound may be a useful modality to examine the cavity, and if retained products of conception are seen, a gentle dilation and curettage, often with suction, should be performed. One must recognize that an overly aggressive curettage of the endometrial cavity after a delivery is the main risk factor for Asherman syndrome, so these procedures must be performed with great care. In the setting of an immediate PPH, ultrasound is less useful because it frequently looks like there is significant debris in the cavity after an uncomplicated delivery. Instead, the evaluation consists of carefully examining the placenta and membranes (if available) to look for evidence of a retained portion of the placenta or a succenturiate lobe. Direct evaluation of the cavity may be performed by a digital examination with palpation once adequate anesthesia is available. If that examination is suggestive of retained products that cannot be manually removed, then a gentle curettage should be performed with care.


If there is no evidence of retained products of conception or uterine bleeding persists despite their removal, other nonsurgical approaches are available. Intrauterine balloon tamponade is an effective treatment for PPH, particularly those related to bleeding from the lower uterine segment such as a relative low placental implantation (4). This balloon is useful both in terms of treating atony and also as a means of deciding who will probably need surgical management (4). In centers that have interventional radiology services available, embolization of the uterine arteries or hypogastric arteries will frequently control bleeding and avoid surgery. The interuterine balloon may also be placed to decrease hemorrhage while the IR team is being assembled. If these nonsurgical methods fail and it is clear that the etiology of the bleeding is uterine rather than from another site, a laparotomy will be required. Surgical ligation of the uterine or hypogastric arteries may decrease the pulse pressure and control the bleeding adequately. If uterine atony persists, the B-Lynch Brace suture has been shown to be an effective measure. This stitch uses rapidly absorbable sutures to squeeze the uterus in an attempt to simulate the ongoing uterine massage or compression. The B-Lynch has been combined with an intrauterine balloon tamponade to maximize compression in a technique referred to as the “uterine sandwich” (5). If all of these surgical measures fail, hysterectomy may be required. This is usually performed as a supracervical hysterectomy because it can be difficult to identify the cervix after a vaginal delivery, and the surgeon usually leaves the cervix to make sure none of the vaginal is taken.

Because chorioamnionitis and endometritis may increase the likelihood of uterine atony, signs such as an elevated white blood cell count, c-reactive protein, uterine fundal tenderness, and fever should be evaluated. If there is suspicion of infection, appropriate treatment includes admission to the hospital for inpatient intravenous antibiotics.

In an immediate PPH, evaluation for other etiologies would include a careful examination of the vagina and the cervix for lacerations. Bleeding lacerations should be repaired with an intermediate-duration absorbable suture. In a delayed PPH when the bleeding is from a prior repair, antibiotic coverage is appropriate. If the repair does not appear infected, a few stitches can be placed to address the bleeding. If the repair is broken down and appears badly infected, a full repair is best postponed until the infection is well-controlled with antibiotics.

Finally, in some patients, there may be coagulopathies, either because of inherent bleeding disorders or because of disseminated intravascular coagulation secondary to their ongoing PPH. Coagulation parameters should be measured, and blood product components replaced as necessary. A number of obstetrical disorders, including familial thrombophilias with a bad obstetric history, a history of thromboembolism, and antiphospholipid antibody syndrome, are now treated with anticoagulation, at both prophylactic and therapeutic doses. A careful history of past medical conditions and medications once again plays an important role here.


THROMBOEMBOLISM

The risk of thromboembolism is increased during pregnancy. In fact, a number of factors come together to make pregnancy and the postpartum period perhaps the highest-risk period in a woman’s life. Stasis, vessel wall injury, and altered clotting factors promoting clotting, the classic triad leading to intravascular thrombosis that was proposed by Virchow, are all present. All of the clotting factors except XI and XIII are increased in pregnancy, and there is mixed evidence that activity of the fibrinolytic system may be decreased during pregnancy. Venous stasis occurs in
maternal leg veins primarily through two mechanisms. First, the gravid uterus compresses the inferior vena cava and iliac veins. This leads to both venous stasis and the lower extremity edema commonly experienced by pregnant women in the third trimester. Venous dilation also plays a role, most likely due to progesterone, allowing for more pooling in the leg veins. After delivery, decreased mobility, particularly after a c-section, may play an additional role in promoting stasis. Blood vessel damage may occur directly from delivery. These factors all come together after delivery and put the woman at high risk for thrombosis. Thromboembolism in pregnancy is often the first clue that a patient has a familial or acquired thrombophilia, and a workup to identify these is appropriate (Table 15.2).


Superficial Thrombophlebitis

Superficial thrombophlebitis is the most common thrombosis identified during pregnancy occurring in 11 per 1,000 deliveries (6). Patients present with pain, redness, and warmth over the affected area. The affected vein may be swollen, but this may be hard to identify. Occasionally, the clot itself is palpable as a “cord.” Superficial thrombosis poses no direct risk to the patient beyond discomfort. It is usually treated with heat, elevation, analgesics (especially aspirin), and occasionally, anticoagulation. If there is evidence of cellulitis, prescription of an antibiotic with coverage for skin flora (e.g., Staphylococcus and Streptococcus) such as dicloxacillin is appropriate. Superficial thrombophlebitis, particularly of the saphenous vein, can progress to deep venous thrombosis, so if there is any question of the extent of the clot, appropriate studies to rule out deep vein thrombosis must be obtained.


Deep Venous Thrombosis

Unlike the more benign superficial thrombophlebitis, DVT poses a direct risk to the patient because it may lead to a pulmonary embolism (PE). Consequently, it is of utmost importance to accurately identify and expeditiously treat this condition. The main complaint women present with is pain and leg swelling. This is usually unilateral leg swelling, which helps distinguish it from the normal lower extremity swelling of pregnancy. If a clot reaches the inferior vena cava, bilateral swelling may occur, which can lead to the false

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Jun 17, 2016 | Posted by in OBSTETRICS | Comments Off on Postpartum Emergencies

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