Trauma and Critical Care

The management of critically ill obstetric patients most commonly involves treatment of disease processes that occur as a direct consequence of pregnancy. Although sometimes life-threatening, these conditions are usually reversible. Delivery of the infant often attenuates or ablates the disease process, and the mother typically recovers with supportive and resuscitative measures. Primary obstetric disorders account for 50% to 80% of intensive care unit (ICU) admissions for pregnant patients; approximately 80% of these admissions result from preeclampsia, sepsis, and/or hemorrhage ( Box 53.1 ). The estimated ICU admission rate for obstetric patients is 0.5% to 1% in the United States; the mortality rate among this population is 12% to 20%.

Box 53.1

Causes of Critical Illness in Pregnancy

Obstetric Causes

•
Acute fatty liver of pregnancy
•
Amniotic fluid embolism
•
Cardiomyopathy
•
Chorioamnionitis
•
HELLP syndrome
•
Hemorrhage
•
Pelvic septic thrombophlebitis
•
Placental abruption
•
Preeclampsia/eclampsia
•
Puerperal sepsis

Nonobstetric Causes

•
Acute renal failure
•
Autoimmune disorders
•
Chronic respiratory disease
•
Diabetic ketoacidosis
•
Substance use disorder
•
Pneumonia
•
Pulmonary thromboembolism
•
Trauma
•
Urinary tract infection

HELLP , Hemolysis, elevated liver enzymes, low platelet count.

Trauma accounts for 45% to 50% of all maternal deaths in the United States, and it is the most common nonobstetric cause of maternal death. Other common nonobstetric causes of ICU admission are respiratory failure, endocrine disorders, preexisting autoimmune disease, and thromboembolic disorders. Ethnic minorities and women with low socioeconomic status have the highest rates of morbidity and mortality. Modern medicine has allowed women with complex medical problems such as congenital heart disease and cystic fibrosis to survive into childbearing age, and these patients are at increased risk for complications during pregnancy and have a higher incidence of ICU admission. Among critically ill obstetric patients admitted to an ICU, the most common cause of death is acute respiratory distress syndrome (ARDS), which can complicate both obstetric and nonobstetric disease processes.

Critical maternal illness places the fetus at significant risk for morbidity and mortality. Important fetal risk factors include maternal shock, transfusion of blood products, and early gestational age at the time of critical maternal illness.

TRAUMA DURING PREGNANCY

Epidemiology

Trauma affects 5% to 8% of pregnancies in the United States and is a leading nonobstetric cause of maternal death; as many as 20% of affected women require emergency surgery. It is likely that the reported incidence of maternal trauma is underestimated due to underreporting, especially in cases of domestic violence. Motor vehicle crashes are the most common cause of injury-related maternal deaths (49% to 70%), followed by domestic violence (11% to 25%) and falls (9% to 23%). Not using a seat belt is a major risk factor for maternal and fetal injury in motor vehicle trauma. Penetrating trauma and burns are less common than blunt mechanisms of injury. Regardless of the mechanism of injury, trauma is a threat to the life of the mother and fetus. The rate of maternal trauma admission to an ICU increases with each trimester: 8% occur in the first trimester, 40% in the second trimester, and 52% in the third trimester. Most women are able to continue their pregnancy at home, but up to 38% are hospitalized until delivery.

Risk factors for maternal trauma include age < 25 years, low socioeconomic status, minority race, use of illicit drugs or alcohol, and domestic violence. It is important to remember that any female patient of reproductive age who is a victim of trauma could be pregnant at the time of injury.

Complications and Outcomes

As in the general population, hemorrhagic shock and brain injury are the most common mechanisms of death in pregnant trauma victims. Pelvic and acetabular fractures also pose a significant risk, with pelvic fractures being the most common maternal injury contributing to fetal death. Injuries and complications that are unique to pregnant trauma victims include uterine rupture, placental abruption, preterm labor, and direct fetal injury. Although rare (0.6% of injuries), uterine rupture is a major threat to the life of both the mother (10% mortality) and the fetus (near 100% mortality). Placental abruption complicates 1% to 5% of minor injuries and 20% to 60% of major trauma and usually occurs from 16 weeks’ gestation onward. Placental abruption can cause major overt and occult hemorrhage and coagulopathy and should be considered as a possible source of bleeding in the unstable pregnant trauma patient. Preterm labor is a common (25%) complication of trauma and can be precipitated even in cases of apparently minor injury. Premature rupture of membranes increases the risk for both preterm labor and infection. Amniotic fluid embolism is a rare complication of maternal trauma, but it should be considered as part of the differential diagnosis in patients who are refractory to resuscitation.

Fetal-maternal (transplacental) hemorrhage can occur after trauma and result in maternal isoimmunization with the D antigen of the fetal red blood cell (RBC) Rhesus protein complex (Rh ₀ [D]) in the Rh-negative mother. The Kleihauer-Betke test is used to identify fetal blood in the maternal circulation after maternal injury. Acid applied to a peripheral maternal blood smear eliminates adult hemoglobin, while fetal hemoglobin is resistant. Subsequent staining lights up the intact fetal cells against a background of pale maternal cells, and the ratio of fetal to maternal cells can be used to calculate the total volume of fetal RBCs in the maternal circulation. When fetal-maternal hemorrhage is present, treatment with Rh ₀ (D) immune globulin (RhoGAM) is generally indicated. In a study performed at the R. Adams Cowley Shock Trauma Center of the University of Maryland, more than 50% of evaluated pregnant trauma victims were positive for fetal-maternal hemorrhage as determined by a positive Kleihauer-Betke test. Essentially all patients with a positive test had uterine contractions, whereas patients with a negative Kleihauer-Betke test did not have contractions. The investigators concluded that the Kleihauer-Betke test was a sensitive and specific predictor of preterm labor in pregnant trauma patients and should be performed in all victims regardless of blood Rh phenotype.

Fetal Trauma and Outcome

The fetal mortality rate after maternal blunt trauma has been reported to range from 3.4% to 38.0%; placental abruption, uterine rupture, maternal shock, and maternal death are the most frequent factors associated with fetal demise ( Box 53.2 ). The risk for direct fetal trauma increases with gestational age because the bony pelvis protects the uterus and fetus before 13 weeks’ gestation. Pregnant women who sustain blunt trauma have a lower risk for bowel injury than nonpregnant patients because the uterus acts as a shield and pushes the abdominal contents into the upper abdomen. Maternal pelvic fractures are associated with uteroplacental injury and fetal skull fractures. A skull fracture is the most common direct fetal injury and has a reported fetal mortality rate of 42%.

Box 53.2

Factors Associated With Fetal Demise After Trauma

•
Ejection from vehicle
•
Maternal pelvic fracture
•
High maternal Injury Severity Score (>15)
•
Maternal death
•
Maternal hypotension
•
Uterine rupture
•
Uterine tenderness
•
Placental abruption
•
Vaginal bleeding
•
Abnormal fetal heart rate pattern
•
Amniotic fluid on pelvic examination
•
Maternal history of alcohol use
•
Maternal history of smoking

The relationship between the Injury Severity Score (ISS) (see later discussion) and fetal outcome is controversial. Analysis of outcomes from 1075 pregnant trauma victims showed that an ISS > 15 was associated with increased risk for fetal demise. In contrast, a study using data from the state of Washington found no correlation between ISS and pregnancy outcomes. Fetal demise occurred even in women with low ISS. Evidence suggests that decreased serum bicarbonate, an indicator of systemic hypoperfusion, is associated with fetal demise after maternal trauma. Altered maternal mental status and the presence of head trauma have also been linked to adverse fetal outcomes.

It is crucial to preserve maternal cardiac output, blood pressure, and oxygen delivery to optimize maternal recovery and protect fetal well-being. However, fetal loss can occur even if the mother has not incurred serious injuries. Thus, all pregnant women should be evaluated in a medical setting after trauma, regardless of the apparent severity of injury. The fetus remains at risk for delayed complications after maternal discharge from the hospital. Delayed complications include a twofold increase in the risk for preterm delivery and a ninefold increase in the risk for fetal death. Late complications of trauma, such as cerebral palsy, have also been reported in children born to mothers who experienced trauma during pregnancy.

Initial Assessment and Resuscitation

The initial assessment and resuscitation should focus on the mother; it is axiomatic that maternal resuscitation typically facilitates fetal resuscitation. A systematic approach to initial resuscitation and stabilization should be used ( Fig. 53.1 ). Immediate interventions are initiated to identify and treat life-threatening conditions based on the principles of Advanced Trauma Life Support. The initial, primary survey should focus on ensuring adequate airway protection, ventilation (breathing), and circulation (the “ABCs” of resuscitation). Pregnant women experience significant changes in cardiopulmonary and metabolic function that must be considered during resuscitation ( Table 53.1 ).

A flowchart outlines steps for managing a pregnant woman after trauma, starting with stabilization and progressing through examination, fetal monitoring, and evaluation. — Fig. 53.1

Table 53.1

Physiologic Changes of Pregnancy That May Affect Trauma Management

BUN , Blood urea nitrogen.

Parameter	Effect of Pregnancy	Implications
Airway
Functional residual capacity	Decreased by 20%	More rapid oxyhemoglobin desaturation during periods of apnea
Oxygen consumption	Increased by 15%–20%
Airway edema	May be present	Tracheal intubation more difficult
Lower esophageal sphincter tone	Decreased	Increased risk for aspiration
Gastric emptying	Decreased during labor	Increased risk for aspiration
Breathing
Diaphragm	Displaced cephalad	Place chest tubes at higher intercostal space
Respiratory rate	No change
Tidal volume	Increased 35%–45%
pH	7.42–7.46, partially compensated respiratory alkalosis
Pa co ₂	28–32 mm Hg	Reflects normal hyperventilation
HCO ₃ ⁻	19–22 mEq/L	Reduced buffering capacity
Base deficit	2–3 mEq/L
Pa o ₂	100–107 mm Hg
Circulation
Blood volume	Increased by 40%–50%	Significant blood loss may occur before onset of symptoms and hypotension
Cardiac output	Increased by 40%–50%
Heart rate	Increased by 15%–25%	Early diagnosis of hypovolemia more difficult
Systolic blood pressure	Decreased by 5–15 mm Hg (more pronounced during mid-pregnancy)
Diastolic blood pressure	Decreased by 5–15 mm Hg (more pronounced during mid-pregnancy)
Hemoglobin	10–12 g/dL	Physiologic anemia
Gravid uterus	Aortocaval compression	Decreased cardiac output in the supine position; left uterine displacement required
Other
Coagulation factors	Increased	Hypercoagulable state
BUN, creatinine	Decreased	Abnormal measurements often overlooked
Symphysis pubis/sacroiliac joints	Widened	May alter radiographic interpretations

Airway

Airway patency, stabilization, and protection should be ensured as quickly as possible in all critically injured patients, including those who are pregnant. The status of the patient’s airway can be quickly assessed by eliciting a verbal response. The inability to speak is an indication of severely impaired mental status or the inability to move adequate air to mediate phonation, either of which should prompt interventions to secure and protect the airway. Additional means of assessing airway patency include auscultation of the chest, assessment of chest movement, and assessment of air movement at the mouth and nose. Immediate interventions to establish airway patency include head-tilt and jaw-thrust maneuvers, as well as placement of an oral or nasopharyngeal airway to facilitate bag-and-mask ventilation and oxygenation.

It is essential to consider the possibility of cervical spine injury, facial fractures, and skull base injuries. Excessive head-tilt maneuvers can worsen injury if a cervical spine fracture is present. Patients who have sustained severe trauma should be suspected of having a cervical spine injury until proven otherwise. Cervical spine injury must be ruled out by radiographic and physical examination criteria. The cervical spine should be stabilized with a hard collar and in-line stabilization until the severity of injury has been established. In cases of documented cervical spine injury, great care must be taken not to worsen spinal cord injury. A nasopharyngeal airway should not be placed in patients with suspected facial or skull base fractures to avoid further trauma and worsening of preexisting conditions.

Most patients who require interventions to open or support the airway, as just described, will ultimately require tracheal intubation. Indications for tracheal intubation include impaired mental status, airway obstruction, inability to clear secretions or blood from the airway, inadequate spontaneous ventilation, and hypoxemia that is refractory to supplemental oxygen administration. Tracheal intubation of pregnant patients is complicated by changes in respiratory system structure and function (see Table 53.1 ) (see Chapter 29 ). Among the most prominent alterations are airway (including vocal cord) edema, decreased functional residual capacity, and increased oxygen consumption. Airway edema impairs vocal cord visualization, thus complicating laryngoscopy and tracheal intubation. Decreased functional residual capacity and increased oxygen consumption result in more rapid oxyhemoglobin desaturation during periods of apnea. These factors increase the risk for failed tracheal intubation and hypoxemia.

Gastric emptying is normal in pregnant women before the onset of labor (see Chapter 28 ). However, lower esophageal sphincter tone is commonly decreased in pregnant women (see Table 53.1 ). Thus, pregnant women are at increased risk for regurgitation and pulmonary aspiration of gastric contents and, similar to all trauma victims, are considered to have a full stomach on arrival in the emergency department or operating room. Therefore, in most cases, rapid-sequence induction of general anesthesia is performed to facilitate tracheal intubation. However, the specific tracheal intubation technique will depend on the practitioner’s skills and resources, as well as on the location of the patient’s injuries. Alternative approaches to rapid-sequence induction include awake tracheal intubation and tracheostomy.

Several factors can complicate tracheal intubation in the trauma patient. The patient may be combative, which complicates awake tracheal intubation strategies. Blood in the airway can limit the use of a fiberoptic bronchoscope and impair visualization of the glottis when using a standard or video laryngoscope. The presence of facial fractures, direct airway injuries, trauma-induced airway edema, and tracheal deviation can limit access to the airway.

Finally, airway management, including tracheal intubation, is more challenging in the presence of cervical spine injury. If cervical spine injury is present or suspected, it is crucial to avoid flexion, extension, or lateral movement of the neck. The spine is protected using in-line stabilization and/or a hard cervical collar. Airway management devices such as a gum elastic bougie, a video laryngoscope, a lighted intubating stylet, and/or an intubating supraglottic airway (SGA), among others, should be available for use if standard laryngoscopy is difficult or impossible. An SGA such as a laryngeal mask airway can be used to temporarily provide ventilation in cases in which mask ventilation and tracheal intubation have failed, but an SGA will not provide protection from aspiration and should be replaced by a secure airway device as soon as possible. In some cases, cricothyroidotomy or tracheostomy may be necessary to provide a secure airway.

Breathing

Adequate ventilation and oxygenation should be ensured for the benefit of both the mother and the fetus. Supplemental oxygen should be administered immediately, even if the patient is breathing spontaneously. Mechanical ventilation is often necessary after tracheal intubation in patients with respiratory failure and/or hypoxemia. Ventilation can be compromised by trauma-associated factors such as pneumothorax, hemothorax, lung contusion, mediastinal compression, and chest wall injuries. These problems must be identified during the primary survey and treated to optimize ventilation and oxygenation. In women with advanced pregnancy, it may be necessary to place chest tubes in a more cephalad location than normal owing to the cephalad displacement of the diaphragm and intraabdominal structures by the gravid uterus. Pregnant trauma patients should be ventilated to maintain Pa co ₂ at a level that is normal for pregnancy (28 to 32 mm Hg) (see Table 53.1 ). Positive end-expiratory pressure (PEEP) may be added to improve oxygenation, if indicated; however, PEEP should be titrated carefully in the hypovolemic patient because it may impair venous return and worsen cardiac output and organ perfusion.

Circulation

Once respiratory stabilization has been achieved, it is essential to assess cardiovascular function and to determine whether the patient is in shock. Two large-bore peripheral intravenous catheters should be placed in the upper extremities to facilitate resuscitation. Central venous access facilitates rapid resuscitation but may be difficult to obtain. Intraosseous cannulation should be considered if it is difficult or impossible to obtain peripheral or central venous access.

Fluid resuscitation should be initiated using crystalloid solution, but blood transfusion should be considered if significant blood loss is apparent or suspected. Left uterine displacement should be initiated immediately to prevent or minimize aortocaval compression by the gravid uterus. The adverse effects of aortocaval compression may be exacerbated during periods of trauma-associated hypovolemia. The use of the pneumatic antishock garment to stabilize fractures or control hemorrhage is relatively contraindicated in pregnant women owing to its adverse effects on venous return.

The hallmark clinical signs of shock are listed in Box 53.3 . The presence of these signs indicates a need for timely and appropriate fluid resuscitation. A rapid assessment of sources of blood loss should be performed. In trauma victims, the most common locations of exsanguinating blood loss are the chest, abdomen, retroperitoneum, long bones, and external sites. In the pregnant trauma patient, placental abruption and uterine rupture are also potential sources of hemorrhage. A brief physical examination will identify fractures of the long bones and external sites of bleeding. Thoracic blood loss and pelvic fractures can be identified by chest and pelvic radiographs, respectively. Focused abdominal sonography in trauma (FAST) or diagnostic peritoneal lavage can be used to identify intraabdominal bleeding. However, diagnostic peritoneal lavage may be difficult to perform safely in advanced pregnancy. FAST can be rapidly performed to assess the hepatorenal, splenorenal, and pelvic spaces, which are the most common sites of major hemorrhage in trauma patients. FAST can also be used to assess uteroplacental integrity and the presence of intrauterine bleeding. Finally, ultrasonography facilitates assessment of cardiac filling and recognition of cardiac tamponade in patients with thoracic trauma.

Box 53.3

Clinical Signs of Shock in the Trauma Patient

•
Agitation
•
Confusion
•
Poor capillary refill
•
Mottled appearance
•
Cool extremities
•
Diaphoresis
•
Tachypnea
•
Tachycardia
•
Weak distal pulses
•
Hypotension
•
Decreased pulse pressure
•
Decreased urine output
•
Lactic acidosis

It is important to recognize that pregnant trauma patients may lose a significant amount of blood before the development of hypotension. Pregnant patients have a 40% to 50% increase in blood volume by the third trimester. Classic signs of hypovolemia, such as tachycardia, hypotension, and poor capillary refill, may not be evident until blood loss approaches 1.5 to 2 L. Therefore, it is likely that a pregnant trauma victim will have lost significantly more blood volume and oxygen-carrying capacity than a comparable nonpregnant patient when signs of cardiovascular deterioration become evident. Resuscitation should be guided by apparent blood loss to maintain adequate maternal cardiac output and uteroplacental perfusion. Because of the physiologic anemia of pregnancy, oxygen-carrying capacity may be significantly impaired at the time that hypovolemia becomes evident. In addition, maternal perfusion of vital organs is often sustained at the expense of uteroplacental perfusion. Uterine blood flow may decrease by as much as 30% before the mother shows signs of hypovolemia. Therefore, a nonreassuring fetal heart rate (FHR) pattern may be the first sign of significant intravascular volume loss. Fluids should be warmed to minimize the risk for hypothermia, which can contribute to coagulopathy, arrhythmias, and altered drug responses.

Fluid resuscitation

Current practice supports the use of crystalloid solutions to resuscitate the hypovolemic trauma victim during the early phases of resuscitation, with the caveat that recent studies show the benefits of early damage control resuscitation using blood products. Furthermore, the benefits and harm of crystalloid versus colloid have yet to be fully resolved. The Saline versus Albumin Fluid Evaluation (SAFE) did not show any difference in survival in nonpregnant trauma patients randomized to receive resuscitation with colloid or crystalloid, with the exception of patients with head trauma, who had poorer outcomes when resuscitated with albumin. The CRISTAL trial also did not demonstrate differences in 28-day mortality when comparing crystalloid to colloid, but 90-day mortality was lower in patients who received colloid. However, the authors considered the results exploratory and cautioned against conclusions about the efficacy of colloid solutions until further investigations are completed.

Balanced salt solutions (lactated Ringer’s solution, PlasmaLyte) are typically preferred over normal saline in patients without closed head injury. Balanced salt solutions have significant buffering properties and are less likely than normal saline solution to cause hyperchloremic metabolic acidosis during high-volume resuscitation. A 2018 trial showed that the use of balanced crystalloids for resuscitation of critically ill patients was associated with a lower incidence of the composite outcome (death, need for renal-replacement therapy, or renal dysfunction) compared with normal saline. Other buffered salt solutions, such as Ringer’s ethyl pyruvate and Ringer’s hydroxybutyrate, also may have value. Currently, no evidence supports the use of one buffered isotonic crystalloid solution over another.

The use of hypertonic crystalloid solutions such as 3% sodium chloride is controversial; currently, no evidence supports their routine use in pregnant trauma victims who did not suffer traumatic brain injury (TBI). Hypernatremia is a risk in patients resuscitated with hypertonic saline, and some studies have shown increased mortality in patients resuscitated with hypertonic crystalloid solutions. In a 2017 systematic review, Wu et al. did not identify significant survival or complication risk associated with hypertonic saline resuscitation compared with isotonic saline in patients with hemorrhagic shock. In contrast, Asehnoune et al. reported improved adjusted 90-day survival in trauma patients with TBI and intracranial hypertension treated with continuous hyperosmolar therapy. Metaanalyses from 2020 and 2022 showed that treatment of trauma patients suffering TBI and intracranial hypertension with hypertonic saline results in decreased intracranial pressure (ICP) and secondary brain injury. The use of 3% saline was most effective and provided more sustained decreases in ICP and improvement in cerebral perfusion compared to mannitol. In general, hypertonic resuscitation does not appear to be beneficial to trauma patients without TBI but likely benefits patients with TBI and elevated ICP.

Some practitioners have advocated hypovolemic resuscitation in patients with major hemorrhage after trauma. This technique employs permissive hypotension (systolic blood pressure of 80 to 90 mm Hg) until hemorrhage can be controlled in the operative setting. The underlying premise of hypovolemic (hypotensive) resuscitation is that overresuscitation worsens ongoing blood loss because of higher perfusion pressure and dilution of clotting factors. Small boluses of fluids are administered to maintain perfusion in patients without evidence of closed head injury. The use of hypotensive resuscitation is likely detrimental in patients with closed head injury because it is crucial to maintain adequate cerebral perfusion pressure (CPP) in patients with elevated ICP. (CPP is the difference between mean arterial pressure [MAP] and ICP.) No definitive published data support the use of hypotensive resuscitation in pregnant trauma patients. Current guidelines do not support this approach because it may compromise uteroplacental perfusion.

The resuscitative endovascular balloon occlusion of the aorta (REBOA) catheter is a large-vessel occlusion device that is typically deployed into the aorta during periods of severe intraabdominal and pelvic hemorrhage, and is becoming increasingly utilized in cases of major trauma. A proximal pressure transducer is used to titrate balloon inflation to maintain central pressures and limit downstream bleeding as reparative procedures are executed. The device is a less invasive alternative to emergency department thoracotomy and aortic cross-clamping to temporize noncompressible torso hemorrhage. In patients without penetrating thoracic injury, Brenner et al. reported a survival benefit for REBOA compared with patients who received resuscitative thoracotomy. A 2023 randomized clinical trial among trauma victims with hemorrhagic shock in the United Kingdom found increased mortality with the use of REBOA (odds ratio, 1.58; 95% credible interval 0.72 to 3.52). Thus, the efficacy of using the REBOA during trauma resuscitation remains to be fully determined in all subsets of trauma patients with hemorrhage. The effectiveness and safety of the REBOA catheter remain to be established in critically injured pregnant patients.

Damage control principles and resuscitation

The traditional approach to treatment of traumatic life-threatening injuries has been definitive operative repair. However, some patients experience progressive physiologic decline during long surgical procedures and develop severe derangements such as hypothermia, metabolic acidosis, and coagulopathy, a combination that has become known as the deadly triad. These pathologic alterations require rapid and effective treatment to prevent severe morbidity and death. More recently, practitioners have advocated the use of a more targeted surgical approach, termed damage control surgery, which is initiated to control hemorrhage without providing early definitive repair of injuries. Major surgical bleeding is controlled, and the thoracic and abdominal cavities are packed to provide hemostasis. Gastrointestinal diversion is performed, and body cavities are temporarily closed, often using vacuum-type closure systems. Active volume resuscitation is performed using blood products rather than crystalloids, an approach known as damage control resuscitation, to achieve metabolic homeostasis. Once stable hemodynamic and acid-base status, coagulation function, and temperature are achieved, the patient is returned to the operating room for definitive repair of injuries.

Blood products

All trauma centers should have rapid access to type O, Rh-negative blood for emergency use before type-specific or cross-matched blood is available. Trauma specialists advocate for damage-control resuscitation using packed RBCs, platelets, and plasma units mixed in equal proportions (1:1:1). Several investigators have reported the value of this approach in military practice, and they have specifically observed that this approach results in more effective resuscitation, less coagulopathy, and improved survival than more traditional approaches utilizing crystalloids. Based on experience over the last few years, damage-control resuscitation is also considered to be the optimal strategy for managing civilian patients with exsanguinating trauma. The Pragmatic, Randomized, Optimal Platelet and Plasma Ratios (PROPPR) trial showed that damage-control surgery and balanced blood product resuscitation (1:1:1 ratio) is associated with improved hemostasis at 3 hours after intervention and a decreased incidence of death by exsanguination at 24 hours after injury, although overall mortality at 24 hours and 30 days after injury was not improved compared with patients receiving damage-control surgery with blood products in a 1:1:2 ratio. Based on current evidence, the Eastern Association for the Surgery of Trauma recommends the use of balanced blood product resuscitation in exsanguinating trauma patients.

Despite implementation of damage-control resuscitation, coagulopathy remains a significant problem for trauma patients requiring large-volume resuscitation. Damage-control resuscitation provides clotting factors via transfused plasma and direct administration of platelets. However, tissue injury and release of endogenous anticoagulants often result in sustained alterations in coagulation. Consequently, some practitioners advocate adopting a goal-directed approach to treat trauma-induced coagulopathy based on viscoelastic monitoring, either with thromboelastography or rotational thromboelastometry (see Chapter 44 ). Gonzalez et al. reported that goal-directed treatment of trauma-associated coagulopathy, compared with standard assessment of coagulation status, was associated with lower mortality and decreased use of plasma and platelets during the acute phase of resuscitation. However, the study had limitations, and further work is needed to define the benefits of goal-directed treatment of coagulopathy in the trauma patient suffering large-volume hemorrhage.

Secondary Survey

As in all trauma cases, it is crucial to evaluate the mother for significant abdominal, thoracic, orthopedic, and neurologic injuries. A head-to-toe examination should be performed to determine the presence of injuries and the need for intervention. A more detailed evaluation of neurologic function, as well as examination of the head and neck, should be performed. This survey includes examination of posterior structures that may be obscured by the supine position and the presence of a cervical collar. The torso should be examined to identify thoracic and abdominal injuries. The thoracic examination should include chest auscultation, inspection, and palpation. Palpation of the abdomen should be performed to evaluate abdominal tenderness, and a rectal examination should be performed to identify evidence of intraluminal bleeding. The extremities must be examined to identify deformities, and each joint should be manipulated. Distal perfusion of the extremities must be continuously monitored, especially in limbs that show signs of significant injury. This is accomplished by evaluation of distal pulses and capillary refill. In cases of penetrating injury, the sites of entry and exit should be identified. It is especially important to carefully examine the areas that are difficult to access such as the oral cavity, perineum, axilla, scalp, and back. Once the secondary survey has been performed, more targeted assessments of suspected injuries can be performed using radiologic imaging.

Fetal survey

After initial stabilization of the mother, information about the pregnancy should be gathered through a focused history and physical examination. The history should include the date of the last menstrual period, expected date of delivery, and status of the pregnancy. In cases in which there is uncertainty regarding fetal age, an approximate determination can be made by measuring fundal height. The fetal age is estimated to be 1 week for each centimeter of fundal height above the symphysis pubis. In addition to the assessment of fundal height, the abdominal examination should include an assessment of uterine tenderness and consistency, the presence or absence of uterine contractions, and fetal position and movement.

A pelvic examination should be performed to evaluate cervical dilation and effacement, fetal station, and the presence of amniotic fluid and blood. The FHR is assessed by Doppler auscultation or ultrasonography. If maternal stability permits, ultrasonography facilitates estimation of fetal age and assessment of uteroplacental injury.

If no fetal cardiac activity is identified, fetal resuscitation should not be attempted (see Fig. 53.1 ). In a series of 441 pregnant trauma patients, the absence of a detectable FHR was associated with fetal death in all cases. When an FHR is detected, an assessment of fetal viability should be performed. An estimated gestational age of 23 to 24 weeks and an estimated fetal weight of 500 g are common thresholds for extrauterine fetal viability. The FHR should be monitored in cases in which the fetus is determined to be viable. In cases in which a nonviable fetus is present, the importance of FHR monitoring is unclear. However, alterations in FHR and FHR variability may signal maternal deterioration and serve as a good monitor of the effectiveness of maternal resuscitation.

FHR monitoring is generally performed with external Doppler auscultation, and a tocodynamometer is used to assess uterine contractions. Adverse fetal outcomes are unlikely in cases with a reassuring FHR tracing (see Chapters 6 and 8 ) and no early-warning signs of uteroplacental injury (bleeding, abdominal pain). In contrast, an abnormal FHR tracing or evidence of uteroplacental injury (vaginal bleeding, uterine contractions, uterine tenderness, presence of amniotic fluid on vaginal examination) predicts poor fetal outcome in approximately 50% of cases.

Fetal Monitoring

Continuous electronic FHR monitoring is the current standard of care for pregnant trauma victims with a viable fetus. FHR monitoring should be initiated as soon as maternal stabilization allows because placental abruption can occur early during the course of resuscitation. Continuous electronic FHR monitoring is more sensitive for placental abruption than ultrasonography, physical examination, or Kleihauer-Betke testing. Occasional uterine contractions are common after trauma and are usually not associated with poor fetal outcome. Random uterine contractions usually resolve within a few hours of the trauma. However, regular and prolonged uterine contractions (eight contractions per hour for more than 4 hours) are associated with placental abruption, which has a high fetal mortality rate. The diagnosis of placental abruption should trigger immediate cesarean delivery for both fetal and maternal indications; a large percentage of viable fetuses can be rescued if expedited delivery is performed, and placental abruption will exacerbate maternal hemorrhage and coagulopathy. The presence of fetal bradycardia and/or frequent late FHR decelerations should also prompt delivery if the mother is stable and adequately resuscitated.

The ideal duration of FHR monitoring has not been determined. However, a common practice, based on a prospective study of 60 pregnant trauma patients at more than 20 weeks’ gestation, is to monitor the FHR for 4 hours. If maternal-fetal abnormalities are not detected within 4 hours, it is generally considered safe to discontinue FHR monitoring because a normal FHR tracing has a negative predictive value of 100% when combined with a normal maternal physical examination. However, the presence of abnormalities such as vaginal bleeding, spontaneous rupture of membranes, category II and III FHR patterns (see Box 8.3 ), persistent uterine contractions, uterine tenderness, abdominal pain, and/or need for maternal analgesia should prompt further FHR monitoring. The sensitivity of ultrasonography for placental abruption ranges from 50% to 80%, but ultrasonography is a safe and effective means of assessing fetal viability, FHR, placental location, gestational age, and amniotic fluid volume. It is particularly valuable in the presence of maternal tachycardia, when it can be difficult to differentiate maternal and FHRs using Doppler auscultation.

Laboratory Studies

Laboratory evaluation in pregnant trauma patients does not differ from the evaluation for nonpregnant patients, with a few exceptions. As for all trauma patients, the laboratory evaluation will be driven by the type and severity of injury. For most patients with significant injury, standard analysis includes a complete blood cell count, coagulation studies, serum electrolyte measurements, blood glucose and lactate levels, liver function tests, arterial blood gas analysis, urinalysis, and toxicology screening, as well as sending a blood sample for typing and cross-matching for compatible blood products ( Box 53.4 ).

Box 53.4

Initial Laboratory Analysis for the Pregnant Trauma Patient

•
Blood type and cross-match
•
Complete blood cell count
•
Prothrombin (INR) and partial thromboplastin times
•
Fibrinogen
•
Serum electrolytes, BUN, creatinine, glucose
•
Liver function tests
•
Serum amylase level
•
Blood lactate
•
Arterial blood gas measurement
•
Toxicology screen
•
Kleihauer-Betke assay
•
Urinalysis

BUN , Blood urea nitrogen; INR , international normalized ratio.

The presence of disseminated intravascular coagulation (DIC) and low blood bicarbonate levels is associated with poor fetal outcome. Both abnormalities reflect severe maternal injury and should prompt aggressive maternal resuscitation. Of special consideration in pregnant trauma patients is maternal-fetal hemorrhage. The Kleihauer-Betke test is used to detect the entry of fetal blood into the maternal circulation. Although typically performed in Rh ₀ (D) antigen–negative mothers to detect transplacental hemorrhage and the potential for developing Rh ₀ (D) sensitization, this test may help predict adverse fetal outcomes in all pregnant trauma patients (see earlier discussion).

Imaging Studies

The pregnant trauma patient often requires imaging to evaluate orthopedic, head, thoracic, and abdominal injuries. Although many patients and physicians are concerned about the fetal effects of ionizing radiation, the risks for teratogenesis, malignancy, and gene mutation are small with a radiation exposure < 5 to 10 rads (see Chapter 18 ). Less than 1% of trauma patients receive more than 3 rads of radiation exposure. Shielding of the fetus with lead is no longer recommended as this provides negligible benefits and may negatively affect the efficacy of the examination. Intravenous pyelography subjects the fetus to as much as 1.4 rads of exposure, but the test can be invaluable in diagnosing injuries to the kidneys, ureters, and bladder. Computed tomography (CT) is associated with greater radiation exposure than plain radiography, but exposure levels are generally below that considered to be dangerous to the fetus. Modern multidetector (multislice) CT results in higher fetal radiation exposure, but it has significant advantages in speed and image resolution. Overall, the small risk for fetal radiation exposure is outweighed by the benefits to the injured mother and, by extension, the fetus.

Injury Scoring

Several injury scoring scales have been developed over the past 40 years. The scoring systems provide a framework for standardizing clinical management, benchmarking outcomes, and planning research. Presently, no reliable scoring tool exists for predicting maternal or fetal outcome after trauma. Currently used scoring systems include (1) anatomic injury scales that rely on physical examination and diagnostic procedures, (2) physiologic injury scales that rely on assessment of physiologic responses and function, and (3) combination injury scales.

One of the first anatomy-based injury scales was the Abbreviated Injury Scale (AIS) developed by the Association for the Advancement of Automotive Medicine. Each of nine body regions is given an ISS that ranges from 1 (minor) to 6 (maximal [currently untreatable]). Although the AIS effectively describes the severity of injuries at specific locations, it provides a limited assessment of the overall pathophysiologic impact of all injuries. The ISS , which was developed to address this issue, is obtained by summing the square of the three highest severity scores from the AIS. The ISS ranges from 1 to 75. Minor injuries are classified as an ISS of less than 9; moderate, from 9 to 15; serious, from 16 to 25; and severe, greater than 25. The ISS correlates with the risk for preterm delivery after trauma, but its value in predicting fetal death, placental abruption, and other adverse outcomes is controversial. The American Association for the Surgery of Trauma developed the Organ Injury Scale ; this organ-based severity scale is designed to facilitate clinical investigation and outcomes research.

The value of injury scoring scales in predicting adverse maternal and fetal outcomes remains to be established. Distelhorst et al. reported improved birth outcomes in pregnant patients treated at dedicated trauma centers. However, after controlling for the ISS, the level of trauma designation was not associated with any differences in most birth outcomes, with the exception of higher risk for preterm labor and meconium-stained amniotic fluid at level 1 and 2 centers compared with level 3 and 4 centers. It is not known whether trauma-level designation correlates with level of maternal care designation (see Chapter 11 ) or whether level of maternal care designation predicts trauma outcomes during pregnancy.

Anatomic scoring systems have value in describing the extent and severity of injuries to specific organ systems. However, physiologic scoring systems may add prognostic value. The Glasgow Coma Scale (GCS) , which is among the most widely used physiologic scoring systems, evaluates the neurologic status of the trauma patient. The GCS evaluates eye opening, verbal response, and motor activity; scores range from 3 to 15, with 3 indicating the absence of neurologic activity and 15 representing intact neurologic function. A GCS score < 9 reflects severe impairment, whereas a score of 9 to 12 reflects moderate disability. However, concerns have been raised about interrater reliability and lack of prognostic utility for the GCS. Some researchers have proposed that a simplified motor score would be more reliable. Evidence suggests that the GCS score has a poor correlation with fetal outcome.

Traumatic Brain Injury

Brain injury is common in patients who suffer from motor vehicle crashes, and it is a major cause of mortality among pregnant trauma victims. It is important to perform a thorough neurologic examination with particular attention to level of consciousness. Altered mental status may be an indicator of evolving intracranial pathology, intoxication, hypoperfusion, and/or metabolic disturbances. Mental status should be reevaluated frequently because intracranial pathologic processes may not be apparent on initial evaluation and may evolve during resuscitation.

Elevated ICP is a common finding in patients with TBI and may be a significant threat to life. A head CT is the imaging study of choice for identifying the site and severity of intracranial pathologic processes in trauma patients, and it should be performed within 1 hour of arrival in the emergency department.

Crystalloid or damage control resuscitation using blood products should be used for resuscitation in patients with TBI; resuscitation with albumin is deleterious in patients with TBI (see earlier discussion). Evidence indicates that selective use of 3% hypertonic saline in patients with TBI and intracranial hypertension may be beneficial. Hypotensive resuscitation is contraindicated in patients with TBI and elevated ICP. It is crucial to maintain MAP and CPP to minimize the risk for brain ischemia and permanent brain injury. The extent of brain injury will worsen if CPP is not maintained. It is also important to maintain cerebral oxygen delivery by optimizing maternal cardiac output and blood oxygen-carrying capacity.

It may be necessary to intubate the trachea of patients with deteriorating mental status for airway protection and provision of ventilatory support. Hypoventilation should be avoided because it increases ICP. Hyperventilation to a Pa co ₂ between 25 and 30 mm Hg will provide a transient decrease in ICP and may be useful until definitive treatment can be initiated. However, hyperventilation can be disadvantageous for the fetus because it can decrease uteroplacental blood flow by decreasing maternal cardiac output and blood pressure, and perhaps by causing uteroplacental vasoconstriction. Therefore, it is prudent to maintain Pa co ₂ at levels that are normal in pregnant women (28 to 32 mm Hg). Additional maneuvers to decrease ICP include treatment with a diuretic such as mannitol or furosemide and elevation of the head 30 to 45 degrees. Treatment with hypertonic saline can also decrease intracranial volume and ICP, and may improve outcomes in patients with TBI.

Corticosteroids are no longer recommended for patients with TBI because their administration in this setting is associated with increased mortality. Barbiturates decrease cerebral oxygen use and blood flow and may provide cerebral protection in patients with severe impairment. Both mannitol and furosemide cross the placenta and could cause alterations in fetal plasma osmolality and decrease fetal intravascular volume. However, concern regarding adverse fetal effects should be overridden by the needs of the mother in cases of TBI.

Cardiopulmonary Resuscitation

The incidence of cardiac arrest in pregnancy is reported to be 1:20,000 to 1:40,000 patients in industrialized countries. Cardiac arrest during hospitalization for delivery is more common because it includes postpartum cardiac arrest. The most frequent causes are trauma, peripartum hemorrhage, embolic phenomena, stroke, preeclampsia/eclampsia, sepsis, status asthmaticus, and anesthesia-related complications.

Cardiopulmonary resuscitation should be initiated immediately (see Chapter 41 ). The 2020 American Heart Association (AHA) guidelines highlight the importance of initiating high-quality chest compressions to facilitate circulation. Guidelines have simplified the list of modifications to cardiopulmonary resuscitation during pregnancy ( Box 53.5 ) ; pregnant women benefit from standard high-quality cardiopulmonary resuscitation similar to that performed in nonpregnant patients. Hands should be placed in the usual location on the center of the victim’s chest; there is no scientific evidence to support changing the hand position from that used to resuscitate nonpregnant patients. Chest compressions should be performed at a rate of 100 per minute at a depth of at least 5 cm. Interruptions should be minimized. Cardiac arrest in the pregnant patient is complicated by the physiologic changes of pregnancy, particularly the effect of the gravid uterus on aortocaval blood flow. Well-performed chest compressions in the nonpregnant patient typically result in cardiac output that is approximately 30% of normal. In pregnant patients, aortocaval compression reduces the cardiac output that results from chest compressions. Therefore, the AHA guidelines advocate manual left uterine displacement with the patient in the supine position ( Fig. 53.2 ).

Box 53.5

Modification of Cardiopulmonary Resuscitation During Pregnancy

Summarized from Jeejeebhoy FM, Zelop CM, Lipman S, et al. Cardiac arrest in pregnancy: a scientific statement from the American Heart Association. Circulation . 2015;132:1747–1773; Lipman S, Cohen S, Einav S, et al. The Society for Obstetric Anesthesia and Perinatology consensus statement on the management of cardiac arrest in pregnancy. Anesth Analg . 2014;118:1003–1016.

•
Perform manual left uterine displacement (see Fig. 53.2 ).
•
Anticipate difficult airway management.
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Obtain intravenous access above the diaphragm.
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If patient is receiving magnesium sulfate, discontinue magnesium infusion and administer calcium chloride or calcium gluconate.
•
Remove all fetal monitors before delivery; internal fetal monitors may be cut externally. Fetal monitor removal should not delay defibrillation.
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If spontaneous circulation does not return with usual resuscitative measures, resuscitative hysterotomy or cesarean delivery should be performed if gestational age is 20 w or greater, aiming for delivery within 5 min of cardiac arrest.
•
Continue all resuscitation efforts during and after cesarean delivery.

An illustration shows two medical staff performing manual left uterine displacement on a pregnant woman lying on her back. — Fig. 53.2

Due to the increased propensity for pregnant patients to become hypoxic, if an arrest occurs in the hospital setting, the airway should be quickly secured and the mother ventilated with 100% oxygen. Chest impedance is unchanged during pregnancy; therefore, the usual voltage levels for defibrillation should be used in pregnant patients. Electric cardioversion during pregnancy appears to be safe for the fetus (see Chapter 41 ); removal of fetal scalp electrodes should not delay maternal defibrillation. Intravenous or intraosseous access should be secured to facilitate resuscitation. Advanced Cardiac Life Support guidelines should be followed to identify and treat causes of cardiopulmonary arrest. The use of transthoracic echocardiography (TTE) to identify causes of cardiac arrest in pregnancy may prove difficult, as the traditional subxiphoid view may be impossible in a pregnant patient at term. Chest compressions should not be delayed for TTE. Important etiologies of maternal cardiac arrest, such as pulmonary embolism and amniotic fluid embolism, may reveal profound right heart dysfunction on bedside exam, while cardiac arrest due to hypovolemic shock may reveal an underfilled left ventricle.

If the return of spontaneous circulation does not occur with the usual resuscitative measures, and if the fundal height is at or above the umbilicus (approximately 20 weeks’ gestation), the AHA recommends that cesarean delivery ( resuscitative hysterotomy ) should be performed within 5 minutes of cardiac arrest. Timely delivery facilitates successful resuscitation of both the mother and the infant. If possible, preparations for perimortem cesarean delivery should occur while resuscitative measures are initiated. The patient should not be moved to the operating room for the procedure, but rather it should be performed at the location of the cardiac arrest. Early uterine evacuation optimizes maternal resuscitation, even if the fetus has already died.

A 2012 systematic review of case reports identified 54% survival to hospital discharge among 94 women suffering cardiac arrest during pregnancy; increased survival was associated with decreased time to cesarean delivery. In a prospective descriptive study performed in the United Kingdom, Beckett et al. reported a 42% mortality rate for women suffering cardiac arrest during pregnancy. Survival was lowest among women who arrested at home, for whom timely cesarean delivery was not available. After 24 weeks’ gestational age, delivery improved perinatal survival. In the UK cohort, 79% (46/58) of infants delivered during maternal cardiac arrest survived, including the offspring of 14 women who did not survive.

The 2020 AHA guidelines recommend targeted temperature management for post–cardiac arrest care in the pregnant patient. However, targeted temperature management for out-of-hospital cardiac arrest in nonpregnant patients has recently been challenged. Therefore, it should be considered on a case-by-case basis in the pregnant population; if pregnant patients are therapeutically cooled, continuous fetal monitoring is warranted.

Management of the Brain-Dead Patient

Brain death in the pregnant patient is a rare occurrence; however, several summaries of case reports have been published. Esmaeilzadeh et al. summarized 30 cases published between 1982 and 2010. Nontraumatic brain injury, primarily intracranial hemorrhage, was the cause of death in 26 of 30 cases. The mean gestational ages at times of injury and delivery were 22 and 30 weeks, respectively. Twelve viable infants survived beyond the neonatal period.

In cases of maternal brain death, care providers should focus on saving the life of the fetus; maternal organ preservation for harvest and donation is a secondary consideration. Maintenance of vital functions in mothers with catastrophic brain injury is justified to meet these two goals, but in many cases ethical and legal concerns must be addressed. Consideration must be given to gestational age and the chance for fetal survival. Before 23 weeks’ gestation, the chance for extrauterine fetal survival is small. In general, management should follow current guidelines for organ preservation therapy.

The question of whether to preserve maternal circulation and organ function to facilitate fetal development is an ethical, legal, and social dilemma. A fundamental issue relates to the support of the brain-dead mother as an incubator for the unborn fetus. It is important to recognize that, in the case of maternal brain death, the primary patient is no longer the pregnant woman, but the fetus. In many cases, the mother’s wishes are not known, but it in most cases it is ethically permissible to consider corporeal support to allow for delivery at a later gestational age. Currently, there is no generally accepted lower limit of gestational age for maintenance of maternal support. A systematic review by Dodaro et al. specifically examined cases of brain death in pregnancy in which attempts were made at maternal somatic support to maximize fetal outcomes. The researchers found, much like previously published case reports, a predominance of brain death due to intracranial hemorrhage, subarachnoid hemorrhage, and hematoma. A predominance of fetuses were born via cesarean, and most (77%) survived, with increasing survival at later gestational ages. While these data may help to frame the decision-making process around maternal somatic support, each case must be addressed on an individual basis, with close communication among the family, a cohort of care providers, and the hospital ethics committee.

CRITICAL CARE DURING PREGNANCY

Stroke

Ischemic Stroke

Pregnant women are at increased risk for ischemic stroke compared with their nonpregnant counterparts. This risk increases with the presence of hypertensive disorders of pregnancy. New data suggest that the presence of infection on the delivery admission is an important risk factor for peripartum stroke. Pregnancy is a hypercoagulable state characterized by decreased fibrinolysis, increased levels of clotting factors, and decreased levels of certain natural anticoagulants (e.g., protein S). The increased preload associated with pregnancy can combine with a hypercoagulable state to increase the risk of stroke due to a patent foramen ovale.

Clinical manifestations of ischemic stroke are similar to those seen in the young, nonpregnant population and include focal neurologic symptoms, seizures, decreased level of consciousness, and abnormal cranial nerve function. Once the diagnosis is suspected, and initial evaluation and therapy—including airway protection—have been addressed, a non–contrast-enhanced CT should follow immediately. The fetal radiation exposure from this test is less than 1 rad. If the CT shows no evidence of hemorrhagic stroke, the patient is assumed to have an ischemic stroke. Magnetic resonance imaging (MRI) is more sensitive in detecting early ischemic events; however, the test is more time-consuming and may not be emergently available. Consideration of thrombolytic therapy should follow, including evaluation of contraindications for thrombolytic therapy ( Box 53.6 ). Thrombolytic therapy with recombinant tissue plasminogen activator (r-tPA) has been reported during pregnancy and appears to be safe for the fetus; transplacental passage of r-tPA is minimal. However, retroplacental bleeding with pregnancy loss has been reported. A consultation with an experienced neurologist is recommended.

Box 53.6

Major Contraindications for Thrombolysis in Ischemic Stroke Patients

Summarized from Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke . 2018;49:e46–e110.

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History of a previous intracranial hemorrhage
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Genitourinary or gastrointestinal bleeding in the previous 3 w
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Closed head trauma in the previous 3 mo
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Major surgery in the previous 2 w
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Blood pressure > 185/110 mm Hg despite antihypertensive therapy
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Acute active bleeding
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Evidence that symptoms are clearing spontaneously
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Hemorrhagic transformation on initial imaging
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Massive ischemic stroke (hypodensity affecting more than one-third of the cerebral hemisphere)
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Platelet count < 100,000/μL
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Concurrent heparin or warfarin therapy with prolonged PT or aPTT
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Blood glucose < 50 mg/dL (symptoms may be caused by hypoglycemia)
•
Evidence of a seizure with postictal residual neurologic impairment

aPTT , Activated partial thromboplastin time; PT , prothrombin time.

The r-tPA is administered intravenously at a dose of 0.9 mg/kg (maximum, 90 mg) over 1 hour (10% of the dose is commonly administered as an initial bolus over the first minute). The therapeutic window (i.e., time from onset of symptoms to administration of the agent) is 4.5 hours. Patients who are candidates for this therapy should be watched closely in an ICU environment that includes fetal surveillance by a maternal-fetal medicine specialist. Blood pressure should be maintained below 180/105 mm Hg during r-tPA therapy with the use of agents such as labetalol or nicardipine. Neurologic deterioration during thrombolytic infusion should raise the suspicion of hemorrhagic transformation ; the infusion should be stopped immediately and the head CT should be repeated. If hemorrhagic transformation is present, reversal of r-tPA is achieved with administration of cryoprecipitate (10 units) with the goal of maintaining a serum fibrinogen level above 150 mg/dL. The added benefit of platelet transfusion is not clear. If cryoprecipitate or fibrinogen concentrate is not available, tranexamic acid 1 g intravenously may be administered.

Patients with ischemic stroke who are not candidates for r-tPA therapy should receive aspirin (162 to 325 mg/day) for 1 to 2 weeks; subsequently, the dose may be decreased to 100 mg/day. Deep vein thrombosis prophylaxis with unfractionated heparin or low-molecular-weight heparin should also be started on admission unless contraindicated.

Outcome data related to blood pressure management in patients with acute ischemic stroke are inconsistent. In 2018 the AHA and the American Stroke Association recommended that in patients who are not receiving thrombolytic therapy, emergency antihypertensive medication should be withheld unless the blood pressure is higher than 220/120 mm Hg. This recommendation does not apply to women with ischemic stroke in the presence of preeclampsia, in whom current guidelines recommend treatment with antihypertensive agents if the blood pressure is greater than 160/110 mm Hg. If the patient has received thrombolytic therapy, aspirin and prophylactic doses of heparin should be withheld for 24 hours after completion of the infusion. Fever should be aggressively treated to achieve normothermia. Blood glucose control with a target between 140 and 180 mg/dL is recommended in the setting of ischemic stroke. Intravenous insulin may be used as needed. Seizure prophylaxis in ischemic stroke is not recommended.

Cerebral sinus and vein thrombosis may occur during pregnancy and the puerperium, but most cases occur postpartum. The practitioner should suspect cerebral sinus thrombosis in the presence of severe headache, focal neurologic signs, and/or papilledema. The diagnostic test of choice is magnetic resonance venography (MRV). Most cases involve the transverse sinuses. Initial imaging reveals concomitant areas of hemorrhage in as many as 40% of these cases. Despite the latter, treatment involves immediate therapeutic anticoagulation with unfractionated heparin or low-molecular-weight heparin unless a massive hemorrhage is present.

Hemorrhagic Stroke

Pregnancy typically is accompanied by a 40% to 50% increase in both cardiac output and effective blood volume. These changes, coupled with hormone-induced increased fragility of vessel wall structures (secondary to increased levels of estrogen, progesterone, matrix metalloproteinases, and relaxin), may render pregnant patients more susceptible to hemorrhagic stroke resulting in intracerebral and subarachnoid hemorrhage. Half of strokes in pregnancy are hemorrhagic.

Intracerebral hemorrhage

Intracerebral hemorrhage is usually a secondary complication of hypertensive emergencies (e.g., preeclampsia, hypertensive encephalopathy). Clinical presentation is similar to that in nonpregnant individuals. The diagnosis is confirmed with non–contrast-enhanced CT.

As in any other stroke victim, initial management involves securing the airway and facilitating oxygenation and ventilation. ICP monitoring should be considered in patients with a GCS score < 8, clinical evidence of transtentorial herniation, or evidence of significant intraventricular hemorrhage or hydrocephalus.

Blood pressure control in the setting of intracerebral hemorrhage is controversial. Past evidence suggested that acute blood pressure control with the aim of reducing systolic pressure to 140 mm Hg is safe and could be associated with improved functional outcomes. However, evidence from recent clinical trials does not support benefit from strict blood pressure control (systolic blood pressure goal below 140 mm Hg) compared with traditional management (systolic blood pressure goal below 180 mm Hg). In some studies, patients randomized to strict blood pressure control had a higher risk for acute kidney injury. Blood pressure control is currently recommended in patients with intracerebral hemorrhage and a systolic blood pressure >160 to 200 mm Hg. In cases of intracerebral hemorrhage associated with preeclampsia, most practitioners recommend maintenance of systolic and diastolic blood pressures between 140 and 160 mm Hg and 90 to 110 mm Hg, respectively, to maintain uteroplacental perfusion pressure (see Chapter 35 ). Blood pressure should be monitored invasively and treated with a titratable intravenous agent such as labetalol or nicardipine.

In the setting of intracerebral hemorrhage associated with warfarin use, rapid reversal of the anticoagulation effect is of paramount importance. Vitamin K (10 mg intravenously over a minimum of 20 minutes) should be administered, along with prothrombin complex concentrate , which contains the vitamin K–dependent clotting factors II, VII, IX, and X. Prothrombin complex concentrate can be infused over 15 to 30 minutes. The role of recombinant activated factor VII in this setting is limited, and its use is not recommended at this time.

The risk for seizures after intracerebral hemorrhage is higher in cases of lobar hemorrhage; the risk is small if hemorrhage is localized to the basal ganglia, and even less if limited to the posterior fossa. Unless clinical seizures are observed or nonconvulsive activity is noted on the electroencephalogram (EEG), routine seizure prophylaxis in patients with intracerebral hemorrhage is not recommended; therapy may be associated with poorer long-term functional outcome. The exception is intracerebral hemorrhage in the setting of preeclampsia, for which magnesium is indicated for seizure prophylaxis. As with most brain injuries, glucose control is paramount in the management of intracerebral hemorrhage. Blood glucose should be maintained between 140 and 180 mg/dL in critically ill patients with brain injuries. Once bleeding cessation is documented by repeat imaging, deep vein thrombosis prophylaxis with unfractionated heparin or low-molecular-weight heparin should be initiated (usually 1 to 4 days after the intracerebral hemorrhage). Patients should also receive mechanical prophylaxis with sequential compression devices.

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Oct 18, 2026 | Posted by drzezo in ANESTHESIA | Comments Off

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