Critical Care Obstetrics



Critical Care Obstetrics


Luis D. Pacheco

Antonio F. Saad

Mohamed Ibrahim



Introduction

Shock is a condition in which circulation fails to meet the nutritional needs of the cell and remove metabolic wastes.1 Shock may be further divided into four types: hypovolemic, distributive, cardiogenic, and obstructive. Table 25.1 summarizes the characteristics of the most common forms of shock. Table 25.2 describes the most significant pregnancy-induced changes in hemodynamic variables that need to be considered when making the diagnosis of shock in the pregnant patient.

Hypovolemic shock, the most common form seen in obstetrics, is due to excessive blood loss. When the circulating blood volume is less than the capacity of its vascular bed, hypotension with diminished tissue perfusion results, leading to cellular hypoxia, acidosis, and cell death.2 Depending on the duration and severity of the insult, irreversible organ damage or even death may occur. Distributive shock occurs in the setting of pathogenic peripheral vasodilation, resulting in decreased systemic vascular resistance (SVR). Vasodilation occurs typically in septic shock, anaphylactic shock, and neurogenic shock following spinal cord injury. Obstructive shock is characterized by an acute obstruction of blood flow and may be secondary to acute decreases in preload from a tension pneumothorax, cardiac tamponade, or pulmonary embolism. Cardiogenic shock is due to failure of either the right or left ventricle, resulting in inadequate cardiac output. The latter may be secondary to coronary ischemia, acute myocarditis, and nonischemic cardiomyopathies such as peripartum cardiomyopathy.









Initial General Management of Shock in Pregnancy

Algorithm 25.1 summarizes the initial basic management of patients in shock. Several important initial steps should be performed when the diagnosis of shock is made in the obstetric patient. First, two large-bore intravenous (IV) lines, preferably 16-gauge, are placed for rapid expansion of intravascular volume. The use of fluids is usually discouraged in patients with shock due to acute right or left ventricular failures (cardiogenic shock) because it may result in overdistention of a failing right ventricle, and, in cases of a failing left ventricle, fluid will result in pulmonary edema. An indwelling bladder catheter is placed for hourly determination of urine output. An arterial line
allows continuous measurement of systemic blood pressure, as well as easy access for laboratory investigations. Oxygen may be administered via a face mask at 8 to 10 L/min, and the inspired oxygen concentration adjusted according to arterial blood gas results. Inability to protect the airway, poor arterial oxygenation, and airway obstruction may require early endotracheal intubation and mechanical ventilation. In viable pregnancies, electronic fetal monitoring and ultrasound examination are recommended. Importantly, during the initial phase of shock resuscitation, maternal care should not be interrupted or delayed due to fetal concerns.









Screening

Initial laboratory investigation usually includes blood type and cross-match, complete blood count, platelets, fibrinogen, electrolytes, blood urea nitrogen, creatinine, and arterial blood gas. Urine should be sent for analysis and microscopic evaluation as indicated. In cases of suspected sepsis, early cultures (blood, urine, respiratory, genital tract) and serum lactate levels should be obtained without delay.3

An ultrasound-focused initial assessment may easily identify the cause of shock in cases of hypovolemia, left ventricular failure, right ventricular failure, cardiac tamponade, and tension pneumothorax. Hypovolemia is usually suspected in the presence of a collapsed inferior vena cava (IVC) and a “hyperdynamic” appearance of the left ventricle (ie, empty cavity with complete obliteration during systole). Shock from a pulmonary embolism may be suspected with a dilated hypokinetic right ventricle (right ventricle larger than the left ventricle on a four-chamber view) and a distended IVC. Similarly, cardiogenic shock may be diagnosed in a patient with hypotension and pulmonary edema whose imaging reveals a severely dilated and hypokinetic left ventricle.



Nonpharmacologic Treatment


Volume Replacement Therapy

Volume replacement is commonly the first intervention in the management of hypovolemic and distributive shock. In general, fluids may be divided into colloids and crystalloids. Colloids have the theoretical advantage of increasing colloid osmotic pressure, thus resulting in more efficient resuscitation. Despite the latter, there is no evidence that colloids improve outcomes compared to crystalloids.4 In the United States, the only colloid currently recommended in clinical practice is albumin (5% or 25%). In the past, hydroxyethyl starch (HES) was

commonly utilized. However, data have demonstrated that HES leads to acute kidney injury, coagulopathy, and increased mortality (the latter mainly in septic patients). HES should not be used for volume replacement anymore.5






The three most commonly used crystalloids are normal saline, Lactated Ringer’s, and PlasmaLyte. Normal saline contains high concentrations of chloride, which may lead to hyperchloremic nongap metabolic acidosis and acute kidney injury from renal vasoconstriction (induced by hyperchloremia). The electrolyte concentration of balanced crystalloid solutions (PlasmaLyte, Lactated Ringer’s) resembles that of normal plasma, consequently hyperchloremia does not occur. A 2018 clinical trial concluded that, in critically ill patients, use of balanced crystalloids (as opposed to saline) resulted in less mortality, reduced need for renal replacement therapy, and lower incidence of new-onset acute kidney injury.6 As expected, pregnant patients were excluded from the trial; however, there is no reason to believe that the findings would be different in pregnancy. We recommend the use of balanced crystalloids as opposed to normal saline for shock resuscitation. Current guidelines recommend 30 mL/kg of crystalloids in cases of suspected septic shock.7

Overzealous fluid resuscitation should be avoided since there is a linear correlation between positive fluid balance and mortality among critically ill patients.8 The use of passive measurements of preload, such as central venous pressure and pulmonary artery occlusion pressure, to guide fluid resuscitation is discouraged because they do not predict fluid responsiveness.9 We recommend that fluid therapy in shock resuscitation be guided by dynamic measures of preload such as pulse pressure variation (PPV) and/or passive leg raising (PLR). The use of PPV and PLR to predict fluid responsiveness is strongly recommend as opposed to just administering volume indiscriminately because there is a direct correlation between a positive fluid balance and mortality among critically ill patients.

PPV is a dynamic measure of volume responsiveness based on the concept that volume-responsive individuals will have a variation in pulse pressure (systolic-diastolic pressure) above 13% during the respiratory cycle. PPV only predicts fluid responsiveness in patients on mechanical ventilation not triggering the ventilator and on sinus rhythm. An arterial line is necessary to document the variability in pulse pressure.10 Briefly, during inspiration, when the ventilator delivers a preset tidal volume, the intrathoracic pressure increases with a concomitant decrease in preload. The opposite occurs during expiration. This variability in preload will result in different amounts of preload to the left ventricle, with resultant variability in stroke volume (and consequently in pulse pressure) only among individuals who are in fact fluid responsive (stroke volume increases with increased preload and vice versa).

During PLR, the clinician raises the patient’s legs to 30° to 45° for 2 to 3 minutes. This maneuver results in an acute increase in preload to the heart of 300 mL. If the patient is volume responsive, an increase in stroke volume will be present. The latter may be documented with the concomitant use of a noninvasive cardiac output monitor,11 which may utilize pulse contour analysis, bioreactance, or bioimpedance, or are Doppler based with estimation of blood velocity within the thoracic aorta. If baseline cardiac output increases after performing the PLR maneuver, the patient is considered fluid responsive, and fluid should be administered. However, during late pregnancy, the uterus may compress the IVC so that a PLR may fail to increase preload, resulting in a false-negative test.12 To avoid this, we recommend performing a bolus challenge instead. A small fluid bolus (250-500 mL) may be administered through an IV access in an upper extremity. If the cardiac output increases, then the patient will respond to further fluid.

Ultrasound evaluation of the IVC diameter to predict fluid responsiveness has been validated in mechanically ventilated patients. The latter, unfortunately, has not been adequately studied during pregnancy. However, if a collapsed IVC is visualized in a mechanically ventilated pregnant patient with hypotension, it is very likely she will be fluid responsive.

The use of sodium bicarbonate is not recommended during the resuscitation process as it has not been associated with improved outcomes. Specifically, in septic patients, current guidelines discourage its use as long as the pH is above 7.15.7 A recent study failed to document any benefit of bicarbonate administration among critically ill patients with severe metabolic academia.13 Although bicarbonate by itself does not cross the placenta, its administration in a pregnant patient may result in fetal respiratory acidosis because it increases CO2 levels, which can diffuse transplacentally toward the fetus after buffering hydrogen ions.



Blood Component Therapy

Hypovolemic shock frequently requires blood product transfusion. Resuscitation based on crystalloids and packed red cells is strongly discouraged as it results in dilutional coagulopathy and increased mortality. Many massive transfusion protocols now incorporate the concept of hemostatic resuscitation, in which similar ratios of packed red cells, fresh frozen plasma (FFP), and platelets are given regardless of laboratory values. This approach simulates whole blood and has been associated with faster achievement of hemostasis and decreased mortality from exsanguination in trauma patients.14

Transfusion of multiple blood products may result in transfusion-related acute lung injury (TRALI). TRALI is due to the presence of antibodies in the blood product transfused against human leukocyte antigens present in the recipient’s leukocytes. The binding of such antibodies results in leukocyte activation with secretion of proteases and elastases that injure the lung endothelial cells with subsequent noncardiogenic pulmonary edema. The management of TRALI is supportive care with mechanical ventilation when indicated.15

Packed red blood cells (PRBCs) are administered to increase oxygen-carrying capacity to the tissues. Each unit of PRBCs (volume of 200-250 mL) will increase the hemoglobin by 1 g/dL and the hematocrit by 3%. Each unit of FFP (200-250 mL) contains all clotting factors. On average, each unit contains 500 mg of fibrinogen and will raise the serum fibrinogen by 10 mg/dL. Once a unit of FFP is thawed, it should be used within the next 5 days. Ideally, FFP should be ABO compatible, although it does not require cross-matching. If no ABO compatible units are available, the “universal donor type” of FFP is AB because there are no naturally occurring anti-A or anti-B antibodies in these donors. However, due to the rarity of the AB blood type, the use of type A FFP is a safe alternative. In the actively bleeding patient, the platelet count should ideally be maintained above 50,000/mm3. Each unit of platelets (20-40 mL) will increase the platelet count by 5000 to 10,000/mm3. Commonly, platelets are administered as “six-packs”; each six-pack will consequently increase the platelet count by 30,000 to 60,000/mm3. Platelets are stored at room temperature and have a shelf half-life of 1 week.

In the setting of severe obstetrical hemorrhage, we recommend early administration of FFP together with PRBCs and platelets to avoid dilutional coagulopathy.16 In addition, although most massive transfusion protocols do not include cryoprecipitate, during obstetrical hemorrhage we recommend that early administration of cryoprecipitate be strongly considered as early severe fibrinogen consumption is common.

Recently, the use of fibrinogen concentrates has been used to raise serum fibrinogen in actively bleeding patients. It is currently recommended that serum fibrinogen be maintained above 150 to 200 mg/dL with the use of cryoprecipitate or fibrinogen concentrates.17 Cryoprecipitate contains fibronectin and factors I, VIII, von Willebrand, and XIII. Each unit is approximately 20 to 40 mL and contains 150 to 350 mg of fibrinogen. One unit will raise serum fibrinogen by 10 mg/dL and is effective without the need to administer large amounts of volume.


Vasopressor and Inotrope Therapy

Vasopressors (norepinephrine, phenylephrine, vasopressin) are agents that increase blood pressure by increasing SVRs and are usually indicated when a patient is unable to maintain a mean arterial blood pressure (MAP) above 65 mm Hg. Vasopressors are mainly used in the setting of distributive shock (ie, septic, anaphylactic, and neurogenic).

Norepinephrine is the vasopressor of choice in most clinical situations, including septic shock complicating pregnancy.3 It should be administered through a central line to avoid extravasation. The usual starting dose is 0.05 µg/kg/min, which is then titrated until the patient reaches a desired MAP (usually above 65 mm Hg).

Phenylephrine increases blood pressure mainly by increasing SVR. The usual starting dose is 0.5 µg/kg/min. Phenylephrine may result in decreases in cardiac output as it does not provide any inotropic support, and low cardiac output may be worsened by an isolated increase in afterload. Bradycardia is a common side effect.

Vasopressin is a stress hormone secreted by the posterior pituitary. The rationale for the use of exogenous vasopressin during distributive shock is that, in the setting of severe stress, a relative deficiency of endogenous vasopressin may occur.18 In the setting of sepsis, vasopressin is a second-line pressor with a recommended dose of 0.03 U/min. Importantly, the dose is fixed and should not be titrated as higher doses may result in ischemia to different organs, including the heart, kidneys, bowel,
and skin. The use of vasopressin in pregnancy is not recommended as it may activate oxytocin receptors, resulting in uterine contractions.

Pure inotropes (dobutamine, milrinone) act mainly by increasing cardiac output. Dobutamine is indicated when increases in cardiac output are required. The starting dose is 2.5 µg/kg/min and may be titrated to the desired effect (improved cardiac output as evidenced by improved blood pressure, urine output, resolution of hyperlactatemia, and improved mental status). The most common side effects are tachycardia and hypotension, but dobutamine administration may also result in vasodilation with decreased SVR. Milrinone, another pure inotrope, inhibits cellular processes which, in turn, allow calcium to enter the myocardial cells. The starting dose is 0.125 µg/kg/min. Main side effects are similar to those of dobutamine: hypotension and tachycardia.

Epinephrine is both a powerful vasoconstrictor and inotrope. The usual starting dose is 0.03 µg/kg/min. Common side effects from epinephrine include a higher rate of tachyarrhythmias (as compared to norepinephrine and vasopressin) and mild elevations in lactate.



Hemodynamic Monitoring

The pulmonary artery catheter (PAC) was introduced in 1970 for the direct measurement of central venous pressure, pulmonary artery systolic and diastolic pressure, and pulmonary capillary wedge pressure.19 PAC-derived hemodynamic data have provided invaluable information regarding normal hemodynamic measurements during pregnancy.20,21 However, their use has fallen out of favor as they have not been shown to improve clinical outcomes,22 and we do not recommend the use of the PAC in the obstetric patient. In lieu of this invasive strategy, different noninvasive techniques have become available and may guide hemodynamic resuscitation in the vast majority of critically ill patients. The use of transthoracic echocardiography (TTE) by noncardiologist physicians has dramatically changed the management of patients with shock.23 The learning curve for a focused TTE examination aimed at identifying the cause of shock is not steep and may be easily accomplished by many physicians.

Another significant advance in hemodynamic monitoring is the availability of different noninvasive cardiac output monitors. These monitors allow for continuous measurement of cardiac output and SVR in many cases. They are useful in predicting acute changes in cardiac output in response to fluid administration, either actual administration of fluid or during a PLR maneuver to decide if the patient will respond to a fluid challenge. With the use of an arterial line, bedside TTE, and a noninvasive cardiac output monitor (when needed), most clinicians will be able to guide appropriate resuscitation without the need of more invasive techniques such as a PAC.


Hemorrhagic (Hypovolemic) Shock

Hemorrhagic shock is the most common form of shock in obstetrics. Most cases occur secondary to postpartum hemorrhage due to uterine atony and abnormal placentation.


Management of Hemorrhagic Shock in Pregnancy

The obstetrical management of bleeding is beyond the scope of this chapter; however, medical and surgical treatments usually involve administration of uterotonics; repair of genital lacerations as indicated; and a variety of surgical procedures, including uterine artery ligation, B-Lynch stitches, placement of intrauterine balloons, and hysterectomy. The latter interventions constitute the mainstay of treatment. From a critical care point of view, the most important intervention is to maintain hemodynamic stability until the bleeding is controlled (usually surgically).



Nonpharmacologic and Pharmacologic Treatments

As discussed previously, overzealous administration of fluids (crystalloids or colloids) is not recommended in the setting of massive hemorrhage as this will result in dilutional coagulopathy, hypothermia, and acidosis (mainly seen with saline as large concentrations of chloride decrease serum bicarbonate).24 Instead, early administration of blood products (PRBCs at a ratio of 1:1:1 with platelets and FFP) results in improved outcomes.14

Guidance of blood product administration with the use of viscoelastic tests, such as thromboelastography or thromboelastometry, results in fewer total blood products transfused and improved survival.25 We recommend the use of these tests when available. Certain adjuvant pharmacological products may be used in the management of severe hemorrhage. In the recent past, recombinant activated
factor VII was commonly utilized. Although this product does decrease the number of blood products transfused, no improved survival has been consistently documented; however, a significant risk of arterial thrombosis (stroke, myocardial infarction, peripheral arterial occlusions) with its use has been documented.26 We do not recommend the use of recombinant activated factor VII routinely as it may result in more harm than benefit.

Where available, fibrinogen concentrates may be used to maintain the serum fibrinogen above 150 to 200 mg/dL in the actively bleeding patient. Prothrombin complex concentrates (PCCs) are concentrates of vitamin K-dependent clotting factors (II, VII, IX, X). PCCs are the recommended antidote for warfarin reversal. Despite off-label use in bleeding patients (trauma, cardiovascular surgery), more data are required, and we do not use PCCs routinely in obstetrical hemorrhage.

Among patients with postpartum hemorrhage, the antifibrinolytic agent tranexamic acid (TXA) within 3 hours of birth is currently recommended to treat established postpartum hemorrhage that is unresponsive to first-line measures such as uterotonics. TXA has been shown to decrease bleeding-associated mortality rates and the need for reoperations for uncontrolled hemorrhage27 and has not been associated with an increased risk of thrombotic complications.

Administration of blood products may result in TRALI. TRALI usually presents with acute onset of hypoxic respiratory failure within 6 hours of administration of a blood product (most cases occur within 1 hour). Chest x-ray will show bilateral pulmonary edema. Most cases will resolve with supportive treatment.


Distributive Shock


Anaphylactic Shock


Clinical Presentation

Anaphylactic reactions are rare events but may be fatal in as many as 10% of cases.28 Antibiotics, anti-inflammatory agents, oxytocin, anesthetic agents, blood products, colloid solutions, and latex exposures are some of the most common causes of anaphylaxis during pregnancy. Anaphylaxis is a series of events that occur in a sensitized individual on subsequent exposure to a specific antigen. It classically refers to an immunoglobulin (Ig) E-mediated, type I hypersensitivity response, produced by the release of antigen-stimulated mast cells and basophil mediators (eg, prostaglandins, leukotrienes, histamine, tumor necrosis factor alpha). The latter may result in a life-threatening systemic reaction with urticaria, angioedema, hypotension from severe vasodilation, increased vascular permeability with third spacing, airway obstruction from edema, and multiorgan system failure. Anaphylactic reactions may also be non-IgE-mediated responses (ie, reactions to IV immunoglobulins, dialysis circuit membranes, dextrans, and iron). In the past, the latter were referred as anaphylactoid reactions; however, this term is no longer recommended.29


Clinical Assessment and Management of Anaphylactic Shock in Pregnancy

Early recognition and management of anaphylactic reactions is essential. Risk factors, including a prior history of anaphylaxis, should be noted carefully at admission. Anaphylaxis usually presents with acute onset of urticaria, hypotension, bronchospasm, angioedema, and cardiovascular collapse. Cardiac output may be decreased due to cytokine-mediated cardiac depression.30 Acute management of anaphylaxis in the obstetrical patient should not differ from that in the nonpregnant patient. A stepwise approach has been suggested and consists of first assessing the airway and supplementing oxygen. Early tracheal intubation is recommended in the setting of significant airway edema.



Pharmacologic Treatment

Epinephrine is the cornerstone of treatment; 0.3 to 0.5 mg (0.3-0.5 mL of a 1:1000 [1 mg/mL] solution) of intramuscular epinephrine should be administered as soon as possible (usually apply in the midlateral thigh). The latter may be repeated every 5 to 15 minutes as needed.29 If IV or intraosseous (IO) access is available and no response to IM epinephrine is obtained, epinephrine can be given by IV or IO at a dose of 50 to 100 µg (0.5-1.0 mL of a 0.1 mg/mL, or 1:10,000 solution). A continuous infusion of epinephrine may be required starting at a dose of 0.03 µg/kg/min. Attempts to remove the inciting antigen, if applicable, should be undertaken. IV fluid resuscitation should accompany the use of epinephrine in the hypotensive patient.

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  4. Fetal Malpresentation

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Jun 19, 2022 | Posted by in OBSTETRICS | Comments Off on Critical Care Obstetrics

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