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Shock and Pregnancy

Author: Marie Rosanne Baldisseri; Chief Editor: David Chelmow, MD more...

Updated: Jan 4, 2012

Background

Shock is a state of compromised tissue perfusion that causes cellular hypoxia. It is defined as a syndrome

initiated by acute hypoperfusion, leading to tissue hypoxia and vital organ dysfunction. Shock is a systemic

disorder affecting multiple organ systems. Perfusion may either be decreased globally or distributed poorly, as in

septic shock. During shock, perfusion is insufficient to meet the metabolic demands of the tissues; consequently,

cellular hypoxia and end organ damage ensue. [1]

The treatment of shock in a pregnant person differs in 2 important respects from the treatment of shock in adults

who are not pregnant. First, normal physiologic changes occur in the most organ systems during pregnancy.

Second, 2 patients are vulnerable, the mother and the fetus. Therefore, obstetric critical care involves simultaneous

assessment and management of both patients (mother and fetus), who have differing physiologic profiles. See the

image below.

Determinants of cardiac function and oxygen delivery to tissues. Adapted f rom Strange GR. APLS: The Pediatric Emergency MedicineCourse. 3rd ed. Elk Grove Village, Ill: AmericanAcademy of Pediatrics ; 1998:34.

For excellent patient educationresources, visit eMedicine's Shock Center, Pregnancy and Reproduction Center,

and Public Health Center. Also, see eMedicine's patient education articles Shock, Pregnancy, and

Cardiopulmonary Resuscitation (CPR).

Cardiovascular Physiology During Normal Pregnancy

During pregnancy, significant cardiovascular changes occur, including changes in the blood volume, heart rate,

stroke volume, cardiac output, and systemic vascular resistance. Furthermore, pregnant women also experience

respiratory changes in lung volumes, minute ventilation, and acid-base status. Understanding and appreciating the

normal physiologic adaptations to gestation are important for treating pregnant women.

Blood volume

Maternal blood volume increases from 25-52% by late pregnancy.[2] The plasma volume increases by 45-50%,

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compared with a 20% increase in red blood cell mass. This disproportionate increase in plasma volume accounts

for the hemodilution or anemia of pregnancy, which is at its maximum by 32 weeks' gestation. The erythropoiesis

occurs secondary to progesterone and other placental hormones. Elevated levels of estrogen and progesterone

increase plasma aldosterone levels and renin activity; these promote sodium retention and an increase in total

body water, the hypervolemia of pregnancy. During pregnancy, blood volume increases 1-1.5 L, total body sodium

levels increase by 950 mEq/L, and the volume of total body water is 6-8 L, 4 L of which is extracellular. The

expansion in blood volume and extracellular fluid volume is required for optimal uteroplacental circulation.

Blood pressure

Both the systolic and diastolic blood pressures decrease until mid pregnancy, with gradual recovery to

nonpregnant values by late gestation.[3] The blood pressure decrease likely occurs because of decreased vascular

resistance. In pregnancy, interpret the blood pressure relative to gestational age. A blood pressure measurement

of 130/80 mm Hg may be normal at term but is abnormal at 28 weeks' gestation, when it should be approximately

110/60 mm Hg. The venous pressure in the legs increases progressively during pregnancy, caused by

compression of the pelvic veins and inferior vena cava by the uterus. The elevated femoral venous pressure returns

to a normal level following labor.

The measurement of brachial artery pressure is not indicative of the uterine arterial blood pressure because the

uterine arterial pressure can be extremely low, even when the blood pressure of the arm measures normal.

Heart rate

The maternal heart rate becomes elevated by 12 weeks' gestation; this reaches and stays at 120% of the baseline

by 32 weeks of pregnancy.[4] The maternal tachycardia may be secondary to cardiac adaptation to volume

overload and elevated free thyroxine serum levels.

Cardiac output and stroke volume

Maternal cardiac output increases 30-50% during pregnancy. [5, 6] This increase occurs by 10 weeks' gestation and

peaks at the end of the second trimester. The increase in cardiac output during gestation is the result of an

increase in heart rate and stroke volume. In the first half of pregnancy, the stroke volume is increased primarily as

the uteroplacental circulation acts as an arteriovenous shunt. In late pregnancy, the cardiac output is increased

due to the tachycardia rate.[7]Alternate hypotheses for the increase in left ventricular stroke volume have been

suggested; the ventricular pressure volume curve may be shifted to the right because of a hormonally dilated heart,

thereby increasing diastolic filling.

Systemic vascular resistance

Systemic vascular resistance decreases and reaches a nadir by the 24th week of pregnancy, with a progressive

rise towards the baseline value at term. The 2 important factors that reduce systemic vascular resistance are the

dilatation of peripheral blood vessels and the presence of the placental c irculation. The placental vascular bed is a

low-resistance vascular system perfused with a large portion of the maternal cardiac output. Uterine veins increase

enormously in size and number during gestation, and uterine vascular resistance is greatly decreased duringpregnancy.

Effect of maternal posture on maternal hemodynamics

The uterine blood flow increases from approximately 50 mL/min prepregnancy to 500 mL/min at term; this

represents a change of systemic cardiac output from 2% normally to 18% during the third trimester. [8, 9]A

pregnant woman has a greater tendency for pooling of venous blood; marked hypotension and syncope may be

experienced with sudden standing from a sitting or lying position. The supine hypotensive syndrome manifests as

dizziness, pallor, tachycardia, sweating, nausea, and hypotension that occur when a pregnant woman lies on her

back. The heavy gravid uterus compresses the descending aorta and the inferior vena cava. This results in pooling

of blood in the legs, a decrease in venous return to the heart, a fall in cardiac output, and hypotension.

Nonreassuring fetal status may occur from decreased uteroplacental perfusion. Turning the mother to her sidequickly restores the pooled blood to the circulation.

Intrapartum hemodynamics


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Maternal cardiovascular responses can be further modified by uterine contractions, pain, labor, analgesia, surgery,

and peripartum blood loss. Cardiac output increases during various phases of labor. The uterine contractions

augment cardiac output. Each uterine contraction expresses from 300-500 mL of blood.[10] The infusion of blood

back into the maternal circulation increases venous return and augments stroke volume. The magnitude of cardiac

output gained during contract ion is 11% less in women laboring under epidural analgesia.[11] This concept is

important for patients with cardiac disease who may not tolerate hemodynamic fluctuations during labor.

Approximately 500 mL of blood loss occurs with vaginal delivery and 1000 mL with cesarian delivery.[12] The

hypervolemia of pregnancy allows women to lose as much as 30% of predelivery blood volume, with little change in

postpartum hematocrit values. Postpartum diuresis peaks between the second and fifth day after delivery, resulting

in 3 kg of weight loss during the first week. Maternal cardiac output increases by approximately 20-30% above

prelabor values during the first 24 hours following delivery. [13] Cardiac output remains elevated for at least 48 hours

postpartum due to the stroke volume increase despite maternal bradycardia. The return of blood volume from the

lower extremities results in approximately 1 L of autotransfusion at the time of delivery. [14]

Respiratory Physiology

Anatomical changes

Hormonal changes in pregnancy affect the upper respiratory t ract and airway mucosa, producing hyperemia,

mucosal edema, hypersecretion, and increased mucosal friability. Estrogen is probably responsible for producing

tissue edema, capillary congestion, and hyperplasia of mucous glands.

The enlarging uterus and the hormonal effects produce anatomical changes to the thoracic cage. As the uterus

expands, the diaphragm is displaced cephalad by as much as 4 cm; an increase in the anteroposterior diameter

and transverse diameter of the thorax occurs, increasing the chest wall circumference. Diaphragm function

remains normal, and diaphragmatic excursion is not reduced.

Pulmonary functions

Anatomical changes to the thorax produce a progressive decrease in functional residual capacity (FRC), which is

reduced by 10-20% by term. The residual volume can decrease slightly during pregnancy, but this finding is notconsis tent; a decreased expiratory reserve volume is a definite change. The increased circumference of the

thoracic cage allows the vital capacity to remain unchanged, and the total lung capacity decreases only minimally

by term. Hormonal changes do not significantly affect airway function; pregnancy does not appear to change lung

compliance, but chest wall and total respiratory compliance are reduced at term. [15, 16, 17]

Ventilation

The minute ventilation increases significantly, beginning in the first trimester and reaching 20-40% above baseline

at term. Alveolar ventilation increases 50-70%. The increase in ventilation occurs because of increased metabolic

carbon dioxide production and an increased respiratory drive due to the increased serum progesterone level. The

tidal volume increases 30-35%. The respiratory rate remains relatively constant or increases slightly.

Arterial blood gases

Physiological hyperventilation results in respiratory alkalosis with compensatory renal excretion of bicarbonate.

The arterial carbon dioxide pressure reaches a plasma level of 28-32 mm Hg, and bicarbonate is decreased to 18-

21 mmol/L, maintaining an arterial pH in the range of 7.40-7.47. Mild hypoxemia might occur in the supine

position. Oxygen consumption increases at the beginning of the first trimester and increases 20-33% by term

because of fetal demands and increased maternal metabolic processes. [18]

In active labor, hyperventilation increases and tachypnea caused by pain and anxiety might result in marked

hypocapnia and respiratory alkalosis, adversely affecting fetal oxygenation by reducing uterine blood flow. In some

patients, severe pain and anxiety can lead to rapid shallow breathing with alveolar hypoventilation, atelectasis, and

mild hypoxemia.

Uteroplacental and Fetal Physiology

A basic understanding of fetal physiology is required to care for pregnant patients who are crit ically ill. The fetal


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oxygen delivery is dependent on maternal arterial oxygen content and uterine blood flow. The uterine blood flow

increases during pregnancy from 2% of cardiac output in a nonpregnant patient to 18% of cardiac output by the

third trimester in a pregnant patient. Therefore, factors affecting either the arterial oxygen content or uterine blood

flow also affect fetal oxygenation. These factors are hypotension, vasoconstriction of the placental bed, and uterine

contractions. The causes of hypovolemia include supine position, hypovolemia, sepsis, and medications.

Vasoconstriction of the uterine arteries occurs in preeclampsia[19] or with vasoconstrictor drugs, and the fetal

blood flow may decrease by as much as 20% with vasoconstriction. The umbilical vein PaO 2is approximately 35-

40 mm Hg because it is mixed with deoxygenated blood in the fetal inferior vena cava. This level of PaO2is

sufficient to saturate fetal hemoglobin to 80-85% because of the left shift in the hemoglobin oxygen dissociation

curve. The oxygen consumption of the fetus is 20 mL/min, and the oxygen reserve is approximately 42 mL.

However, the fetus has the capability of surviving longer by redistributing blood flow to the vital organs. A 50%

decrease in uterine blood flow may be tolerated for brief periods, and further reduction produces anaerobic

metabolism, brain damage, and fetal death.[20]

Determinants of fetal oxygen delivery

Oxygen delivery to fetal tissues can be affected at many levels, ie, maternal oxygen delivery to the placenta,

placental transfer, and oxygen transport from the placenta to fetal tissues. The major determinants of oxygen

delivery to the placenta are the following:

The oxygen content of uterine blood, which is determined by maternal PaO2

Maternal hemoglobin concentration and saturation

Uterine blood flow, which depends on maternal cardiac output

Thus, a decreased PaO2in the mother can be offset somewhat by augmentation of the blood hemoglobin

concentration or cardiac output. A combination of maternal hypoxemia and decreased cardiac output has a

profoundly deleterious effect on fetal oxygenation.

Variations in maternal pH also influence oxygen delivery; alkalosis causes vasoconstriction of the uterine artery,

resulting in decreased fetal oxygen delivery.

The interaction of maternal and fetal circulations in the placenta most likely follows a concurrent exchangemechanism. This is less efficient than a countercurrent exchange mechanism; this helps explain why the PaO2of

the fetal umbilical vein is in the range of 32 mm Hg, far lower than the uterine vein PaO2. Despite low umbilical vein

PaO2, fetal oxygen content is actually quite close to maternal oxygen content because of the shape of the

oxyhemoglobin saturation curve of the fetal hemoglobin.

The other placental factors that determine fetal oxygenation are the amount of intraplacental shunt, the degree of

matching of maternal and fetal blood flows, and the presence of any placental abnormalities such as placental

infarcts. The fetal arterial blood has an even lower PaO2than umbilical vein blood. This is partially compensated by

a high fetal cardiac output relative to oxygen consumption, thus maintaining abundant oxygen delivery to the

tissues. The umbilical vein PaO2values of less than 30 mm Hg are saturated on the steep part of the fetal

oxyhemoglobin dissociation curve; therefore, small changes in maternal PaO2may cause significant changes infetal oxygen content.[20]

Fetal monitoring

Fetal monitoring is performed via continuous electronic fetal heart rate (FHR) monitoring to identify any changes in

fetal physiology. The baseline FHR is in the range of 120-160 beats per minute. Although fetal tachycardia may be

a nonspecific finding, fetal bradycardia may indicate hypoxia secondary to uteroplacental insufficiency. Absence of

beat-to-beat variability in the FHR may be another indication of fetal asphyxia and anemia. While early

decelerations of FHR are benign, late or variable decelerations, particularly when recurrent and combined with

decreased variability, are highly suggestive of fetal hypoxia.

Abnormalities of FHR patterns may be further evaluated using results from a fetal biophysical profile. The fetal

biophysical profile consists of an ultrasound determination of fetal movements, fetal breathing movements, limb

tone, amniotic fluid volume, and reactivity to nonstress testing. Fetal acid-base measurements from scalp blood

sampling are used in labor to assess the state of fetal physiology. A pH less than 7.20 indicates fetal hypoxia,

whereas a pH greater than 7.25 predicts a favorable outcome. Fetal pH monitoring can only be performed when


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membranes are ruptured.

Fetal oxygen saturation is a new intrapartum fetal monitoring technology, which is expected to provide a more

complete and accurate assessment of the fetal condition. This technique directly and objectively measures fetal

oxygen status during labor and delivery. Fetal pulse oximetry has been approved for use with the conventional fetal

monitor only on patients with nonreassuring heart rates. Because the degree of nonreassuring rates differs, this

new technology requires further study to assess its role in the management of different clinical situations.

Critical Care Monitoring and Support of the Pregnant Patient

The pregnant patient is unique in an intensive care environment. A pregnant patient who is critically ill and in shock

requires special expertise because of the extraordinary underlying physiology.

Intubation and mechanical ventilation

During pregnancy, the nasopharyngeal, oropharyngeal, and respiratory tract mucosa swell. Therefore, intubation

and suctioning may lead to mucosal injury and bleeding. Endotracheal intubation must be performed quickly

because pregnant patients have lower oxygen reserves because of the decrease in FRC. Ventilate pregnant

patients to maintain their PaCO2at approximately 30 mm Hg, the normal level during pregnancy. Avoid respiratory

alkalosis because it may decrease uterine blood flow and, hence, fetal oxygenation. Avoid high ventilatory

pressures at the expense of a rise in PaCO2; maternal hypercapnia has not been reported to be harmful to thefetus.

Cardiopulmonary resuscitation

In an arrest situation, place pregnant patients in a left lateral tilt position to avoid supine hypotension. This can be

achieved by placing a pillow or wedge under the patient's right hip. Advanced cardiac life support (ACLS) is

provided according to ACLS standard protocols. The precipitating events for cardiac arrest in pregnancy include

amniotic fluid embolism (AFE), pulmonary embolism (PE), cardiomyopathy, anesthetic complications, myocardial

infarction, and magnesium overdose.

Hemodynamic monitoring

Pregnant patients who are critically ill and in shock may require insertion of a pulmonary artery catheter. The

indications for pulmonary artery catheterization are severe preeclampsia with oliguria, pulmonary edema, severe

cardiac disease, acute respiratory distress syndrome (ARDS), septic shock, and AFE. In normal pregnancy, the

cardiac output increases as much as 30-50% compared to prepregnancy levels, but the cardiac filling pressures

are unchanged.

Drug therapy

For sedation, meperidine and fentanyl are commonly used; experience with propofol is limited. Benzodiazepines

may be used, but these may have depressive effects on fetal respiration.

A patient who is critically ill and in shock requires vasoactive drugs. Insufficient human data are available to

assess the effects of these drugs in pregnancy and labor. Animal data suggest that dobutamine, norepinephrine,

and epinephrine adversely affect uterine blood flow. Dopamine and ephedrine have been shown to increase

maternal blood pressure and uterine flow. The pure alpha-adrenergic agents, such as phenylephrine and

norepinephrine, cause vasoconstriction of uterine arteries and should be avoided if possible. Ephedrine, which has

both beta-2 properties and alpha-1 agonist properties, is known to increase uterine blood flow and maternal blood

pressure. It is the vasoactive drug of choice to treat hypotension in pregnant patients.

Hemorrhagic Shock

Trauma and resultant hemorrhage causes 6-7% of all deaths in pregnancy. The cause of trauma can be vehicular

accidents, falls, assaults, or penetrating injuries. Placental abruption occurs in 1-5% of patients with minor trauma

and 20-50% of patients with major trauma. In the United States, obstetric hemorrhages are responsible for 13.4%

of all maternal deaths.[21]Antepartum hemorrhage can occur from disruption of the placenta and spontaneous or

traumatic uterine rupture.[22, 23]


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Placenta previa is implantation of the placenta in the lower uterine segment, with a classic presentation of painless

vaginal bleeding and a soft, nontender uterus.

Abruptio placenta may occur in a normally implanted placenta, manifesting as uterine pain and hemorrhage. The

uterine pain is present between contractions, and the uterus is tender.

The signs and symptoms of uterine rupture include vaginal bleeding, lower abdominal pain, and a nonreassuring

fetal tracing. Uterine rupture commonly occurs when high doses of oxytocin or prostaglandins are infused for

induction.[24] The uterine fundus feels boggy and tender upon palpation. Most obstetric hemorrhages occur

postpartum and are primarily due to uterine atony and cervical or vaginal lacerations; antepartum hemorrhage isless common.

Postpartum hemorrhage may be worsened by thrombocytopenia, coagulopathy secondary to AFE, or sepsis. The

normal blood loss of vaginal delivery (500 mL) or cesarian delivery (1000 mL) is generally well tolerated. Excessive

blood loss results in hypovolemic shock; in an antepartum patient, excessive blood loss diminishes uteroplacental

blood flow and induces fetal distress.

Management

The management of hemorrhagic shock requires immediate resuscitative measures, including administration of

oxygen, placement of 2 intravenous lines, intravenous volume replacement, and blood typing and crossmatching to

replace packed red blood cells.[25] In emergencies, blood that is type-specific and not crossmatched can beadministered. Once the patient is stable, immediately perform an abdominal ultrasound to definitely diagnose the

cause of uterine bleeding. The ultrasound confirms if the hemorrhage is due to placenta previa or placental

abruption. Patients requiring a large amount of volume replacement may develop coagulopathy, which should be

treated with appropriate blood product support. Fetal monitoring should be performed via continuous FHR

monitoring to detect fetal distress or fetal hypoxia, the presence of which should lead to prompt fetal delivery by

the safest possible method.

In postpartum hemorrhage, uterine atony can be treated with uterine massage, intramuscular administration of

methylergonovine (0.2 mg), and intravenous oxytocin infusion. Oxytocin is the first-line drug and is often

administered as an infusion (20-40 U/L) because bolus administ ration can cause peripheral vasodilation,

tachycardia, and hypotension. The next step is prostaglandin administration; prostaglandins increase myometrial

intracellular free calcium concentrations and enhance the activity of other oxytocic agents. Hemabate (15-methylprostaglandin F2-alpha) at a dose is 250 mcg administered intramuscularly every 15-30 minutes as necessary (not

to exceed 2 mg) is the frequently used agent.

Adverse effects include bronchospasm, ventilation-perfusion mismatch, and hypoxemia. Ergonovine and

methylergonovine are the ergot alkaloids that produce rapid tetanic uterine contraction and are used to treat

refractory uterine atony. The dose is 0.2 mg intramuscularly. These drugs can cause serious cardiovascular

problems, such as hypertension, vasoconstriction, and increased pulmonary artery pressures.

If medical management fails, therapeutic embolization of the internal iliac or uterine artery has been used to

control obstetric hemorrhage. Surgical exploration to repair lacerations and decrease blood loss by arterial ligation

or hysterectomy may be required as a life-saving measure.

Transcatheter arterial embolization has been a recognized method of hemorrhage control and has been used

successfully in the control of postpartum hemorrhage. Several advantages of uterine artery embolization include

easy identification of the bleeding site, preservation of the uterus and fertility, and decreased rebleeding from

collaterals. A recent review revealed a success rate of 94.9% and a complication rate of 8.7% in 138 cases of

PPH treated by arterial embolization. The commonest complication is low-grade fever but, rarely, pelvic infection,

groin hematoma, iliac artery perforation, transient buttock ischaemia, transient foot ischaemia and bladder

gangrene may occur.

Septic Shock

Septic shock may occur during pregnancy because of overwhelming infection caused by gram-positive bacteria,viruses, or fungi. Gram-negative bacteria such as Escherichia coli, Klebsiellaspecies, Pseudomonas aeruginosa,

and Serratiaspecies cause most cases of septic shock. The microorganisms produce endotoxins that activate

complement systems and cytokines, initiating an inflammatory response. The mediators of sepsis are responsible

for vasodilation, low peripheral vascular resistance, and hypotension. Furthermore, blood flow is poorly distributed,

resulting in inadequate perfusion of certain organs, leading to cellular damage, multiorgan failure, and death.


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The mediators of inflammation result in increased capillary permeability, causing leakage of intravascular fluid

throughout the body, specifically the pulmonary parenchyma, and resulting in noncardiac or low-pressure

pulmonary edema. During sepsis, injury to type II pneumocytes impairs surfactant production, causing alveolar

collapse, lowering lung compliance, and producing severe hypoxemia. This constellation of clinical and

physiological features is described as ARDS.

The causes of septic shock are septic abortion, chorioamnionic and postpartum infections, pyelonephritis, and

respiratory tract infections.[26]Although septic shock remains one of the major causes of death in obstetric

patients, the incidence of death is lower compared to nonobstetric patients with septic shock (0-3% in obstetric

patients vs 10-80% in nonobstetric patients). Prolonged rupture of membranes, retained products of conception,and instrumentation of the genitourinary tract are other significant risk factors for sepsis. Patients with septic

shock present with chills, fever, hypotension, mental confusion, tachycardia, tachypnea, and flushed skin. As the

septic shock progresses, the patient develops cool clammy skin, bradycardia, and cyanosis.

Intravaginal mifepristone in medical abortions has resulted in fulminant and lethal septic shock due to Clostridium

sordellii. The clinical illness is consistent with toxic shock and had evidence of endometrial infection with C

sordellii,a gram-positive, toxin-forming anaerobic bacteria. By blocking both progesterone and glucocorticoid

receptors, mifepristone interferes with the release and function of cortisol and cytokines. Thus, the failed release of

cortisol and cytokine responses impairs the body's defense mechanism, which is necessary to prevent the

endometrial spread of C sordelliiinfection. Concomitant release of potent exotoxins and an endotoxin from C

sordelliicontribute to the rapid development of lethal septic shock.

Treatment

Treatment of septic shock requires immediate resuscitation, identification of the underlying cause of septic shock,

and treatment with antimicrobial therapy. [27] Cultures of sputum, blood, and urine are sent prior to antibiotic

administration. Provide empiric antibiotic coverage intravenously for both gram-negative and gram-positive bacteria.

Later, antibiotic therapy is adjusted based on the patient's response to therapy and the results of culture and

sensitivities. In puerperal sepsis, also provide anaerobic coverage. A usual combination used often is penicillin,

aminoglycoside, and clindamycin or metronidazole. An alternate combination is a second- or third-generation

cephalosporin combined with metronidazole. Piperacillin-tazobactam is another combination that provides fairly

comprehensive coverage for an intra-abdominal source of sepsis.

In septic shock, maintain adequate tissue oxygenation. Optimum mean arterial pressure, circulating blood volume,

cardiac output, and sufficient oxyhemoglobin saturation are required. Patients in respiratory distress or those with

severe hypoxemia may need to be intubated and mechanically ventilated. Because patients with septic shock

often develop ARDS, the goals of mechanical ventilation are the use of a low tidal volume and a high positive end-

expiratory pressure. This approach results in recruitment of alveoli, makes the lungs more compliant, and improves

oxygenation.

Patients in septic shock require hemodynamic support with restoration of adequate circulating volume followed by

the administration of vasoactive drugs. These patients require aggressive resuscitation with crystalloids and

colloids to maintain sufficient intravascular volume before considering vasopressor therapy. Although dopamine has

been used in the past in patients with septic shock, norepinephrine achieves better perfusion pressure and

maternal hemodynamics and helps restore oxygen delivery to hypoperfused organs. This may be achieved at acost of reduced uterine blood flow. Ephedrine, an alpha and beta agonist, may be the preferred vasopressor in

patients with acute hypotension during pregnancy.

In summary, the principles in the management of septic shock, similar to treatment of any other case of septic

shock, include the following components:

1. Early recognition

2. Early and adequate antibiotic therapy

3. Source control

4. Early hemodynamic resuscitation and continued support

5. Corticosteroids (refractory vasopressor-dependent shock)

6. Drotrecogin alpha (Severely ill if APACHE II > 25)

7. Tight glycemic control

8. Proper ventilator management with low tidal volume in patients with ARDS

Other Causes Of Shock In Pregnancy


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Cardiogenic shock

Cardiogenic shock may also be observed during pregnancy. The major cause of cardiogenic shock is severe

valvular disease. In cardiogenic shock, the left ventricle is not able to pump sufficient blood to meet the metabolic

demands of the tissues. The compensatory response is tachycardia, but, eventually, hypervolemia, pulmonary

venous congestion, and generalized edema occur. Inadequate oxygen delivery leads to cellular damage,

multiorgan failure, and death. The clinical signs of cardiogenic shock are distended neck veins, dyspnea,

tachypnea, the presence of a third heart sound, systolic or diastolic murmurs, and generalized edema.

Peripartum cardiomyopathy is an idiopathic disorder that occurs during the last month of pregnancy and up to 6months postpartum. The incidence of this disease is 1 case in 1500-4000 deliveries. The risk factors include old

age, multiparity, twin gestation, and preeclampsia. Upon presentation, these patients have signs and symptoms of

congestive heart failure. The mortality rate associated with peripartum cardiomyopathy is 25-50%.[28] This disease

tends to recur in subsequent pregnancies. A small percentage of these patients are found to have inflammatory

myocarditis after analysis of endomyocardial biopsy specimens. The treatment consists of diuretics, vasodilators

for afterload reduction, digoxin, and careful follow-up. Inflammatory myocarditis may respond to

immunosuppressive therapy.

Postpartum patients may have a localized abscess, resistant organism, or septic pelvic thrombophlebitis. Patients

with septic pelvic thrombophlebitis usually develop persistent fever; the diagnosis may be suggested by findings

from a CT scan of the pelvis. Treatment consists of a broad spectrum of antibiotics and standard anticoagulation.

Coronary artery disease is uncommon in reproductive-aged women, but myocardial infarction has occurred

because of the excessive hemodynamic stress of pregnancy. Management of coronary artery disease in a

pregnant patient is similar to that for a nonpregnant patient.

Spontaneous coronary artery dissection, a rare event, causes myocardial ischemia and sudden death in younger

age groups and especially postpartum women. The clinical presentation includes angina, myocardial infarction,

cardiogenic shock, and death. No specific cardiac risk factors have been associated with its occurrence. In

postpartum patients, the possible mechanism for dissection is thought to be pregnancy-induced degeneration of

collagen and the additional stresses of parturition. The treatment is usually tailored to the individual patient's

needs.

Amniotic fluid embolism

AFE is a catastrophic peripartum syndrome that manifests as a sudden onset of severe dyspnea, hypoxemia,

hemodynamic collapse, coagulopathy, and seizures. AFE is a rare disorder, occurring in 1 case in 20,000-30,000

pregnancies, but it accounts for 10% of all maternal deaths.[29]AFE may occur at any point during pregnancy,

labor, or delivery. Uterine manipulation or trauma may often precede AFE. Whether the pathogenesis occurs

secondary to embolization of particulate cellular contents or secondary to humoral factors has not been

established.

A recent analysis of 46 verified cases of AFE had none of the previously cited predisposing factors: 12% of the

cases occurred in women with intact membranes, 70% during labor, 11% after vaginal delivery, and 19% during

cesarean delivery with or without labor.

The fetal substance may initiate an anaphylactoid reaction, resulting in endogenous mediator release and causing

hypotension, tachycardia, hypoxemia, and seizures. This may lead to pulmonary arterial vasospasm and transient

pulmonary hypertension, followed by left ventricular failure, decreased cardiac output, and hydrostatic pulmonary

edema. The acute left ventricular dysfunction may be caused by humoral mediators or cytokines contained in

amniotic fluid released during the anaphylactoid reaction.

AFE is totally unpredictable, although most cases occur after the onset of labor, some may occur outside of labor,

and AFE is extremely difficult to predict or prevent. Respiratory distress and cyanosis occur suddenly within the

first few minutes and are quickly followed by hypotension, pulmonary edema, shock, and neurological

manifestations such as confusion, loss of consciousness, and seizures. More than 80% of patients experience

cardiorespiratory arrest at the onset. Approximately 50% of patients do not survive this cardiopulmonary

catastrophe, but of those who do, 40-50% develop coagulopathy and hemorrhage up to 4 hours later, and this may

well be the first indication of AFE. Seizure activity may, at times, be the first manifestation.

The diagnosis of AFE is based on a characteristic clinical picture. Treatment consists of oxygenation and

hemodynamic support. Patients often require invasive monitoring to assess the adequacy of intravascular volume


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status and to guide inotropic therapy. Corticosteroids have been used, but their benefit has not been established.

The mortality rate for AFE is high; 86% of patients may succumb to this disorder. Approximately 40% of cases

have fetal death at the time of presentation, and placental abruption is found in 50% of the cases.

Management includes supportive measures and should begin emergently. The initial principles of dealing with

obstetric emergencies include: airway, breathing, and circulation. The 3 main goals of treatment are (1)

oxygenation, (2) maintaining cardiac output and blood pressure, and (3) correcting coagulopathy. The fetus should

be monitored continuously for signs of compromise. In order to ensure optimal uterine perfusion, the mother should

be placed in the left lateral position.

The first priority is resuscitation of the mother and administration of oxygen (100% concentration). The patient may

need to be intubated and ventilated. The initiation of fluid therapy and the administration of pharmacological agents

to maintain optimal blood pressure and cardiac output is next step. Volume replacement and therapy for left

ventricular dysfunction should be directed toward improving inotropy. A clinical guideline is to maintain systolic

blood pressure at or higher than 90 mm Hg, with acceptable organ perfusion, as indicated by a urine output of 25

mL/h or more. Administration of blood transfusions and blood components is considered the first line of treatment

for correcting coagulopathy associated with AFE. Intravenous steroids to treat underlying inflammatory response

and similarities of AFE to anaphylaxis may be helpful.

Pulmonary embolism

The risk for developing deep venous thrombosis (DVT) and PE increases markedly during the advanced stages ofpregnancy and is greatest during postpartum. Rates of maternal mortality from PE have been reported at 2.6

cases per 100,000 live births in white females and 2.5-fold higher in black females. Incidence increases markedly

following cesarean delivery compared to vaginal delivery. [30] The signs and symptoms of PE are more problematic

because dyspnea and tachypnea are common in pregnancy. In nonpregnant patients, tachypnea, dyspnea, chest

pain (pleuritic), apprehension, and crackles are present in only 50% or more of patients. Chest radiograph findings

are abnormal in 80% or more of patients with PE, and the findings are nonspecific. Electrocardiogram findings are

abnormal in 70% of patients with PE, but they are nonspecific. Arterial oxygen tension is low in most patients with

PE.

Objective diagnostic testing

As with DVT, PE requires objective diagnostic testing to confidently confirm or exclude the diagnosis . This is

particularly true in pregnancies because the diagnosis of DVT or PE requires the following:

Prolonged therapy (potentially heparin for the entire 40 wk of pregnancy)

Prophylaxis during future pregnancies

Avoidance of oral contraceptive pills

The first objective diagnostic test should be compression ultrasonography; if it is not available, impedance

plethysmography is adequate. If findings from the noninvasive leg studies are negative, proceed to ventilation-

perfusion lung scanning. Perfusion scanning alone is recommended initially, adding ventilation scanning when

perfusion defects are noted. Pulmonary angiography might be necessary if lung scan findings are of low probability

or indeterminate but clinical evidence is strong.

Several studies show no increased risk of teratogenicity in patients undergoing radiological procedures for the

diagnosis of maternal venous thromboembolic disease. A complete and adequate evaluation to document the

presence or absence of PE requires less than 0.005 Gy. Obtaining the appropriate diagnostic study in

pregnancies is mandatory.

Management

Immediately treat patients, pregnant or not, in whom PE is strongly considered. Treatment is with intravenous

unfractionated heparin, unless a high risk or contraindication to the use of any anticoagulants exists. Extensive

clinical experience and cohort studies establish heparin as the safest anticoagulant to use during pregnancy

because it does not cross the placenta. The initial loading dose should be 5000-10,000 U. Following loading, startan infusion of 18 U/kg. Monitor and keep the activated partial thromboplastin time in the therapeutic range, which

is 1.5-2 times the baseline value.

Although data are relatively modest, low molecular weight heparin (LMWH), which does not cross the placenta,

can be administered once a day and does not require monitoring. LMWH has not been shown to have an


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increased risk of bleeding with surgical procedures, including cesarian deliveries, in a small number of patients. In

one report, dalteparin was used safely and effectively for prophylaxis in 47 women throughout their pregnancies.

The recommended dose was 5000 U, once or twice daily, with a target trough plasma heparin level of 0.1-0.2

U/mL.

However, data on the use of LMWH during pregnancy are limited; most come from diverse case series involving

prophylaxis rather than therapy. These data provide no clear conclusions as to the efficacy and adverse effects of

LMWH; no optimal dose regimen; and insufficient information on risks of obstetric, fetal, or neonatal problems.

Additionally, cases of epidural hematoma have occurred after epidural anesthesia.

Warfarin should be avoided throughout pregnancy because it can cause embryopathy characterized by mental

retardation, optic atrophy, cleft lip, cleft palate, cataracts, and hemorrhage. The teratogenic effects are particularly

common during the first trimester. Warfarin crosses the placenta; it can cause fetal and neonatal hemorrhage and

placental abruption.

Vena cava filters (Greenfield, stainless steel or titanium; bird's nest; Simon-Nitinol) are positioned within the

infrarenal inferior vena cava to trap thrombi arising from the lower extremities. Patients with documented venous

thromboembolic disease who have contraindications to anticoagulation therapy or in whom conventional therapy

has failed are candidates for inferior vena cave filter placement. Vena cava filters and filter placement are

associated with a favorable safety profile; however, both fatal and nonfatal complications have been reported. Fatal

complications are rare, and most nonfatal complications are of minimal clinical significance.

Duration of anticoagulation

Patients who develop DVT or PE antepartum should receive anticoagulation therapy with heparin throughout

pregnancy. After delivery, warfarin should be started; the heparin can be discontinued once an adequate

International Normalized Ratio is achieved. Continue the warfarin for at least 6 weeks postpartum or until at least 3

months of anticoagulant therapy have been completed.

Complications of treatment

Osteopenia has been reported with unfractionated heparin administered for more than 6 months. No information is

available about the beneficial effects of concomitant multivitamins, calcium, or vitamin D supplementation. The

problem of osteopenia and osteoporosis might be less severe if LMWH is used, but providing optimum calciumand vitamin D supplementation to all patients receiving long-term heparin administration during pregnancy is

reasonable.

Contributor Information and DisclosuresAuthor

Marie Rosanne Baldisseri MD, FCCM, Associate Professor, Department of Critical Care Medicine, University

of Pittsburgh Medical Center

Marie Rosanne Baldisseri is a member of the following medical societies:American College of Physicians,

Neurocritical Care Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal

Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep

Medicine,American College of Chest Physicians,American College of Physicians-American Society of Internal

Medicine,American Thoracic Society, Canadian Medical Association, Royal College of Physicians and

Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical

Association


Specialty Editor Board

Steven David Spandorfer, MD Assistant Professor, Department of Obstetrics and Gynecology, New York

Presbyterian Hospital, Weill Cornell Medical College
http://www.wma.net/e/http://www.sccm.org/http://www.rsm.ac.uk/http://rcpsc.medical.org/index.php?pass=1http://www.cma.ca/index.cfm/ci_id/121/la_id/1.htmhttp://www.thoracic.org/http://www.acponline.org/http://www.chestnet.org/http://www.aasmnet.org/http://www.sccm.org/http://www.neurocriticalcare.org/http://www.acponline.org/


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Steven David Spandorfer, MD is a member of the following medical societies:American College of Obstetricians

and Gynecologists,American Society for Reproductive Medicine, and Endocrine Society


Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center

College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

David Chelmow, MD Leo J Dunn Dist inguished Professor and Chair, Department of Obstetrics and

Gynecology, Virginia Commonwealth University Medical Center

David Chelmow, MD is a member of the following medical societies: American College of Obstetricians and

Gynecologists,American Medical Association,American Society for Colposcopy and Cervical Pathology,

Association of Professors of Gynecology and Obstetrics, Council of University Chairs of Obstetrics and

Gynecology, Phi Beta Kappa, Sigma Xi, Society for Gynecologic Investigation, and Society for Medical

Decision Making


Timothy D Rice, MD Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent

Medicine, St Louis University School of Medicine

Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatricsand

American College of Physicians


Chief Editor

David Chelmow, MD Leo J Dunn Dist inguished Professor and Chair, Department of Obstetrics and

Gynecology, Virginia Commonwealth University Medical Center

David Chelmow, MD is a member of the following medical societies: American College of Obstetricians and

Gynecologists,American Medical Association,American Society for Colposcopy and Cervical Pathology,

Association of Professors of Gynecology and Obstetrics, Council of University Chairs of Obstetrics and

Gynecology, Phi Beta Kappa, Sigma Xi, Society for Gynecologic Investigation, and Society for Medical

Decision Making


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