Contrary to other developed nations, maternal mortality has not decreased and may
have even increased over time in the United States.[1] The rise in the prevalence of coexisting cardiovascular disease and obesity, among
others, has changed the field of obstetrics and maternal–fetal medicine (MFM) dramatically.
Unfortunately, most obstetrical programs do not provide adequate training in management
of acute maternal care; as a result, obstetricians (OB) and MFM specialists must usually
rely on multiple consultants in managing common medical emergencies during pregnancy.
While multidisciplinary management of complex medical conditions is optimal, it often
falls on the obstetrical team of providers to make the correct diagnosis and manage
the patient before the arrival of consultant services. This initial interaction with
the obstetrical service, including arriving at a differential diagnosis that will
inform further evaluation and management, is critical for determining outcomes. The
obstetrical service is therefore the first line of defense when patients present with
life-threatening conditions. As such, OB and MFM physicians should have basic medical
knowledge to initiate such evaluation and interventions since they may be the only
provider available initially. The goal of this article is not to extensively discuss
management of complex medical diseases during pregnancy, rather we provide a concise
review of key early medical interventions that will likely result in improved clinical
outcomes. The goal for the obstetrician is to arrive at the appropriate differential
diagnosis and institute the initial phase of management until the appropriate consultants
arrive.
Sepsis
Sepsis is defined as the presence of an infectious process leading to a dysregulated
inflammatory response resulting in acute organ dysfunction.[2] Sepsis should be suspected in any patient with an infectious process and evidence
of any organ dysfunction (e.g., confusion, hypotension, oliguria, dyspnea and hypoxemia,
ileus, abnormal coagulation studies, and elevated liver enzymes). Early source control
is fundamental and achievable in many cases (e.g., delivery for chorioamnionitis,
dilation and curettage for retained infected placental products, and wound debridement
as indicated). Together with early source control, other vital interventions include
obtaining cultures as indicated (e.g., blood, urine, wounds, and vaginal) and serum
lactate.[3] Lactate levels should be followed during early resuscitation; a progressive decline
in lactate correlates with decreased mortality.[3] Early administration of broad-spectrum antibiotics (in most cases providing coverage
against anaerobic and gram-positive and gram-negative bacteria), together with fluid
resuscitation with 1 to 2 L of crystalloid (preferably lactated Ringer's solution
or plasma-lyte A) aiming for a mean arterial blood pressure (MAP) of 65 mm Hg, should
not be delayed. If hypotension and hypoperfusion persist, norepinephrine (0.05 µg/kg/minute
as a starting dose) should be initiated targeting a MAP of 65 mm Hg.[3]
[4] During the midtrimester, physiologic vasodilation may result in MAP below 65 mm
Hg; the latter should not be the sole indication for aggressive fluid resuscitation
and vasopressor support in the absence of other markers of hypoperfusion such as oliguria,
confusion, tachycardia, cold extremities, and elevated serum lactate.
Ischemic Stroke
Ischemic stroke should be suspected with the acute onset of neurologic deficits, such
as paresthesia, hemiparesis or hemiplegia, seizures, dysarthria, facial droop, or
confusion/obtundation, among others. Once suspected, stroke protocols should be activated
immediately. Most hospitals have such a protocol or have a process for emergency consultation
of a stroke team. Obstetrical care providers should be familiar with their particular
institutional approaches. Imaging with computed tomography (without contrast, followed
by angiography in many centers) should procced without delay, as this will identify
optimal candidates for reperfusion therapy.[5] Early measures to prevent secondary brain injury must be undertaken as soon as possible.
If the airway cannot be protected, the patient should be immediately intubated, aiming
for a normal arterial partial pressure of oxygen (above 80 mm Hg) and carbon dioxide
(35–45 mm Hg in nonpregnant patients, 30 mm Hg in pregnancy). Hypotonic fluids (e.g.,
the lactated Ringer's solution or plasma-lyte A) should be avoided, as they will result
in hyponatremia, potentially worsening cerebral edema.[5] Normal saline should be the initial fluid utilized. Hyperglycemia and hypoglycemia
should be avoided, targeting glucose levels between 140 and 180 mg/dL.[5] Any temperature elevation should be managed as soon as possible since hyperthermia
worsens neuronal injury. Cooling blankets targeting normothermia are indicated.
If the patient is a candidate for reperfusion with systemic tissue plasminogen activator
(tPA; window between presentation and onset of symptoms of 4.5 hours or less), blood
pressure control is important. In nonpregnant individuals, treatment is required if
the blood pressure is above 185/110 mm Hg prior to administering tPA.[6] For tPA recipients during pregnancy, we recommend targeting blood pressures between
140 and 160/90 and 110 mm Hg with the use of labetalol (sequential boluses of 10,
20, 40, and 80 mg at every 10 minutes with a maximum cumulative dose of 300 mg) or
nicardipine (continuous infusion starting at 2.5 mg/h with increments of 2.5 mg every
5–10 minutes to a maximum of 15 mg/h).[5] The window for endovascular intervention with local thrombolysis and clot stent
retrieval of proximal thrombi is up to 24 hours after onset of symptoms.[7] For this procedure, we recommend targeting the same blood pressures described for
systemic tPA. If tPA is administered, aspirin and deep vein thrombosis (DVT) prophylaxis
should not be started until 24 hours later and after documenting the absence of hemorrhagic
transformation post tPA.
If no tPA or thrombectomy is planned, blood pressure should also be maintained between
140 and 160/90 and 110 mm Hg. In these patients, aspirin 160 to 300 mg/day, together
with DVT prophylaxis, should be started as soon as possible.[8]
Hemorrhagic Stroke
Hemorrhagic strokes from uncontrolled hypertension commonly affect the basal ganglia.
The clinical presentation of a hemorrhagic stroke may be similar to the ischemic counterpart;
suspect it with any acute onset of neurologic dysfunction including seizures, paresthesia,
hemiparesis or hemiplegia, dysarthria, facial droop, or confusion/obtundation. A hypertensive
response usually follows the stroke event in an attempt to increase cerebral perfusion
pressure. Current guidelines recommend blood pressure treatment with values above
220/120 mm Hg.[6] Treatment aiming for lower blood pressures (systolic blood pressure < 140 mm Hg)
does not improve neurologic outcomes and may increase the risk of end organ damage
(acute kidney injury).[9] During pregnancy, we recommend maintaining blood pressure between 140 and 160/90
and 110 mm Hg with labetalol or nicardipine as described above.[5] As with ischemic strokes, prevention of secondary brain injury is paramount: avoid
hypotonic fluids, fever, and hypo/hyperglycemia (target glucose: 140–180 mg/dL). If
the patient is on low-dose aspirin, discontinuation is appropriate; transfusion of
platelets, however, is not indicated unless a neurosurgical procedure is planned.[10] Thrombocytopenia may result in hematoma expansion. Most experts recommend maintaining
a platelet count above 100,00/mm3 with platelet transfusions as needed.[11] Reversal of anticoagulants, such as warfarin (with intravenous [IV] vitamin K and
prothrombin complex concentrates), unfractionated heparin (with protamine sulfate),
and the new direct oral anticoagulants (with idarucizumab or andexanet α) may be required.[10] Intubation with mechanical ventilation may be necessary if the patient is unable
to protect her airway or if hypoxemia and/or hypercapnia develop (as the latter two
result in cerebral vasodilation with worsening intracranial hypertension). If preeclampsia
is suspected in the differential diagnosis, magnesium sulfate should be administered.
Aortic Dissection
The clinical presentation of aortic dissection typically includes sudden onset of
severe chest pain which radiates to the interscapular region. Risk factors for aortic
dissection include Ehlers–Danlos, Marfan's, and Turner's syndromes; fibromuscular
dysplasia; and congenital bicuspid aortic valve. If suspected, the most important
early medical management goal is rapid blood pressure control, as uncontrolled hypertension
will propagate the dissection. Treatment with antihypertensives should begin as soon
as possible, even before imaging, if clinical suspicion is high. Vasodilators should
not be administered prior to adequate β blockade since the acute decrease in afterload
will increase shear stress with further dissection.[12] Instead, treatment is started with IV esmolol (25–300 µg/kg/minute) followed by
an IV vasodilator, such as nicardipine (2.5–15 mg/h) or nitroprusside (0.2–2 µg/kg/min),
aiming for a systolic blood pressure below 120 mm Hg.[6] Alternatively, IV labetalol monotherapy may be utilized, as it is a combined α−
and β-blockers. Proximal aortic dissection (Stanford's A) requires surgical repair.
Most distal dissections (Stanford's B) are managed expectantly.
Myocardial Infarction
Myocardial infarction (MI) usually presents with sudden onset of chest pain which
radiates to the upper extremities and/or jaw. Other symptoms include diaphoresis,
dyspnea, nausea, vomiting, and epigastric pain. Women are prone to atypical presentations
including lack of significant chest pain. Grossly, MI may be divided into ST MI (elevation
of the ST segment) and non-ST MI (without elevation of the ST segment). Elevation
of serum troponins reflects myocardial necrosis. Unlike in nonpregnant individuals,
most MI during pregnancy are due to coronary dissection (especially during the third
trimester and postpartum period).[13] Most coronary dissections affect the left descending coronary artery.
Initial management of a suspected MI includes pain relief with nitroglycerin (0.4-mg
sublingual in every 5 minutes up to three doses) or morphine (2–4 mg IV). Oxygen should
be administered if peripheral oxygen saturation (SpaO2) is below 90%.[14] The cornerstone of management is administration of concomitant anticoagulation and
antiplatelet therapy. IV unfractionated heparin (UFH) should be started (bolus of
60 units/kg, maximum 4,000 units, followed by an initial infusion of 12 units/kg/h,
maximum 1,000 units/h, aiming for an activated partial thromboplastin time of 50–70 seconds)
together with chewed noncoated aspirin (162–325 mg, followed by 81 mg daily).[15] Dual antiplatelet therapy is standard and consists of adding a P2Y12 blocker, such
as clopidogrel, ticagrelor, or prasugrel, to aspirin. Available limited data suggest
that clopidogrel (300 mg oral load followed by 75 mg a day) is safe in pregnancy.[16] No data exist on the safety of ticagrelor or prasugrel during pregnancy. Recent
studies suggest that ticagrelor is the preferred agent for patients treated conservatively,
while prasugrel is optimal among patients undergoing percutaneous coronary intervention
(PCI).[17] If in doubt, addition of a P2Y12 blocker may be delayed until the coronary angiography
is performed (if no PCI is indicated, then clopidogrel or ticagrelor may be added;
if PCI is indicated, then prasugrel will be ideal).[17] If hypertension and tachycardia are present, IV β-blockers are indicated (metoprolol
2.5–5 mg at every 5 minutes to a maximum of 15 mg or esmolol 25–300 µg/kg/min). Persistent
hypertension may be treated with IV nitroglycerin 5 to 100 µg/min (avoid if right
ventricular MI is suspected). If coronary angiography reveals a coronary dissection,
patients are commonly managed conservatively without PCI, as coronary interventions
may worsen the dissection.[18] UFH should be stopped after the diagnosis of coronary dissection, and continuation
of aspirin and β-blockers is recommended.[18] Methergine is contraindicated in patients with acute MI.
Seizures (Noneclamptic)
Most generalized tonic–clonic epileptic seizures are self-limited. During the episode,
administration of oxygen and positioning the patient in the left lateral decubitus
is recommended. First-line medication is IV lorazepam (0.1 mg/kg, usually starting
with 4 mg).[19] If IV access is not available, intramuscular (IM) midazolam (10 mg) is equally effective.[20] Most patients will require a long acting antiepileptic drug (AED) concomitantly.
Commonly used agents include IV phenytoin or phosphenytoin (15–20 mg/kg) or levetiracetam
(500–2,000 mg IV). In patients previously receiving a specific AED, a loading dose
of the maintenance agent is commonly indicated. Refractory cases may require endotracheal
intubation followed by infusions of midazolam (preferred) or propofol.[21]
Acute Right Ventricular Failure
Acute right ventricular failure (RV failure) may occur with any condition that increases
right ventricular afterload (e.g., pulmonary embolism, air embolism, amniotic fluid
embolism, or exacerbation of existing pulmonary hypertension by triggers such as hypoxemia,
acidosis, or hypercarbia). Clinically, patients may present with systemic hypotension,
dyspnea, oxygen desaturation, peripheral edema, hepatic congestion, and distended
jugular veins. The diagnosis may be easily confirmed with limited bedside transthoracic
echocardiography (TTE; [Fig. 1]). The most important aspect of acute treatment is to avoid fluids. Overzealous fluid
administration worsens hypotension by further dilating the RV, with left-sided displacement
of the interventricular septum resulting in left ventricular obliteration and decreased
cardiac output.[22] Instead, hypotension should be treated with vasopressors (IV norepinephrine starting
at 0.05 µg/kg/min and titrated to a MAP of 65 mm Hg). Oxygen should be administered
if hypoxemia is present since the latter worsens RV failure by causing pulmonary vasoconstriction.[22] Contractility of the RV may be improved by starting an inotropic agent, such as
dobutamine (2.5–5 µg/kg/min) or milrinone (0.25–0.75 µg/kg/min). If pulmonary embolism
(PE) is the underlying cause, immediate therapeutic anticoagulation with UFH should
be started (80 U/kg bolus, followed by 18 U/kg/h, aiming for an activated partial
thromboplastin time of 60–85 seconds or an anti-Xa value of 0.3–0.7 U/mL). The presence
of hypotension (systolic blood pressure below 90 mm Hg) in the setting of PE warrants
the use of thrombolytic therapy, such as tPA.[23] For massive PE, the recommended dose of tPA is 100 mg IV over 2 hours.[23] Thrombolysis should not be delayed if indicated during pregnancy.[24] Recent surgery (e.g., cesarean section) is a relative contraindication to using
tPA, but its use in this life-threatening condition may be indicated even in the setting
of a recent surgical intervention.
Fig. 1 Acute right ventricular failure. Please note the massively dilated right ventricle
compressing the left ventricle. Reproduced with permission under Creative Commons
license type BY 2.0 from Jochmann et al.[31]
Acute Left Ventricular Failure
Acute left ventricular failure commonly presents with new onset dyspnea, hypoxemia,
tachypnea, and orthopnea. Clinical examination reveals bilateral pulmonary crackles.
Bedside point-of-care ultrasonography will show B lines (rocket lines, [Fig. 2]).[25] In severe cases, decreased systolic function may result in hypotension, oliguria,
confusion, and cold clammy extremities. The immediate management of acute cardiogenic
pulmonary edema centers on preload and afterload reduction combined with both respiratory
and inotropic support. All fluids should be discontinued. Diuresis with furosemide
(intermittent boluses or a continuous infusion) is indicated.[26] Common doses include 20- to 80-mg IV boluses at every 6 to 8 hours or an infusion
of 1 to 10 mg/h. Besides its diuretic effect, furosemide induces venodilation with
subsequent decreased preload. The use of morphine sulfate (2–4 mg IV) also results
in venodilation and preload reduction. If systemic hypertension is present, afterload
reduction is indicated. Commonly used agents in this setting include IV nitroglycerin
(5–300 µg/min), nitroprusside (0.2–2 µg/kg/min), nicardipine (2.5–15 mg/h), and hydralazine
(5–10 mg every 20 minutes). Nitroglycerin may be particularly effective, as it will
improve pulmonary edema by inducing systemic venodilation with decreased preload.
Beta-blockers should be avoided in acute decompensated left-ventricular failure. Respiratory
support with noninvasive mechanical ventilation (e.g., CPAP) commonly results in improved
oxygenation and improvement in pulmonary edema (a continuous positive airway pressure
of 8–10 cm H2O is a reasonable starting point). In patients with cardiogenic shock (systolic blood
pressure below 90 mm Hg) and evidence of end-organ hypoperfusion, blood pressure support
with norepinephrine (starting at 0.05 µg/kg/min and titrated to a MAP of 65 mm Hg)
is usually indicated. Addition of inotropic agents (e.g., dobutamine or milrinone)
is commonly required, as norepinephrine may further decrease cardiac output after
increasing systemic vascular resistances.[26] Refractory cases may require mechanical support with left ventricular assist devices.
Fig. 2 Hyperechoic B lines extending to the bottom of the screen indicating pulmonary edema.
Reproduced with permission under Creative Commons license type BY 4.0 from Macias.[32]
Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA) usually presents with nonspecific symptoms including nausea,
vomiting, abdominal pain, polyuria, and polydipsia leading to dehydration together
with a gap metabolic acidosis and hyperglycemia. Other findings include deep fast
breathing (Kussmaul's respiration) in an attempt to clear carbon dioxide. A fruity
breath odor indicates acetone clearance. The diagnosis is usually confirmed by identifying
β-hydroxy butyric acid in blood with a wide anion gap. The anion gap is calculated
as (Sodium − [chloride + bicarbonate]), and it is considered increased when above
12 mmol/L. Early management of DKA includes IV fluids, insulin administration, and
potassium replacement. Patients with DKA are usually volume depleted secondary to
osmotic diuresis and require IV fluid resuscitation. This may be accomplished with
1 to 2 L of crystalloid (normal saline, lactated Ringer's solution, or plasma-lyte
A) in the first 1 to 2 hours, depending on the severity of hypovolemia, followed by
an infusion of 150 to 250 cc/h. Once a glucose value of 200 to 250 mg/dL is reached,
5% dextrose may be added to each bag of crystalloid to prevent iatrogenic hypoglycemia.
Normal saline has been associated with a higher risk of acute kidney injury secondary
to hyperchloremia in critically ill patients.[27] Although this has not been described in patients with DKA, if serum chloride is
elevated following use of normal saline, we recommend switching to a balanced crystalloid
solution, such as lactated Ringer's solution or plasma-lyte A. IV insulin should be
started at a rate of 0.1 U/kg/h.[28] If blood glucose does not decrease by at least 50 to 70 mg/dL in the first hour,
the infusion rate should be doubled. Importantly, in patients with significant hypokalemia
(serum potassium <3.3 mEq/L), potassium replacement should be started prior to insulin
to avoid the potential for insulin-induced life-threatening hypokalemia.[28]
[29] Usually, replacement of KCl 20 mEq IV per hour for 2 hours before insulin administration
will suffice. In patients with normal serum potassium, maintenance fluids should contain
potassium (20–40 mEq/L). In women presenting with potassium levels above 5.3 mEq/L,
initial fluids are administered without potassium; however, serial potassium measurements
are indicated since hypokalemia will be “unmasked” as IV fluids and insulin are administered.
Clinicians should actively seek out any treatable precipitating factor, such as infection.
Fetal heart rate anomalies, including minimal or absent variability, are frequently
seen with maternal acidosis and should not lead to a rush for cesarean delivery. The
latter should be reserved for prolonged bradycardia that does not resolve with maternal
resuscitation. Beta mimetics should be avoided in patients with DKA.
Thyroid Storm
Thyroid storm usually presents with systolic hypertension (wide pulse pressure), tachycardia,
hyperthermia, diaphoresis, tremor, nausea, vomiting, diarrhea, and agitation. Acute
management is directed at blocking synthesis, release, and peripheral action of thyroid
hormones. Propylthiouracil (PTU) should be started immediately at a dose of 1 g orally
(nasogastric or orogastric tube if unable to swallow), even before the laboratory
testing results are available. Once the diagnosis is confirmed, the loading dose is
followed by 200 mg at every 6 hours.[30] One hour after PTU is started and iodide is administered. Iodide may be given as
potassium iodide (KI; 5 drops orally every 8 hours) or Lugol's solution (10 drops
every 8 hours). IV sodium iodide is another option (1 g every 8 hours).[30] Dexamethasone 2 mg IV every 6 hours for four doses also will decrease thyroid hormone
production and secretion. Hypertension and tachycardia usually require management
with β-blocking agents (propranolol, labetalol, or esmolol). IV esmolol (25–300 µg/kg/min)
is particularly useful in patients at risk of high-output cardiac failure (e.g., severe
tachycardia with mild pulmonary edema secondary to decreased ventricular filling time)
since iatrogenic worsening of cardiac output following β-blockade is easily reversible
after stopping the infusion (esmolol half-life is only a few minutes long). [Table 1] provides a summary of our recommendations.
Table 1
Key points on early acute management of medical emergencies in pregnancy
|
Medical emergency
|
Management
|
|
Sepsis
|
Suspect with any infectious process and evidence of any organ dysfunction (e.g., confusion,
hypotension, oliguria, dyspnea and hypoxemia, ileus, abnormal coagulation studies,
and elevated liver enzymes)
|
• Early volume administration (1–2 L crystalloid); add norepinephrine if no response
to fluids
• Obtain cultures and serum lactate
• Start broad spectrum antibiotics
• Achieve source control
|
|
Ischemic stroke
|
Suspect with acute onset of neurologic deficits such as paresthesia, hemiparesis or
hemiplegia, seizures, dysarthria, facial droop, and confusion/obtundation
|
• Early head imaging and stroke protocol activation
• Secure airway if needed
• Blood pressure control (<160/110 mm Hg in pregnancy)
• Normal saline as maintenance fluid
• Avoid hyponatremia, fever, or hyperglycemia
|
|
Hemorrhagic stroke
|
Suspect with acute onset of neurologic deficits, such as paresthesia, hemiparesis
or hemiplegia, seizures, dysarthria, facial droop, and confusion/obtundation
|
• Early head imaging
• Secure airway if needed
• Blood pressure control (<160/110 mm Hg during pregnancy)
• Normal saline as maintenance fluid
• Avoid hyponatremia, fever, or hyperglycemia
• Magnesium sulfate if preeclampsia suspected
|
|
Aortic dissection
|
Usually presents with sudden onset of severe chest pain which radiates to the interscapular
region. Risk factors for aortic dissection include Ehlers–Danlos, Marfan's, and Turner's
syndromes; fibromuscular dysplasia; and congenital bicuspid aortic valve
|
• Early blood pressure control, aim for systolic <120 mm Hg
• Avoid pure vasodilators in absence of early β-blockade
• Avoid misdiagnosis with acute coronary syndrome
|
|
Myocardial infarction
|
Sudden onset of chest pain which radiates to the upper extremities and/or jaw. Other
symptoms include diaphoresis, dyspnea, nausea, vomiting, and epigastric pain
|
• Pain control with morphine sulfate or sublingual nitroglycerin
• Oxygen if saturations below 90%
• Start aspirin
• Start intravenous unfractionated heparin
• Intravenous β-blockade if hypertension and tachycardia
|
|
Non eclamptic seizures
|
Acute onset of generalized tonic clonic movements
|
• Oxygen administration
• Left lateral decubitus
• Early benzodiazepine administration
• Load with long acting antiepileptic drug
|
|
Acute right ventricular failure
|
Systemic hypotension, dyspnea, oxygenation desaturation, peripheral edema, hepatic
congestion, and distended jugular veins.
Confirm with bedside transthoracic echocardiography if available
|
• Bedside transthoracic echocardiography if available
• Treat hypotension with vasopressors/inotropes in lieu of fluids
• Avoid hypoxemia, acidosis, or hypercarbia
• If pulmonary embolism, start intravenous unfractionated heparin. If hypotension,
administer systemic tissue plasminogen activator
|
|
Acute left ventricular failure with pulmonary edema
|
Dyspnea, hypoxemia, tachypnea, and orthopnea. Clinical examination reveals bilateral
pulmonary crackles. Bedside point of care ultrasonography will show B lines (rocket
lines) and decreased left ventricular function
|
• Discontinue all fluids
• Administer furosemide
• Positive pressure ventilation as needed (invasive or noninvasive)
• Treat hypertension with vasodilators
• Vasopressors and/or inotropes if systemic hypotension
|
|
Diabetic ketoacidosis
|
Nausea, vomiting, abdominal pain, polyuria, and polydipsia leading to dehydration.
Kussmaul's respiration and fruity breath odor. Hyperglycemia and metabolic acidosis
with wide anion gap
|
• Start intravenous fluids
• Check potassium level prior to starting insulin infusion
• Insulin infusion
• Identify potentially treatable triggering factors (e.g., infection)
|
|
Thyroid storm
|
Systolic hypertension (wide pulse pressure), tachycardia, hyperthermia, diaphoresis,
nausea, vomiting, diarrhea, tremor, and agitation
|
• Early propylthiouracil (PTU)
• Iodide following PTU
• Corticosteroids
• Beta blockers as needed
|
