OBSTETRIC CATASTROPHES
Highlights from Vanderbilt University School of Medicine’s 32nd Annual High-Risk OB Seminar
George A. Saade, MD, Professor, Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine,
University of Texas Medical Branch, Galveston, TX
Stroke and Pregnancy
| Epidemiology: hypertension major contributor to stroke in pregnancy; risk for peripartum stroke 6 times
higher in patient with hypertension, compared to normotensive patient; postpartum stroke 13 to 14 times
more likely than if patient normotensive; strokes in pregnant patients with hypertension similar to
strokes in nonpregnant patients (except for edema); cerebrovascular edema common in preeclampsia;
hypoxic-ischemic encephalopathy cerebrovascular complication more common in older women; stroke
and cerebrovascular accident (CVA) major contributors to maternal death; stroke responsible for ≈12%
of maternal deaths; some evidence of CVA in almost 50% of women who die from eclampsia
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| Diagnosis: difficult to determine whether patient had pre-eclampsia before having stroke, or had stroke
and then manifested signs and symptoms resembling preeclampsia; treat patient having stroke as though
they have preeclampsia/eclampsia
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| Pathophysiology: preeclampsia associated with endothelial damage (believed to be caused by free radicals
and oxidative stress); endothelial damage—leads to cerebrovasospasm and capillary leakage; decreased
oncotic pressure—lower albumin level in preeclampsia results in capillary leakage; endothelial
damage decreases brain perfusion, increasing risk for stroke; loss of normal cerebral autoregulation— primary
reason for stroke in patient with preeclampsia; occurs before symptoms of preeclampsia manifest
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| Presentation: headache most common presentation; onset sudden and severe; patient may describe as
worse headache ever experienced; lethargy and confusion, nausea and vomiting, labile hypertension
(suspect CVA, especially if preeclampsia diagnosed)
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| Diagnosis: initially clinical diagnosis; brain imaging with computed tomography (CT) or magnetic resonance
imaging (MRI) recommended (MRI better for cerebellum and brainstem); CT may be negative in
first 24 hr of stroke; with high index of suspicion, repeat CT or order MRI; indications for cerebral
imaging—persistent seizures despite therapeutic magnesium levels; residual neurologic deficit after seizure
(inability to move one side of body or weakness on one side of body, presence of Babinski’s sign);
data show postpartum stroke becoming more common (range, 8-28 days postpartum); mortality in one
third of cases; some neurologic deficit in almost 50% of patients who survive; ≈66% of cases believed to
be nonpreventable; perinatal deaths ≈25% and number of preterm births significant
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| Management: correct hypoxemia with oxygen supplementation or intubation if necessary; correct hyponatremia;
control body temperature (use warm air blower, eg, Bare Hugger); magnesium sulfate best
choice for controlling seizures; if effective, add another antiseizure medication (eg, phenobarbital,
phenytoin [Dilantin]); monitor coagulation and treat laboratory abnormalities; surgical intervention
rarely beneficial; prevent induced hypertension (lability of BP likely to occur during intubation and suctioning;
pretreat patient with antihypertensive; labetalol recommended); lower BP gradually over 6 to 12
hr (cerebral perfusion decreases if lowered too quickly) and not more than 25% of mean arterial pressure
(MAP); nitroprusside—ideal antihypertensive for pregnant patient; nitric oxide potent vascular smooth
muscle relaxant; short half-life; BP can be titrated by adjusting infusion rate; nimodipine—selective calcium
channel blocker (selective to brain vessels); good medication if seeing patient within first few
hours of onset of hypertension; do not use in combination with nitroglycerin; cerebral edema—more
common than stroke; elevate head 45°; restrict fluids; decrease PCO 2 by hyperventilation (when CO2 decreased,
blood vessels of brain constrict, preventing further edema); increasing oxygen controversial;
correct hyponatremia; intracranial pressure monitoring rare; treatment centered on osmotic therapy and
diuresis (mannitol over 10 min or continuous infusion with furosemide [Lasix] 10-40 mg intravenously
[IV]); magnesium sulfate—data clearly show does not prevent stroke or decrease mortality or morbidity;
prevents only seizure
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| Factors predisposing pregnant patient to stroke: protein peaks—seen in cerebrospinal fluid (CSF) of
women with severe preeclampsia; peaks shown to be derivative of hemoglobin; patients with severe pre-
eclampsia may have subtle bleeding in CSF, predisposing them to CVA; thrombophilias—predispose
pregnant patient to preeclampsia and nonpregnant patient to stroke; thrombophilia work-up recommended
for any patient having stroke; data show strong association between stroke and preeclampsia;
data show patients developing preeclampsia have preexisting pathophysiology; data looking at mortality
25 yr after pregnancy showed significant mortality in patients who had severe preeclampsia, compared
to patients who had normal pregnancies; patients experiencing problems in pregnancy (eg, preeclampsia,
gestational diabetes, intrauterine growth restriction, preterm labor, stillbirth) have more complicated
health issues in future; risk for stroke and epidemiology of stroke and eclampsia have changed over time;
data show 80% of patients developed eclampsia >48 hr after delivery, and stroke follows same pattern
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Amniotic Fluid Embolism (AFE)
| Mortality: not every patient with amniotic fluid in circulation develops AFE; decrease in maternal mortality,
but slight increase in perinatal mortality; slight increase in rate of disseminated intravascular coagulation
(DIC); routine discharge 72%; residual health consequences in ≈30% of survivors
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| Causes: not primary vascular effect from amniotic fluid; transient initial pulmonary vasospasm occurs
(not from clotting or clogging in pulmonary arteries); currently believed amniotic fluid in certain patients
causes anaphylactoid reaction that manifests as pulmonary vasoconstriction (initial manifestation)
and other symptoms
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| Diagnosis: complex constellation of symptoms; manifests initially with respiratory distress; patient reports
chest pain or dyspnea (often overlooked because of short duration); cardiovascular and hematologic
symptoms follow; patient may develop multisystem organ failure (from DIC, blood loss, and
ischemia) if she survives cardiorespiratory collapse; presence of fetal squames not necessary for diagnosis;
diagnosis based on exclusion (temporal relationship of symptoms and progression of symptoms);
if patient still pregnant, first sign often prolonged fetal bradycardia
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| Management: prompt and aggressive approach critical; perform cardiopulmonary resuscitation; employ
multidisciplinary approach (eg, intensive care unit staff, anesthesiologist, intensivists); early intubation
and oxygenation necessary; hemodynamic and hematologic monitoring; maintain systolic blood pressure
(SBP) at 90 mm Hg, urine output at 25 mL/hr, and O2 at 90%; correct coagulopathy (do not wait for
bleeding to occur); treat left ventricular failure (digitalis [Digoxin]); high-dose hydrocortisone (500 mg
IV q6h); heparinization not recommended; perform cesarean delivery as soon as possible if patient still
pregnant; survival of fetus increased if delivered within 15 min of cardiac arrest; at >15 min, survival
and intact survival rates decline significantly; successful pregnancies reported; theoretic risk for recurrence
low
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Postpartum Hemorrhage
| Definition: defined historically as 500 mL in first 24 hr postpartum; current definition, 10% change in hematocrit
between admission and delivery, or need for erythrocyte transfusion, or both; average measured
blood loss 500 mL for vaginal delivery, 1000 mL for cesarean delivery; pregnancy adds ≈1 L of blood
volume; pregnant woman can lose ≈1 L (≈15%) of blood volume without showing signs or symptoms;
early intervention (before manifestation of signs and symptoms) critical if excessive postpartum bleeding
suspected; causes—uterine atony; obstetric trauma; retained placenta; coagulopathy
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| Treatment of uterine atony: halothane and isoflurane potent smooth muscle relaxants; discontinue if
uterus fails to contract
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 | Pharmacologic (uterotonic) agents: oxytocin—ad-ministered IV, intramuscularly (IM) or intramyometrially;
100 units; do not administer bolus (significant hypotension); methylergonovine (Methergine)—potent
smooth muscle constrictor; dose 0.2 mg (not 1 ampule); IV administration not recommended (significant
vasospasm); constricts vascular smooth muscle; contraindicated if patient has hypertension, coronary
artery disease (CAD), or preeclampsia; 15-methyl-prostaglandin F 2 alpha (PGF2 a )—dose 0.25 mg,
administered IM or intramyometrially over 15 to 90 min (maximum 8 doses); contraindicated in patients
with cardiac or pulmonary (eg, asthma) complications; Misoprostol (PGE1 )—1000 µg rectally
shown effective 100% of time (speaker starts with 500 µg); light and heat stable (15-methyl-PGF2 a
must be refrigerated and kept from light)
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| Mechanical interventions: uterine massage—needs to be vigorous, using 2 hands; aortic compression—if
performing after cesarean delivery, compress above promontory point of aorta; after vaginal delivery,
compression performed with closed fist at level of umbilicus; partially occludes aorta and decreases BP
in legs and femoral pulses; uterine packing—must cover entire uterine wall; SOS Bakri tamponade balloon
catheter— use in achieving tamponade
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| Surgical interventions: B-Lynch compression suture—tamponades bleeding (constricts uterus); use only absorbable
suture; speaker believes effective 50% of time; uterine artery ligation—effective with localized
bleeding, bleeding in lower cervical area, or if cesarean delivery incision extends into broad
ligaments; take sufficient cervical tissue to avoid tearing vessels; stepwise uterine devascularization—
cuts off all blood supply to uterus; entails 5 successive steps until bleeding stops; uterus does not necrose,
and ovarian failure does not occur; case reports of successful pregnancies after procedure; hypogastric
artery ligation—not as effective as uterine artery ligation and stepwise uterine
devascularization; associated with more complications and higher blood loss than cesarean hysterectomy;
consider patient’s level of stability before performing conservative approach; selective arterial
embolization—reported success 97%; ideal for patient with retroperitoneal bleeding; management of
stable retroperitoneal hemorrhage is expectant (no drainage); pelvic pressure pack—used after hysterectomy;
sterile plastic bag filled with gauze brought out through vagina; traction of weight at end produces
pressure against pelvic floor
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| Coagulopathy: general hematologic goal—maintain fibrinogen 100 mg%, platelets 50,000 /mm3 , and hematocrit
28%; correcting coagulopathy—to increase fibrinogen by 100 mg, give fresh frozen plasma
(FFP) 3 to 4 mL/unit (if patient actively bleeding) or cryoprecipitate 16 to 20 units (if patient in renal
failure); to increase platelets by 50,000/mm3 , give 5 units of platelets; give Rh-immune globulin
(RhoGAM) if patient RhD-negative
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| Additional therapies: activated Factor VII, recombinant factor VIIa, and fibrin glue used with cryoprecipitate
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Suggested Reading
Aurangzeb I et al: Amniotic fluid embolism. Crit Care Clin 20:643, 2004; Belfort MA et al: A comparison
of magnesium sulfate and nimodipine for the prevention of eclampsia. N Engl J Med 348:304, 2003;
Martin SR et al: Intensive care in obstetrics: an evidence-based review. Am J Obstet Gynecol 195:673,
2006; Mousa H et al: Treatment of primary postpartum hemorrhage. Cochrane Database Syst Rev.
24:CD003249, 2007; Riskin-Mashiah S et al: Cerebrovascular hemodynamics in chronic hypertensive
pregnant women who later develop superimposed preeclampsia. J Soc Gynecol Investig. 12:28, 2005; Soncini
E et al: Uterine artery embolization in the treatment and prevention of postpartum hemorrhage. Int J
Gynaecol Obstet. Feb 5; [Epub ahead of print], 2007; Witlin AG et al: Cerebrovascular disorders complicating
pregnancy—beyond eclampsia. Am J Obstet Gynecol 176:1139, 1997.
Educational Objectives
| The goal of this program is to reduce the morbidity and mortality associated with critical disorders in pregnancy.
After hearing and assimilating this program, the clinician will be better able to:
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| 1. Distinguish the primary pathologic feature associated with cerebrovascular accident (CVA) in pregnancy.
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| 2. Identify patients at risk for CVA in pregnancy and care for patients suspected of having a CVA.
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| 3. Recognize patients experiencing amniotic fluid embolism and provide aggressive treatment.
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| 4. Define and list the causes for postpartum hemorrhage.
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| 5. Integrate into practice the management interventions for postpartum hemorrhage.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to
disclose relevant financial relationships within the past 12 months that might create any personal conflicts
of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality
in health care and not a proprietary business or commercial interest. For this program, the faculty reported
nothing to disclose.
Acknowledgements
Dr. Saade was recorded at the 32nd Annual High-Risk OB Seminar, sponsored by Vanderbilt University School of
Medicine, and held on December 8-9, 2006, in Nashville, TN. The Audio-Digest Foundation thanks the speaker and
the sponsor for their cooperation in the production of this program.
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