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preexisting diagnosis of asthma, because compliance is gen-
BOX 55.1 ASTHMA SIGNS AND SYMPTOMS
Symptoms ofAsthma
erally poor despite having appropriate diagnostic tests and
therapy. In one study examining patient’s medication usage,
40% of patients were noncompliant with inhaled corticoste-
• Wheezing
Historyof:
roids and 16% of patients did not use their inhalers appropriately.16 Healthcare providers should identify changes in
symptoms over time, especially in the parturient. In addition
• Cough, especially nocturnal
• Difculty breathing
to subjective changes in symptoms, providers should also ask
about changes in frequency of use of rescue inhalers.
Spirometry is used to both diagnose asthma and its
• Chest tightness
Worsening symptomswhen:
responsiveness to treatment. e diagnosis of asthma is
supported by the presence of airow obstruction and
reversibility of the obstruction following administration
• Exercising
• ExperiencingURI
of inhaled beta- 2 agonists. Current guidelines dene an
increase of FEV1 greater than 200 mL and/ or 12%, or more,
from baseline following the inhalation of a SABA as being
• Experiencingstress
Exposures to these worsen symptoms:
diagnostic for asthma.10 If a patient describes intermittent
asthma symptoms, a bronchoprovocation test using methacholine may be used to trigger airway hyperresponsiveness
• Allergens
• Smoke
and generate a denitive diagnosis.
Dierential diagnosis for asthma includes chronic
obstructive pulmonary disease (COPD), gastroesophageal
• Strong chemical smells, such as perfumes
reux disease (GERD), and vocal cord dysfunction (VCD).
Spirometry can be used to rule out GERD and VCD with
high degrees of spe cicity. If the clinician is unable to diagnose
shortness of breath (see Box 55.1). Patients may experience
variability in symptoms– some will have episodic symptoms
related to triggers such as an upper respiratory infection while
others will experience signicant symptoms year- round.
It is important to obtain a detailed medical history
when diagnosing a patient with suspected asthma. Patients
should be asked about constituent symptoms and whether
they experience any patterns in their symptoms, such as seasonality. Patients frequently report worsening symptoms
at night. Onset, duration, and frequency of exacerbations
should also be noted. Use of short- acting beta- 2 agonists
asthma versus COPD based on the patient’s history, diusing capacity for carbon monoxide (DLCO) may be ordered.
e DLCO is normal in asthmatic patients and decreased
in patients with COPD. Additionally, patients with asthma
demonstrate symptomatic resolution with the use of inhaled
corticosteroids while the patient with COPD does not.17 In
COPD, a chest x- ray may also reveal hyperinatedlungs.
Patients diagnosed with asthma are categorized into
intermittent, mild- persistent, moderate- persistent, or
severe. Table 55.1 describes criteria used when categorizing
disease severity.
(SABA), such as albuterol, or daily inhalers should be identied. Any recent emergency department visits and hospitalizations should be identied, as well as any exacerbations
requiring oral steroids or intubation.
It is important to identify what triggers, if any, worsen
the symptoms of asthma. Common exacerbating factors are
upper respiratory infections and environmental allergens
such as dust mites, animal dander, pollen, molds, and mildew. Asthmatic patients can also have a worsening of symptoms when exposed to cold air or during exercise. Finally,
female patients may notice changing symptoms during their
menses or during pregnancy.
It is important to obtain information related to compliance with medications in patients who present with a
MANAGEMENT
e four components of care for the asthmatic patient
are education, control of environmental factors, medications, and monitoring of symptoms. Each is important for
obtaining control and providing stable, long- term, asthma
management.
Education is essential for patients for both maintaining symptomatic control and exacerbation self- treatment.
Patients who undergo self- management education have
reduced urgent care visits and hospitalizations, an increased
adherence to inhaled corticosteroids, and an improved
quality of life.
10,18– 21
Education programs should provide
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TABLE55.1 CLASSIFICATION OFASTHMA SEVERITY
Classication
Intermittent 2days/ week
Mild 2- 6days/ week 2- 6days/ week,
Moderate Daily Daily Some Limitation
Severe Throughout the
Symptoms Need for SABA
≤2days/ week None
or fewer
not more than
1×/ day
Several times/
Day
day
Interference with
Normal Activity
Minor limitation
Extremely
Limited
a basic understanding of the role of inammation in the
development of asthma, treatment goals and details of
medication usage, instructions on how to take medications
correctly, and instructions on how to reduce environmental
exposures that result in asthma exacerbations. It is important to stress the dierence between long- term control
medications, such as inhaled corticosteroids, and quickrelief medications, such as SABAs, and the importance of
medication compliance to disease management.
Eective environmental control strategies identify and
reduce exposure to allergens that result in asthma exacerbations. Patients may be counseled to obtain skin testing for a
variety of allergens then follow up with a treatment plan to
control inciting environmental factors. Some nonmedical
steps can include the use of high- eciency particulate air
(HEPA) lters in bedrooms to reduce pollen exposure and
using mattress encasement wraps to reduce exposure to dust
mites. Alternatively, immunotherapy (allergy shots) may be
recommended to patients demonstrating signicant reactions to pollens and other environmental factors.
Current management guidelines for the asthmatic patient
follow a stepwise approach, demonstrated in Figure 55.1.
Patients with a new diagnosis are oen started on a SABA to
use as needed during exacerbations, and additional therapies,
including inhaled corticosteroids, depend on disease severity.
Examples of low- dose corticosteroids include beclomethasone HFA, 80 mcg/ pu, 1– 3 pus per day, or uticasone
HFA, 44 mcg/ pu, 2 pus perday.
10
Patients who are more symptomatic at initial diagnosis
or are experiencing asthma exacerbations are treated with
increasing immunomodulation and long- acting beta- 2 agonists. Patients in Step 5 requiring high- dose inhaled corticosteroids can be prescribed as much as 480 mcg per day of
beclomethasone or 440 mcg per day of uticasone. Patients
with the most severe symptoms are also prescribed oral corticosteroids in addition to inhaled corticosteroids and longacting beta- 2 agonists.
10
Frequent monitoring of asthma symptoms provides
patients and healthcare providers information on therapeutic success and can reduce the number and severity of
exacerbations. Eective monitoring includes patient logs
to detail the frequency of SABA use and compliance with
Intermittent
Asthma
Step 3
Medium-dose
inhaled
corticosteroids
Step 2
Step 1
Short Acting Beta
Agonist PRN
Figure55.1 Stepwise approach for managing asthma in adults.
ASTHMA AND PREGNANCY 397
Low-dose inhaled
corticosteroids
or
Inhaled cortical
steroids and long-
acting inhaled
agonist
beta
2
Persistent Asthma
Step 4
Medium-dose
inhaled
corticosteroids
and long-acting
inhaled beta
agonist
2
Step 5
High-dose inhaled
corticosteroids
and long-acting
inhaled beta
agonist
Consider
omalizumab in
patients with
allergies
2
Step 6
High-dose inhaled
corticosteroids,
long-acting
inhaled beta
agonist, and oral
corticosteroid
Consider
omalizumab in
patients with
allergies
2
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maintenance medications. Patients with more severe symptoms may be instructed to use peak expiratory ow meters
on a regular basis. Spirometry should be repeated at least
every 1– 2years to monitor the response to therapy. Finally,
30– 32
eects.
All volatile inhaled agents reduce respiratory
resistance when administered at 1 MAC, however desurane has been shown to cause increased airway resistance
when administered at 2 MAC.
33– 35
patients should be seen frequently following initial diagnosis to reinforce education eorts and to ensure pharmaceutical management is optimized.
PREGNANCY- SPECIFIC CONCERNS
For an average parturient, minute ventilation increases by
TREATMENT OFASTHMA EXACERBATIONS
Patients experiencing asthma exacerbations may be
instructed to increase use of SABA to relieve acute symptoms. In addition, inhaled anticholinergics, such as ipratropium bromide, can be prescribed for use during moderate
to severe exacerbations. Finally, patients experiencing a
moderate to severe exacerbation may be prescribed a systemic corticosteroid to speed recovery. Long- acting beta- 2
agonists are not recommended for treatment of exacerbations because of their association with adverse outcomes,
including higher rates of mortality.
22
50% due primarily to increases in tidal volume by the third
trimester secondary to elevated progesterone levels.36 As
a result of increased intra- abdominal mass, the functional
residual capacity (FRC) decreases by 18%. In an otherwise
healthy patient, spirometry results for FEV1, FVC, and
peak expiratory ow rate remain unchanged.
37
Asthma’s progression during pregnancy is highly variable. Improvement in symptoms can be seen in 18%– 34%
of patients, while worsening of symptoms can be seen in
20%– 42% of patients.
1– 3
Some of this variability can be
attributed to increased treatment options, including inhaled
corticosteroids. Women with moderate to severe symptoms
prepregnancy are more likely to experience exacerbation
STATUS ASTHMATICUS
Status asthmaticus (SA) is development of respiratory
failure following a severe asthma attack. Risk factors for
developing SA include previous intubations, hospitalization despite chronic oral steroid use, recent steroid taper,
and medication noncompliance.
23,24
In the acute phase, an
arterial blood gas may demonstrate mild hypoxemia and
a respiratory alkalosis. Respiratory acidosis can be indicative of a tired patient with impending respiratory failure.
In addition, patients with more prolonged symptoms may
begin to demonstrate a metabolic acidosis.
25
Treatment of the patient with status asthmaticus
includes inhaled beta- 2 agonists. e severity of the exacerbation may warrant larger and more frequent doses to
improve the patient’s respiratory status. Albuterol nebulizers are frequently used to optimize medication benet.
Other medications that may be considered in the
treatment of status asthmaticus may be intravenous
methylprednisolone, 60 to 125 mg every 6 hours, and
ipratropium bromide. A recent multicenter randomized
controlled trial demonstrated improved FEV1 in patients
receiving 2 g of IV magnesium in conjunction with albuterol nebulizers.
26
Ketamine has also been used to treat intubated patients
with severe asthma exacerbations and has been demonstrated to reduce the number of intubations in children with
respiratory failure secondary to asthma.
27– 29
Midazolam,
lidocaine, and propofol all demonstrate bronchodilatory
while pregnant. Most episodes occur during the late second
semester.
ated with viral illnesses or upper respiratory infections.
38,39
Exacerbations during pregnancy may be associ-
38
Because uncontrolled asthma is associated with
increased perinatal mortality, preeclampsia, preterm birth,
and low- birth- weight infants, current treatment guidelines
emphasize the importance of maintaining lung function
(see Box 55.2).
10,40,41
Albuterol is the preferred SABA rescue inhaler during pregnancy due to its favorable safety
prole. Budesonide is the preferred inhaled corticosteroid
due to signicant clinical data on safety and is classied as
pregnancy category B. Clinical trials do not demonstrate
specic safety concerns for other inhaled corticosteroids,
yet they are classied as pregnancy category C due to insufcient trials in humans.10 Treatment with chronic inhaled
corticosteroids can reduce the incidence of exacerbations
by 75%.2 Additionally, the addition of inhaled corticosteroids following exacerbation decreases readmission rates by
55% versus a steroid taper alone.
42
e principals of asthma management during pregnancy are unchanged from prepregnancy guidelines.
Patients must remain vigilant to changes in their underlying symptoms, and patients with moderate to severe asthma
should regularly measure peak expiratory ows to facilitate
early identication and treatment of exacerbations. e
presence of gastric reux can exacerbate asthma symptoms
and should be actively managed. Patient education should
continue to emphasize medication compliance, especially
with inhaled corticosteroids. Finally, healthcare providers
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399
receive terbutaline and develop pulmonary edema should
BOX 55.2 GUIDELINES FORTREATMENT OFASTHMA
INPREGNANCY
• Maintain good asthma control during pregnancy. The risks
of asthma exacerbations are greater to both mother and
baby than asthma medications.
be treated with diuretics and oxygen therapy.
Because a well- functioning neuraxial anesthetic usually
avoids instrumentation of the airway, lumbar epidural and
spinal anesthesia are the preferred anesthetic if cesarean
section is necessary. Labor epidurals also decrease catecholamine release associated with labor pain and can reduce both
• Monitor asthma control during monthly visits to evaluate
the need to increase asthma medications.
• Albuterol is the preferred short- acting beta agonist for pregnancy.
oxygen consumption and minute ventilation duringlabor.
Vigilance should be maintained for maternal hemorrhage following delivery secondary to poor uterine tone
in the patient who has received systemic beta- 2 agonists.
• Inhaled corticosteroids, such as budesonide, are preferred
for long- term control.
• Consider regional anesthesia for cesarean section to
decrease risk of bronchoconstriction triggered by intubation.
Carboprost (Hemabate) should be avoided in asthmatic
patients due to the bronchoconstriction eects of this medication. Oxytocin (Pitocin), prostaglandin PGE1 (Cytotec),
and methylergometrine (Methergine) are generally safe for
treatment of peripartum bleeding in the asthmatic patient.
must emphasize the importance of compliance with pharmacologic therapy, especially inhaled corticosteroids.
According to one study, approximately 18% of women
with asthma will have one emergency visit during pregnancy
and as many as 62% of pregnant patients with severe asthma
exacerbations will require hospitalization.42 However evidence exists that patients with actively managed asthma
have outcomes comparable to those of parturients without
asthma.43 For this reason, patients with moderate to severe
asthma should be considered to be high- risk pregnancies
and have increased frequency of oce visits.
Should an asthmatic parturient require intubation for
an acute asthma exacerbation, anesthesia providers should
note that pregnancy- related changes in the airway may
result in dicult airway management. In addition to the
CONCLUSION
Uncontrolled asthma during pregnancy may lead to many
serious outcomes for both the fetus and mother. However,
patient outcomes may be optimized through education, monitoring, environmental control, and medication maintenance
therapy. Good baseline control and high patient compliance may reduce acute asthma exacerbations and emergency
department visits. It is important for the practitioner to
identify patient- specic triggers and to prescribe appropriate
preventive therapies. Finally, patients with severe symptoms
should be considered to be high- risk for peripartum complications and should have more frequent prenatal visits.
challenges oxygenating secondary to bronchoconstriction,
the decrease in FRC and increased oxygen consumption in
parturients cause a more rapid, and severe, decline in arterial
saturation compared with the nonpregnancy population.
Ventilation in pregnant asthmatics should be maintained
with small tidal volumes and low respiratory rates and by
using capnography to optimize I:E times. While permissive
hypercapnia may be used in the nonpregnant patient, its
use in the parturient can result in fetal acidosis and shiing
of the fetal oxyhemoglobin dissociation curve to the right,
resulting in decreased oxygen delivery to fetal tissues.
Preterm labor presents another challenge for the asthmatic patient. Parturients on SABA therapy are at increased
risk for tocolytic pulmonary edema, a syndrome characterized by tachypnea and tachycardia, bilateral alveolar inltrates on chest x- ray, and an A- a gradient on an arterial
blood gas.44 us, caution should be taken when choosing
tocolytic therapy in asthmatic parturients. Patients who do
CASE- BASED LEARNING DISCUSSION
1. Is the treatment plan for this patient appropriate? Why
or whynot?
2. Instead of her vital signs improving following the
nebulized albuterol, the patient’s condition remained
the same. What are the most appropriate next steps in
her treatment?
3. e patient expresses concern about the use of inhaled
corticosteroids and is particularly worried about their
eects on her baby. How do you address her concerns?
What are the risks of not taking corticosteroids?
4. How would your diagnostic workup dier if this patient
did not have a history of asthma? How would you expect
her symptoms to change as her pregnancy progresses?
ASTHMA AND PREGNANCY 399
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5. If this patient needed to have surgery for a broken ankle,
what would your preferred anesthetic be? How does her
asthma history aect your preference for anesthesia?
21. Guénette L, etal. Eectiveness of an asthma integrated care program on asthma control and adherence to inhaled corticosteroids.
Journal of Asthma. 2015:1– 8.
22. Salpeter SR, etal. Meta- analysis:eect of long- acting β- agonists on
severe asthma exacerbations and asthma- related deaths. Annals of
Internal Medicine. 2006;144(12):904– 12.
REFERENCES
23. Corbridge TC, Hall JB. e assessment and management of adults
with status asthmaticus. American Journal of Respiratory and
Critical Care Medicine. 1995;151(5):1296– 316.
1. Turner ES, Greenberger PA, Patterson R. Management of
the pregnant asthmatic patient. Annals of Internal Medicine.
1980;93(6):905– 18.
2. Stenius- Aarniala BS, Hedman J, Teramo KA. Acute asthma during
pregnancy. orax. 1996;51(4):411– 4.
3. Kircher S, Schatz M, Long L. Variables aecting asthma course
during pregnancy. Annals of Allergy, Asthma and Immunology.
2002;89(5):463– 6.
4. Hernandez E, Angell CS, Johnson JW. Asthma in pregnancy:current concepts. Obstetrics and Gynecology. 1980;55(6):739– 43.
5. Alexander S, Dodds L, Armson BA. Perinatal outcomes in women
with asthma during pregnancy. Obstetrics and Gynecology.
1998;92(3):435– 40.
6. Ford ES. e epidemiology of obesity and asthma. Journal of Allergy
and Clinical Immunology. 2005;115(5):897– 909.
7. Simard B, et al. Asthma and sleep apnea in patients with morbid obesity: outcome aer bariatric surgery. Obesity Surgery.
2004;14(10):1381– 8.
8. Beuther DA, Weiss ST, Sutherland ER. Obesity and asthma.
American Journal of Respiratory and Critical Care Medicine.
2006;174(2):112– 9.
9. Platts- Mills TAE, et al. Is the hygiene hypothesis still a viable
explanation for the increased prevalence of asthma? Allergy.
2005;60:25– 31.
10. Prevention P. Expert Panel Report 3 (EPR- 3): guidelines for the
diagnosis and management of asthma- summary report 2007. Journal
of Allergy and Clinical Immunology. 2007;120(5 Suppl):S94.
11. Sporik R, etal. Exposure to house- dust mite allergen (Der p I) and
the development of asthma in childhood:a prospective study. New
England Journal of Medicine. 1990;323(8):502– 7.
12. Platts- Mills TA, etal. Indoor allergens and asthma: report of the
ird International Workshop. Journal of Allergy and Clinical
Immunology. 1997;100(6):S2– S24.
13. Rosenstreich DL, et al. e role of cockroach allergy and exposure to cockroach allergen in causing morbidity among innercity children with asthma. New England Journal of Medicine.
1997;336(19):1356– 63.
14. Perzanowski MS, etal. Eect of cat and dog ownership on sensitization and development of asthma among preteenage children.
American Journal of Respiratory and Critical Care Medicine.
2002;166(5):696– 702.
15. Sama SR, etal. A longitudinal study of adult- onset asthma incidence
among HMO members. Environmental Health. 2003;2(1):10.
16. Murphy V, et al. Asthma self- management skills and the use of
asthma education during pregnancy. European Respiratory Journal.
2005;26(3):435– 41.
17. Tilles SA. Dierential diagnosis of adult asthma. Medical Clinics of
North America. 2006;90(1):61– 76.
18. Coman JM, et al. Eects of asthma education on children’s use of acute care services: a meta- analysis. Pediatrics.
2008;121(3):575– 86.
19. Guevara JP, etal. Eects of educational interventions for self management of asthma in children and adolescents:systematic review and
meta- analysis. British Medical Journal. 2003;326(7402):1308– 9.
20. Cabana MD, et al. Impact of physician asthma care educa-
24. Peters JI, etal. Status asthmaticus in the medical intensive care unit:a
30- year experience. Respiratory Medicine. 2012;106(3):344– 8.
25. Mountain R, et al. Acid- base disturbances in acute asthma. Chest
Journal. 1990;98(3):651– 5.
26. Silverman RA, etal. IV magnesium sulfate in the treatment of acute
severe asthma: a multicenter randomized controlled trial. Chest
Journal. 2002;122(2):489– 97.
27. Denmark TK, Crane HA, Brown L. Ketamine to avoid mechanical ventilation in severe pediatric asthma. Journal of Emergency
Medicine. 2006;30(2):163– 6.
28. Sarma V. Use of ketamine in acute severe asthma. Acta
Anaesthesiologica Scandinavica. 1992;36(1):106– 107.
29. L’Hommedieu CS, Arens J. e use of ketamine for the emergency
intubation of patients with status asthmaticus. Annals of Emergency
Medicine. 1987;16(5):568– 71.
30. Cheng EY, et al. Direct relaxant eects of intravenous anesthetics on airway smooth muscle. Anesthesia and Analgesia.
1996;83(1):162– 8.
31. Rogliani P, etal. e inuence of propofol, remifentanil and lidocaine on the tone of human bronchial smooth muscle. Pulmonary
Pharmacology and erapeutics. 2013;26(3):325– 31.
32. Koga Y, etal. Comparison of the relaxant eects of diazepam, unitrazepam and midazolam on airway smooth muscle. British Journal
of Anaesthesia. 1992;69(1):65– 69.
33. Dikmen Y, etal. Pulmonary mechanics during isourane, sevourane and desurane anaesthesia. Anaesthesia. 2003;58(8):745– 8.
34. Satoh J- I, Yamakage M. Desurane induces airway contraction
mainly by activating transient receptor potential A1 of sensory Cbers. Journal of Anesthesia. 2009;23(4):620– 3.
35. Nyktari V, etal. Respiratory resistance during anaesthesia with isourane, sevourane, desurane: a randomized clinical trial. British
Journal of Anaesthesia. 2011;107(3):454– 61.
36. Guy ES, Kirumaki A, Hanania NA. Acute asthma in pregnancy.
Critical Care Clinics. 2004;20(4):731– 45.
37. Brancazio LR, Laifer SA, Schwartz T. Peak expiratory ow rate in
normal pregnancy. Obstetrics and Gynecology. 1997;89(3):383– 6.
38. Murphy VE, etal. Severe asthma exacerbations during pregnancy.
Obstetrics and Gynecology. 2005;106(5, Part1):1046– 54.
39. Schatz M, etal. Asthma morbidity during pregnancy can be predicted by severity classication. Journal of allerg y and clinical immunology. 2003;112(2):283– 8.
40. Liu S, etal., Maternal asthma and pregnancy outcomes:a retrospective cohort study. American Journal of Obstetrics and Gynecology.
2001;184(2):90– 96.
41. Murphy V, Clion V, Gibson P. Asthma exacerbations during pregnancy:incidence and association with adverse pregnancy outcomes.
orax. 2006;61(2):169– 76.
42. Wendel PJ, et al. Asthma treatment in pregnancy: a randomized
controlled study. American Journal of Obstetrics and Gynecology.
1996;175(1):150– 4.
43. Schatz M, etal. Perinatal outcomes in the pregnancies of asthmatic
women:a prospective controlled analysis. Critical Care Medicine.
1995;151:1170– 4.
44. Pisani RJ, Rosenow EC. Pulmonary edema associated with tocolytic
therapy. Annals of Internal Medicine. 1989;110(9):714– 8.
tion on patient outcomes. Health Education and Behavior.
2014;41(5):509– 17.
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SECTIOND
NEUROLOGIC CRISES
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56.
STROKE/ SUBARACHNOID HEMORRHAGE AND PREGNANCY
CristinaWood
CASE PRESENTATION
hypotension resulting in poor perfusion can also result in
ischemic stroke.
A 30- year- old G2P1 parturient with a history of migraines
and a diagnosis of preeclampsia is in active labor at 39 weeks
gestation. She is now complaining of a headache, blurred
vision, and dizziness. Her blood pressure is 160/ 100.
ere does not appear to be an increased risk of ischemic stroke during the antepartum period, but there is a
seven- to eightfold increase in the postpartum period.
2
A hemorrhagic stroke is a violation of cranial vasculature
that results in blood leaking into/ around cranial tissue. e
INCIDENCE, EPIDEMIOLOGY AND
PATHOPHYSIOLOGY
Stroke and intracranial hemorrhage are the two leading
neurologic causes of maternal mortality. Athorough understanding of the pathophysiology, assessment, and management of stroke and subarachnoid hemorrhage in pregnancy
is necessary to ensure appropriate and timely care delivery for optimal outcome in the setting of these neurologic
emergencies.
most common etiologies for hemorrhagic stroke are hypertensive disorders in the peripartum period, namely preeclampsia, eclampsia, and gestational hypertension. Compared with
nonpregnant women, there is a 2.5- fold increased risk antepartum and 24- fold risk in the postpartum period, respectively,
for hemorrhagic stroke. e distribution between ischemic
and hemorrhagic stroke in pregnancy appears to be fairly
equal, unlike the general population, where 87% of strokes are
ischemic.
2,3
Hospital admissions for stroke in pregnancy have
almost doubled since 1995, likely due to increasing frequency
of hypertensive disorders in pregnancy.4 In addition, the overall risk of stroke is increased in the peripartum period, with an
STROKE
More women died from neurological causes in 2010– 2012
than from any other single direct cause of maternal death.
In addition, the rate of deaths from neurological causes
has remained essentially unchanged for the past 30years.1
Two of those neurological causes are stroke and intracranial
hemorrhage, which, in addition to being medical emergen-
incidence of 34.2 per 100,000 deliveries versus an incidence
of 11 per 100,000 in the general population. e majority of
strokes occur in the postpartum period (89%) and account for
14% of maternal mortalities.
2,3
When mortality from stroke is
broken down by etiology, intracranial hemorrhage is the most
common cause, followed by cerebral ischemia and cerebral
venous thrombosis. e mortality rate of ischemic stroke is
0.03 per 100,000 and hemorrhagic is 0.75 per 100,000.
1
cies, can also be more challenging to diagnose and treat in
the parturient. is is largely due to the physiologic changes
that occur during pregnancy and in the postpartum period,
but fetal considerations are also a factor.
Stroke results from vascular damage that occurs in the
brain and can be broken down into ischemic and hemorrhagic etiologies. Ischemic stroke is dened by the absence
or blockade of blood ow to an area of the brain. e
most common etiology of ischemic stroke is occlusion of
the arterial vasculature due to atherosclerosis, thrombotic
events, or vasospasm. However, occlusion of the venous
vasculature due to venous embolism and cerebral venous
thrombosis can also induce cerebral ischemia. In addition,
INTRACRANIAL HEMORRHAGE
Subarachnoid hemorrhage (SAH) is a leading cause of indirect maternal mortality, occurring in 5– 17 per 100,000 deliveries. It is involved in 4% of all pregnancy related in- hospital
deaths, with half occurring postpartum. ere are several
etiologies of cerebral hemorrhage in pregnancy, including
aneurysm/ arteriovenous malformation (AVM) and vessel
rupture from intracranial arterial occlusion or preeclampsia/ hypertension. Aneurysms/ AVM are extremely rare and
found in 0.01% to 0.05% of all pregnancies, similar to the
general population (7 versus 5 per 100,000 person years).
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However, rupture of an existing aneurysm/ AVM has been
reported to be ve times higher in pregnancy in some studies
and most commonly occurs late in pregnancy, at delivery, or
postpartum. is increase is possibly due to hemodynamic
changes seen in pregnancy, including a 40%– 50% increase
in circulating blood volume at term gestation.
5,6
Maternal
mortality is also similar to the nonpregnant population at
35%, while fetal mortality is 17% following maternal SAH.6
Hypertension occurs in 40% of SAHs in the peripartum
period5 and is most common commonly associated with
hypertensive disorders of pregnancy.
TABLE56.1 CARDIOVASCULAR CHANGES INPREGNANCY
Measurement Percentage change
Blood Volume +40
Plasma Volume +55
Red Blood Cell Volume +30
Heart Rate +15
Cardiac Output +40–50
Peripheral Systemic Resistance - 20
Other causes of intracranial or subarachnoid bleeding
during pregnancy include cerebral vascular thrombosis and
dural puncture. Seventy- ve percent of adult cases of cerebral
venous/ arterial thrombosis are women of childbearing age, and
cases usually involve the cortical veins (12 per 100,000 deliveries). Cases are seen more frequently in the last trimester and
2– 3 weeks postpartum. rombosis may also occur secondary to trauma (i.e., compromise of the endothelial lining during the second stage of labor), or simply the hypercoagulable
state of pregnancy.7 Post– dural puncture headaches (PDPHs)
occur in <1% of parturients receiving neuraxial anesthesia/
analgesia; those at highest risk for bleeding related to dural
puncture are those with the largest dural insult and greatest
degree of intracranial hypotension. e loss of cerebrospinal
uid (CSF) creates traction on the bridging veins, leading to
rupture. Maternal intracranial hemorrhage occurs in approximately 6 per 100,000 deliveries, which is similar to SAH, but
mortality may be twice that of SAH (20% versus 10%).
8,9
placenta, and fetus. As mentioned above, increased cardiac
output and blood volume can lead to increased intracranial
perfusion and potentially increased vessel wall tension. If
intracranial ischemia or hemorrhage does occur, decreased
oxygen delivery may worsen the neurologic insult.
Increased minute ventilation occurs in parturients, likely
secondary to progesterone sensitization of the central respiratory centers. is results in an increase in respiratory rate (15%)
and tidal volume (40%). Normal CO2 in pregnancy is about
32mmHg, versus 40mmHg in the nonpregnant patient. ere
is increased renal excretion of sodium bicarbonate to compensate for this hypocapnia, resulting in a minimal increase in pH
(7.41–7.44).13 Cerebral autoregulation related to carbon dioxide level should not change to a signicant degree.
Gestational thrombocytopenia is observed in a small
number of parturients (90,000– 100,000). ere is no associated platelet dysfunction or increased risk of bleeding complications, including intracranial events. However, there is an
IMPACT OFPHYSIOLOGIC CHANGES
INPREGNANCY
increase in production of coagulation factors Ι, VII, VIII, and
X, a decrease in protein S, and inhibition of brinolysis. ese
changes result in a prothrombotic state, placing the parturient
ere are many physiologic changes occurring in pregnancy
that place parturients at risk for neurologic complications
and alter management and treatment. In the cardiovascular
at risk for thrombotic events14 such as stroke.
RISK FACTORS
system, the blood volume increases by approximately 40%
(approximately 1.5 L) by the third trimester.
logic dilutional anemia develops where normal HCT is 30%–
35%. Heart rate also increases 10%– 20%. e combination
of these results is a 30%– 60% increase in cardiac output seen
as early as the rst trimester. e vascular circulation compensates by decreasing peripheral vascular resistance, resulting in an overall slight decrease in systemic blood pressure.
See Table 56.1. Aortocaval compression starting at approximately 20 weeks gestation may decrease cardiac output if the
patient is not positioned with appropriate le uterine displacement (at least 30° displacement).12 Oxygen consumption and metabolic demand increases up to 40%– 60% from
prepregnancy values, secondary to the enlarged uterus, the
10,11
Aphysio-
ere are several conditions in pregnancy that place the
parturient at risk for stroke and cranial hemorrhage, including hypertension, diabetes, heart disease, anemia, and other
blood dyscrasias. Operative delivery places the parturient at
a 3- to 12- fold increased risk for stroke. Migraine headaches
have also been associated with a 17- fold increased risk of
stroke. However, hypertensive disorders in pregnancy are by
far the most common etiology of cerebral hemorrhage and
stroke, with an odds ratio of 8.8. In fact, parturients diagnosed with hypertension have a six- to ninefold increased
risk of stroke and intracranial hemorrhage.
2,15,16
Preeclampsia is a hypertensive disorder found only in
pregnancy and is diagnosed as hypertension (blood pressure
404 SECTION D.NEUROLOGICCRISES
Maternal Headache
https://t.me/medicina_free
405
greater than 140/ 90 taken on two occasions at least 4 hours
apart) with associated end- organ damage (thrombocytopenia, increased creatinine, headache, visual disturbances,
elevated liver transaminases, proteinuria, etc.). Preeclampsia
occurs in approximately 5% of pregnancies worldwide and is
thought to be due to poor placental perfusion with the release
of antiangiogenic factors and impaired endothelial function.
Independent risk factors for SAH are similar to
stroke risk factors and include certain ethnicities (African
American and Hispanic), hypertension, coagulopathy, drug
abuse (tobacco, alcohol, illicit drugs), and venous thrombosis. Cerebral venous thrombosis (CVT) can result in stroke
as well as hemorrhage, occurs in 11.6/ 100,000 pregnancies,
and carries a 4.3% mortalityrate.
9
Of parturients diagnosed with stroke, 25%– 45% are women
with a diagnosis of preeclampsia. e increased risk of stroke
and intracranial hemorrhage is due to acute increases in blood
PRESENTINGSIGNS
pressure. Astudy by Martin etal.17 demonstrated that systolic
blood pressure is the most important predictor of stroke,
and in 96% of cases the systolic blood pressure was greater
than 160mmHg; whereas in only 18% of the cases the diastolic blood pressure was greater than 105mmHg. HELLP
syndrome (hemolysis, elevated liver enzymes, low platelets)
occurs in <1% of pregnancies and up to 20% of severe preeclamptic patients. HELLP syndrome is associated with
bleeding complications, including intracranial hemorrhage.
Hypertension/Preeclampsia Neurological Deficits
e most common presenting sign of neurological injury
such as stroke or intracranial hemorrhage is severe headache,
with a frequency up to 77%,18 especially in hemorrhagic
cases. Since headache in the parturient is a common and
nonspecic complaint, timely assessment and diagnosis is
critical (Figure 56.1). Dierential diagnosis should include
stroke, preeclampsia, postdural puncture headache, migraine
or tension headache, meningitis, and caeine withdrawal. In
No neurological
deficits/hypertension
Antihypertensive medications
Magnesium sulfate therapy
If no response
Consider tension or migraine
headache or caffeine
withdrawal
If no response with
appropriate treatment
Consider PDPH
Consyntropin, Fioricet
and/or Epidural Blood Patch
Imaging
Consider Neurology/Neurosurgery Consult
Figur e5 6.1 Maternal headache algorithm.
STROKE/SUBARACHNOID HEMORRHAGE 405
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