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Asthma in Pregnancy 

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Asthma is a chronic inflammatory disease of the airways that is characterized by increased responsiveness of the tracheobronchial tree to multiple stimuli. It is the most common chronic condition in pregnancy. [1]

The disease is episodic, being characterized by acute exacerbations intermingled with symptom-free periods. Most asthma attacks prove to be short-lived, lasting minutes to hours. Although patients appear to recover completely clinically, evidence suggests that patients with asthma develop chronic airflow limitations.

The prevalence of asthma in the general population is 4-5%. In pregnancy, the prevalence ranges from 1-4%.

Asthma-related morbidity and mortality rates in pregnant women are comparable to those in the general population. The mortality rate from asthma in the United States is 2.1 persons per 100,000. [2]

Although women with mild asthma are unlikely to have problems, patients with severe asthma are at greater risk of deterioration. The deterioration risk is highest in the last portion of a pregnancy.

In fact, severe and/or poorly controlled asthma has been associated with numerous adverse perinatal outcomes, including the following:

Preeclampsia

Pregnancy-induced hypertension

Uterine hemorrhage

Preterm labor

Premature birth

Congenital anomalies

Fetal growth restriction

Low birth weight

Neonatal hypoglycemia, seizures, tachypnea, and neonatal intensive care unit (ICU) admission

This risk of giving birth to a small or preterm infant appears to be small and may be minimized by good control of asthma. Studies have indicated that low-birth-weight infants are more common in women with daily symptoms or low expiratory flow than in women without asthma.

Asthma can also lead to the following morbidities in pregnant women:

Respiratory failure and the need for mechanical ventilation

Barotrauma

Complications of (parenteral) steroid use

Death can also occur.

Pregnancy has a significant effect on the respiratory physiology of a woman. While the respiratory rate and vital capacity does not change in pregnancy, tidal volume, minute ventilation (40%), and minute oxygen uptake (20%) increase, with a resultant decrease in functional residual capacity and residual volume of air as a consequence of the elevated diaphragm. In addition, airway conductance is increased and total pulmonary resistance is reduced, possibly as a result of the influence of progesterone.

The consequence of these physiologic changes is a hyperventilatory picture as a normal state of affairs in the later half of pregnancy. This results in the picture of a chronic respiratory alkalosis during pregnancy, with a decreased partial pressure of carbon dioxide (pCO2), decreased bicarbonate, and increased pH.

A normal pCO2 in a pregnant patient may signal impending respiratory failure. The increased minute ventilation and improved pulmonary function in pregnancy promote more efficient gas exchange from the maternal lungs to the blood. Therefore, changes in respiratory status occur more rapidly in pregnant patients than in nonpregnant patients.

Asthma is characterized by inflammation of the airways, with an abnormal accumulation of eosinophils, lymphocytes, mast cells, macrophages, dendritic cells, and myofibroblasts. This leads to a reduction in airway diameter caused by smooth muscle contraction, vascular congestion, bronchial wall edema, and thick secretions.

Go to Asthma for more complete information on this topic.

Problems to consider that can mimic asthma in pregnant patients include the following:

Airway obstruction

Amniotic fluid embolism

Acute congestive heart failure (CHF), secondary to peripartum cardiomyopathy

Physiologic dyspnea of pregnancy

History findings in pregnant and nonpregnant patients may include the following:

Cough

Shortness of breath

Chest tightness

Noisy breathing

Nocturnal awakenings

Recurrent episodes of symptom complex

Exacerbations possibly provoked by nonspecific stimuli

Personal or family history of other atopic disease (eg, hay fever, eczema)

General physical examination findings may include the following:

Tachypnea

Retraction (sternomastoid, abdominal, pectoralis muscles)

Agitation, usually a sign of hypoxia or respiratory distress

Pulsus paradoxicus (>20 mm Hg)

Pulmonary findings are as follows:

Diffuse wheezes – Long, high-pitched sounds on expiration and, occasionally, on inspiration)

Diffuse rhonchi – Short, high- or low-pitched squeaks or gurgles on inspiration and/or expiration

Bronchovesicular sounds

Expiratory phase of respiration equal to or more prominent than inspiratory phase

Signs of fatigue and near-respiratory arrest are as follows:

Alteration in the level of consciousness, such as lethargy, which is a sign of respiratory acidosis and fatigue

Abdominal breathing

Inability to speak in complete sentences

Signs of complicated asthma are as follows:

Equality of breath sounds: Check for equality of breath sounds (pneumonia, mucous plugs, barotrauma). The amount of wheezing does not always correlate with the severity of the attack. A silent chest in someone in distress is more worrisome.

Jugular venous distension from increased intrathoracic pressure (from a coexistent pneumothorax)

Hypotension and tachycardia (think tension pneumothorax)

Fever, a sign of upper or lower respiratory infections

Asthma Control Questionnaire/ Test

The Asthma Control Questionnaire (ACQ)/Test (ACT) is a 7-item, primarily self-administered, validated questionnaire (patients: 6 items; clinicians: 1 item) that is used to gauge the adequacy and change in asthma control in patients. [3] Symptoms (5 items), use of a rescue bronchodilator (1 item), and clinically measured of forced expiratory volume (FEV 1 ) (1 item) are scored on a 7-point scale (0 = completely controlled; 6 = severely uncontrolled).

A Brazilian study reported that the ACQ/ACT is also reliable and valid in pregnant women with asthma on the basis of findings on clinical evaluations and pulmonary function tests and ACQ/ACT results in 40 pregnant asthmatic women over a total of 113 medical visits. [4]

Go to Pediatric Asthma for more information on this topic.

Asthma results from a complex and poorly defined interaction of genetic predisposition and environmental stimulation. The basic mechanism for nonspecific bronchial hyperresponsiveness is unknown. Airway inflammation is the most popular hypothesis.

Implicated stimuli include the following:

Allergens, including pollens, house-dust mites, cockroach antigen, animal dander, molds, and Hymenoptera stings

Irritants, including cigarette smoke, wood smoke, air pollution, strong odors, occupational dust, and chemicals

Medical conditions, including viral upper respiratory tract infections, sinusitis, esophageal reflux, and Ascaris infestations

Drugs and chemicals, including aspirin, nonsteroidal anti-inflammatory drugs, beta blockers, radiocontrast media, and sulfites

Exercise (see Exercise-Induced Asthma.)

Cold air

Menses

Emotional stress

A complete blood count (CBC) is performed to assess the degree of nonspecific inflammation and the possibility of a comorbid anemia or thrombocytopenia. Leukocytosis may be the result of a physiologic response to pregnancy, steroid therapy, upper respiratory tract infections, or the stress of an asthma attack.

Arterial blood gas (ABG) analysis indicates the level of oxygenation and respiratory compensation, giving objective information to the patient’s clinical presentation. Partial pressure of carbon dioxide in the arterial blood (PaCO2) is generally low in the early stages of an exacerbation as a result of hyperventilation. An increase in PaCO2 can be a sign of impending respiratory failure. ABG results often show a decrease in PaO2. Physiologic changes that accompany pregnancy in the pulmonary system slightly alter normal ABG values: pH = 7.4-7.45, pO2 = 95-105 mm Hg, pCO2 = 28-32 mm Hg, and bicarbonate = 18-31 mEq/L.

These must be obtained in patients in whom pneumonia is found or reasonably suggested.

A normal chest radiograph in late pregnancy typically reveals an enlarged heart and some prominent lung markings from elevation of the diaphragm. Chest radiography is indicated when the other coexistent conditions, such as pneumonia, barotrauma, CHF, or chronic obstructive pulmonary disease, are likely. Chest radiographs (2 views) with a shielded maternal abdomen expose the fetus to approximately 0.00005 rad.

Go to Imaging in Asthma for more complete information on this topic.

Hand-held peak flow meters are available in most emergency departments (EDs). If the patient’s baseline is known, clinicians can use measurement to assess the severity of an attack and the patient’s response to medications.

Reversible airflow obstruction is central to the diagnosis and assessment of asthma.

Changes in pulmonary function during acute asthma include the following:

Decreased peak expiratory flow rate (PEFR) and forced expiratory volume in 1 second (FEV1)

Mild reduction in the forced vital capacity (FVC)

An increased residual volume (RV), functional residual capacity (FRC), and total lung capacity (TLC)

Normal diffusing capacity

Patients with asthma usually demonstrate a greater than 15% increase in FEV1, FVC, and PEFR when treated with bronchodilators.

Go to Peak Flow Rate Measurement for more complete information on this topic.

Almost all antiasthma drugs are safe to use in pregnancy and during breastfeeding. In fact, undertreatment of the pregnant patient is a frequent occurrence, because such patients are worried about medication effects on the fetus. [1, 5]

Outpatient management of asthma is similar for the pregnant patient as it is for the nonpregnant patient. Beta-adrenergic agonists remain the mainstay of treating exacerbations and handling mild forms of asthma. Early research suggests a management algorithm for asthma in pregnancy based on fraction of exhaled nitric oxide (FE NO) and symptoms significantly reduces asthma exacerbations. [6]

For moderate-persistent asthma, a beta-adrenergic agonist combined with an inhaled anti-inflammatory agent or inhaled corticosteroid is recommended for treatment. In severe asthma, oral corticosteroids and beta agonists are recommended.

Corticosteroids can be used in the acute and outpatient setting and have been shown to be relatively safe in pregnancy. The intravenous, intramuscular, and oral preparations can be used for acute exacerbations, whereas the inhaled preparations are reserved for outpatient maintenance therapy. Recent data on inhaled glucocorticoids support its relative safety although there is the potential risk for offspring endocrine and metabolic disturbances. [7]  Some studies suggest the “sustained” use of systemic steroids may cause a slight increase in congenital malformation (mainly clef lip), prematurity, low birth weight, preeclampsia, gestational diabetes, and neonatal insufficiency. [8, 9, 10, 11, 12, 13] However, randomized trials have not been performed.

A longer-acting beta2-adrenoreceptor agonist (eg, salmeterol), the bronchodilator effects of which last at least 12 hours, is an effective treatment for nocturnal asthma.

Historically, methylxanthines and oral beta agonists have been used to treat asthma. Both have been shown to be safe in pregnancy but have fallen out of favor for newer medicines and the inhaled forms, respectively.

Magnesium sulfate is another medication that is safe to use in pregnancy. It works as a smooth-muscle relaxant of the airway.

Epinephrine use should be avoided in the pregnant patient. In general, epinephrine is used only in the most severe asthma exacerbations. In pregnancy, employment of the drug can lead to possible congenital malformations, fetal tachycardia, and vasoconstriction of the uteroplacental circulation. In rare cases where a systemic beta-agonist is needed, SQ use of terbutaline may be considered. [14]

A case-control study by Gidaya et al investigated associations between use of β-2-adrenergic receptor (B2AR) agonist drugs during pregnancy and risk for autism spectrum disorders by using Denmark’s health and population registers. The study found that B2AR agonist exposure during pregnancy may be associated with an increased risk for ASD however any intervention must be balanced against benefits of indicated medication use by pregnant women. [15, 16]

Go to Use of Metered Dose Inhalers, Spacers, and Nebulizers for more complete information on this topic.

Prior to arriving at the ED, address the patient’s airway status as needed. Provide early institution of beta-agonist inhalational therapy. Provide supplemental oxygen.

Pregnant patients who present with typical mild exacerbations of asthma may be treated in the same way that a regular asthmatic patient with similar symptoms would be, with bronchodilator therapy and steroids.

Special attention must be given to pregnant patients who present with severe asthma exacerbations, because the resulting maternal hypoxia can have devastating consequences on the fetus.

The American College of Obstetricians and Gynecologists has issued practice guidelines for the management of asthma during pregnancy, Asthma in Pregnancy. [17]

As always in the ED, address the ABCs. The patient should be placed on a cardiac monitor and pulse oximetry. The threshold of intubation should be low to prevent/limit hypoxic episodes to the fetus. Intubate and mechanically ventilate patients who are in or near respiratory arrest and patients who do not respond to treatment as evidenced by the following:

Hypoxemia despite supplemental oxygen

Increasing carbon dioxide retention

Persistent/worsening level of consciousness

Hemodynamic instability

The key to treating asthma in the pregnant patient is to frequently assess the patient, the severity of the attack, and the response to treatment.

Hypoxia, acidosis, unequal breath sounds, pneumothorax, and atypical features serve as warning signs of severe exacerbations.

Inhaled beta2-agonists are the mainstay of treatment. The beta2-agonist, inhaled and/or subcutaneous, is typically given in 3 doses over 60-90 minutes. Beta-adrenergic blocking agents should be avoided owing to bronchospastic effect.

The early use of systemic steroids has been shown to reduce the length of stay in the ED and the admission rate; the effect of steroids is seen within 4-6 hours of the institution of therapy.

Supply supplemental oxygen to maintain oxygen saturation higher than 95%. Intravenous fluids can help to loosen and clear secretions.

Fetal monitoring becomes important after 20 weeks of gestation in severe cases.

Tranquilizers and sedatives should be avoided because of their respiratory depressant effect. Antihistamines are not useful in the treatment of asthma. Mucolytic agents increase bronchospasm.

Less than 1% of all asthmatic patients require mechanical ventilation. Asthmatic patients have higher complication rates from mechanical ventilation. Increased airway resistance may result in extremely high peak airway pressures, barotraumas, and hemodynamic impairment. Mucous plugging is common, increasing airway resistance, atelectasis, and the incidence of secondary pneumonia. Paradoxical increases in bronchospasm may occur from aggravation by the endotracheal tube.

Typical ventilator settings may lead to stacked breaths and increased airway pressures. Decrease the ratio of the duration of inspiration to the duration of expiration (I:E ratio), and set a low respiratory rate to allow for adequate expiration.

Go to Status Asthmaticus for more complete information on this topic.

Criteria for hospital admission are as follows:

Inadequate response to ED therapy

pO2 less than 70 mm Hg

Signs of fetal distress (eg, decreased movement, abnormal cardio tocodynamometry, uterine contractions)

Multiple medication use (ie, requiring 3 or more medications simultaneously)

A protracted course with poor response to outpatient therapy thus far instituted or a history of severe asthma requiring intubation or ICU admission

Inadequate home conditions and transport/access to ED care

Criteria for ICU admission are as follows:

Altered level of consciousness

Poor air flow

Signs of fatigue, a downhill course, or a need for mechanical ventilation

PEFR/FEV1 less than 25% of predicted or pCO2 greater than 35 mm Hg

Criteria for home discharge include the following:

Greatly improved symptoms and physical examination findings

Ability of the patient to walk out of the ED without obvious distress

PEFR/FEV1 greater than 70% baseline

No fetal distress

Good follow-up and access to ED in case of relapse

A follow-up appointment 2-4 days following the ED visit is recommended. Consider referral to an asthma specialist; in addition, involvement of a multidisciplinary team that includes a pulmonologist, neonatologist, obstetrician, and possibly an allergologist should be considered in the follow-up of a pregnant asthma woman. [18] Glucocorticoids at the time of discharge have proven to be useful and to reduce the incidence of ED visits.

Rey E, Boulet LP. Asthma in pregnancy. BMJ. 2007 Mar 17. 334(7593):582-5. [Medline]. [Full Text].

Sly RM, O’Donnell R. Stabilization of asthma mortality. Ann Allergy Asthma Immunol. 1997 Apr. 78(4):347-54. [Medline].

American Thoracic Society. Asthma Control Questionnaire (ACQ). Available at http://www.thoracic.org/assemblies/srn/questionaires/acq.php. Accessed: December 17, 2014.

Monteiro de Aguiar M, Rizzo JA, de Melo Junior EF, Pires Lins E Silva Lima ME, Cavalcanti Sarinho ES. Validation of the Asthma Control Test in pregnant asthmatic women. Respir Med. 2014 Nov. 108(11):1589-93. [Medline].

Hornby PJ, Abrahams TP. Pulmonary pharmacology. Clin Obstet Gynecol. 1996 Mar. 39(1):17-35. [Medline].

Powell H, Murphy VE, Taylor DR, et al. Management of asthma in pregnancy guided by measurement of fraction of exhaled nitric oxide: a double-blind, randomised controlled trial. Lancet. 2011 Sep 10. 378(9795):983-90. [Medline].

Tegethoff M, Greene N, Olsen J, Schaffner E, Meinlschmidt G. Inhaled glucocorticoids during pregnancy and offspring pediatric diseases: a national cohort study. Am J Respir Crit Care Med. 2012 Mar 1. 185(5):557-63. [Medline].

Bakhireva LN, Jones KL, Schatz M, Johnson D, Chambers CD, Organization Of Teratology Information Services Research Group. Asthma medication use in pregnancy and fetal growth. J Allergy Clin Immunol. 2005 Sep. 116(3):503-9. [Medline].

Fitzsimons R, Greenberger PA, Patterson R. Outcome of pregnancy in women requiring corticosteroids for severe asthma. J Allergy Clin Immunol. 1986 Aug. 78(2):349-53. [Medline].

Schatz M. The efficacy and safety of asthma medications during pregnancy. Semin Perinatol. 2001 Jun. 25(3):145-52. [Medline].

Bracken MB, Triche EW, Belanger K, Saftlas A, Beckett WS, Leaderer BP. Asthma symptoms, severity, and drug therapy: a prospective study of effects on 2205 pregnancies. Obstet Gynecol. 2003 Oct. 102(4):739-52. [Medline].

Eltonsy S, Forget A, Beauchesne MF, Blais L. Risk of congenital malformations for asthmatic pregnant women using a long-acting β₂-agonist and inhaled corticosteroid combination versus higher-dose inhaled corticosteroid monotherapy. J Allergy Clin Immunol. 2015 Jan. 135(1):123-30. [Medline].

Schatz M, Dombrowski MP, Wise R, et al. The relationship of asthma medication use to perinatal outcomes. J Allergy Clin Immunol. 2004 Jun. 113(6):1040-5. [Medline].

National Heart, Lung, and Blood Institute, National Asthma Education and Prevention Program Asthma and Pregnancy Working Group. NAEPP expert panel report. Managing asthma during pregnancy: recommendations for pharmacologic treatment-2004 update. J Allergy Clin Immunol. 2005 Jan. 115(1):34-46. [Medline].

Gidaya NB, Lee BK, Burstyn I, Michael Y, Newschaffer CJ, Mortensen EL. In utero Exposure to β-2-Adrenergic Receptor Agonist Drugs and Risk for Autism Spectrum Disorders. Pediatrics. 2016 Feb. 137 (2):1-8. [Medline].

Davenport L. Prenatal Exposure to Asthma Drugs May Boost Autism Risk. Medscape Medical News. Available at http://www.medscape.com/viewarticle/857417. January 19, 2016; Accessed: June 6, 2016.

[Guideline] American College of Obstetricians and Gynecologists (ACOG). Asthma in pregnancy. ACOG practice bulletin; no. 90. Washington (DC): American College of Obstetricians and Gynecologists (ACOG). 2008 Feb. [Full Text].

Mihaltan FD, Antoniu SA, Ulmeanu R. Asthma and pregnancy: therapeutic challenges. Arch Gynecol Obstet. 2014 Oct. 290(4):621-7. [Medline].

Bain E, Pierides KL, Clifton VL, et al. Interventions for managing asthma in pregnancy. Cochrane Database Syst Rev. 2014 Oct 21. 10:CD010660. [Medline].

Namazy JA, Chambers C, Schatz M. Safety of therapeutic options for treating asthma in pregnancy. Expert Opin Drug Saf. 2014 Dec. 13(12):1613-21. [Medline].

Vasilakis-Scaramozza C, Aschengrau A, Cabral HJ, Jick SS. Asthma drugs and the risk of congenital anomalies. Pharmacotherapy. 2013 Apr. 33(4):363-8. [Medline].

Namazy JA, Murphy VE, Powell H, Gibson PG, Chambers C, Schatz M. Effects of asthma severity, exacerbations and oral corticosteroids on perinatal outcomes. Eur Respir J. 2013 May. 41(5):1082-90. [Medline].

Lim A, Stewart K, Konig K, George J. Systematic review of the safety of regular preventive asthma medications during pregnancy. Ann Pharmacother. 2011 Jul. 45(7-8):931-45. [Medline].

Breton MC, Beauchesne MF, Lemiere C, Rey E, Forget A, Blais L. Risk of perinatal mortality associated with inhaled corticosteroid use for the treatment of asthma during pregnancy. J Allergy Clin Immunol. 2010 Oct. 126(4):772-777.e2. [Medline].

Charlton RA, Snowball JM, Nightingale AL, Davis KJ. Safety of fluticasone propionate prescribed for asthma during pregnancy: a UK population-based cohort study. J Allergy Clin Immunol Pract. 2015 Sep-Oct. 3(5):772-9.e3. [Medline].

Namazy J, Cabana MD, Scheuerle AE, et al. The Xolair Pregnancy Registry (EXPECT): the safety of omalizumab use during pregnancy. J Allergy Clin Immunol. 2015 Feb. 135(2):407-12. [Medline].

Hodyl NA, Stark MJ, Osei-Kumah A, Bowman M, Gibson P, Clifton VL. Fetal glucocorticoid-regulated pathways are not affected by inhaled corticosteroid use for asthma during pregnancy. Am J Respir Crit Care Med. 2011 Mar 15. 183(6):716-22. [Medline].

Markus Little, MD Resident Physician, Department of Emergency Medicine, State University of New York Downstate Medical Center

Disclosure: Nothing to disclose.

Richard H Sinert, DO Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Vice-Chair in Charge of Research, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Mark Zwanger, MD, MBA 

Mark Zwanger, MD, MBA is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Jeter (Jay) Pritchard Taylor, III, MD Assistant Professor, Department of Surgery, University of South Carolina School of Medicine; Attending Physician, Clinical Instructor, Compliance Officer, Department of Emergency Medicine, Palmetto Richland Hospital

Jeter (Jay) Pritchard Taylor, III, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Columbia Medical Society, Society for Academic Emergency Medicine, South Carolina College of Emergency Physicians, South Carolina Medical Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Employed contractor – Chief Editor for Medscape.

Assaad J Sayah, MD, FACEP Senior Vice President and Chief Medical Officer, Cambridge Health Alliance

Assaad J Sayah, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, Massachusetts Medical Society

Disclosure: Nothing to disclose.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors A Antoine Kazzi, MD, and Araz Marachelian, MD, to the development and writing of the source article.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors A Antoine Kazzi, MD, and Araz Marachelian, MD, to the development and writing of the source article.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors A Antoine Kazzi, MD, and Araz Marachelian, MD, to the development and writing of the source article.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors A Antoine Kazzi, MD, and Araz Marachelian, MD, to the development and writing of the source article.

Asthma in Pregnancy 

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