Asthma in pregnancy

Asthma in pregnancy

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Pulmonary Disorders

• m/c in pregnancy: asthma (4%) • No evidence that pulmonary function is impaired

because of pregnancy but, advanced pregnancy may intensify the pathophysiological effects of some lung diseases.

- The disparate number of maternal deaths during the influenza pandemics of 1918 and 1957.

- The poor tolerance for pregnancy of women with severe chronic lung disease.

Pulmonary Physiology

• Vital capacity and inspiratory capacity

- increase by 20 percent by late pregnancy

• Expiratory reserve volume

- decreases from 1300 mL to 1100 mL

• Tidal volume

- increases 40 percent

- respiratory stimulant properties of progesterone

Pulmonary Physiology

• Minute ventilation - increases about 30 to 40 percent(d/t tidal volume ↑)

• Arterial pO2 - increases from 100 to 105 mm Hg

• Carbon dioxide production: increases 30 percent

• Diffusion capacity : increases

• pCO2 : decreases from 40 to 32 mm Hg

Pulmonary Physiology

• Residual volume

- decreases 20 percent from 1500 mL to 1200 mL

• The expanding uterus and increased abdominal pr.

-> chest wall compliance to be reduced by a third.

-> the functional residual capacity

(the sum of expiratory reserve and residual

volumes) : decreases.

Pulmonary Physiology

• The sum of these changes

-> substantively increased ventilation

due to deeper but not more frequent breathing.

-> induced by basal oxygen consumption, which

increases incrementally by 20 to 40 mL/min in the

second half of pregnancy.

Asthma

• Prevalence

- increased steadily in many countries beginning

in the mid-1970s

- plateaued in the United States during the past

decade

• almost 8 percent of the general population has asthma.

• prevalence during pregnancy to range between 4 and 8 percent (Kwon and associates,2006)

Pathophysiology of asthma

Pathophysiology of asthma

• Chronic inflammatory airway disorder

• Associated with hereditary component

- increased airway responsiveness and persistent

subacute inflammation have been genes on

chromosomes 5, 11, and 12

(cytokine gene clusters, -adrenergic and

glucocorticoid receptor genes, and the T-cell antigen

receptor gene)

• environmental allergic stimulant

- influenza or cigarette smoke etc.

Pathophysiology of asthma

Reversible airway obstruction from bronchial smooth muscle contraction, vascular congestion, tenacious mucus, and mucosal edema.

Environmental Stimulants

irritants, viral infections, aspirin, cold air, andexercise etc.

Allergent Irritant

Pathophysiology of asthma

• Inflammation : caused by response of mast cells,

eosinophils, lymphocytes, and bronchial epithelium. • inflammatory mediators : histamine, leukotrienes,

prostaglandins, cytokines, and many others.

• IgE also plays a central role in pathophysiology (Strunk and Bloomberg, 2006)

• F-series prostaglandins and ergonovine exacerbate

asthma -> should be avoided if possible.

Clinical Course

• Mild wheezing to severe bronchoconstriction.

• Acute bronchospasm

-> airway obstruction and decreased airflow.

-> work of breathing progressively increases

-> chest tightness, wheezing, or breathlessness.

Clinical Course

• generally reversible and well tolerated by the healthy

nonpregnant individual.

• But even early stages of asthma may be dangerous for the pregnant woman and her fetus.

- smaller functional residual capacity

- more susceptible to hypoxia and hypoxemia.

Effects of Pregnancy on Asthma

• No evidence that pregnancy has a predictable effect

on underlying asthma. • Approximately 20 percent of women with mild or

moderate asthma have been reported to have an intrapartum exacerbation

(Schatz and associates, 2003) • Conversely, reported exacerbations at the time of

delivery in only 1 percent of women. (Wendel and associates,1996)

Pregnancy Outcome

Pregnancy Outcome

• Significantly increased morbidity - associated with progressively more severe disease, poor control, or both. (Källén and Otterblad Olausson, 2007) • Life-threatening complications from status

asthmaticus include muscle fatigue with respiratory arrest, pneumothorax, pneumomediastinum, acute cor pulmonale, and cardiac arrhythmias.

• Maternal and perinatal mortality rates are

substantively increased when mechanical ventilation is required.

Fetal Effects

• With reasonable control of asthma

-> perinatal outcomes are generally good.

• when respiratory alkalosis develops

-> both animal and human studies suggest that fetal

hypoxemia develops well before the alkalosis

compromises maternal oxygenation

(Rolston and associates, 1974)

Fetal Effects

• The fetal response to maternal hypoxemia

-> decreased umbilical blood flow,

-> increased systemic and pulmonary vascular resistance

-> decreased cardiac output.

• Incidence of fetal-growth restriction increases with asthma severity. (Bracken and colleagues ,2003)

• Monitoring the fetal response

-> an indicator of maternal status.

Fetal Effects

• No evidence that commonly used anti-asthmatic drugs

are harmful

(Blais and colleagues, 2007; Källén, 2007; Namazy and Schatz, 2006).

• Despite this, a 13- to 54-percent patient-generated decrease in -agonist and corticosteroid use between

5 to 13 weeks of pregnancy

(Enriquez and co-workers ,2006)

Clinical Evaluation

• The subjective severity of asthma

-> frequently does not correlate with objective

measures of airway function or ventilation.

• Useful clinical signs

-> labored breathing, tachycardia, pulsus paradoxus,

prolonged expiration, and use of accessory muscles.

• Signs of a potentially fatal attack

-> central cyanosis and altered consciousness.

Clinical Evaluation

• Arterial blood gas analysis

-> objective assessment of maternal oxygenation,

ventilation, and acid–base status.

• If used, the results must be interpreted in relation to normal values for pregnancy.

(a pCO2 > 35 mm Hg with a pH < 7.35 is consistent

with hyperventilation and CO2 retention in a pregnant

woman.)

Clinical Evaluation

• Pulmonary function testing

-> should be routine in the management of chronic and

acute asthma.

• Sequential measurement of the FEV1 or the peak expiratory flow rate (PEFR)

-> the best measures of severity.

• An FEV1 less than 1 L, or less than 20 percent of predicted value -> correlates with severe disease defined by hypoxia, poor response to therapy, and a high relapse rate. (Noble and colleagues, 1988)

Clinical Evaluation

• PEFR (peak expiratory flow rate) -> correlates well with the FEV1 -> can be measured reliably with inexpensive portable meters.

• Each woman determines her own baseline when

asymptomatic—personal best—to compare with values when symptomatic.

• PEFR did not change during the course of pregnancy in normal women. ( Brancazio and associates ,1997)

Management of Chronic Asthma

Guidelines of the Working Group on Asthma and Pregnancy • Patient education—general asthma management and its

effect on pregnancy.

• Environmental precipitating factors—avoidance or control.

• Objective assessment of pulmonary function and fetal well-being—monitor with PEFR or FEV1.

• Pharmacological therapy— appropriate combinations and doses to provide baseline control and treat exacerbations

(National Heart, Lung and Blood Institute, 2004)

Management of Chronic Asthma

• Women with moderate to severe asthma

-> FEV1 or PEFR twice daily.

• The FEV1 ideally is >80 percent of predicted.

• For PEFR, predicted values range from 380 to 550 L/min.

Management of Chronic Asthma

Management of Chronic Asthma

• Theophylline

- Methylxanthine

- bronchodilators and anti-inflammatory agents.

- used less frequently since inhaled corticosteroids became available.

- Some theophylline derivatives are considered useful

for oral maintenance therapy if the initial response is

not optimal to inhaled corticosteroids and -agonists

Management of Chronic Asthma

• Leukotriene modifiers - inhibit their synthesis - include zileuton, zafirinkast, and montelukast. - orally or by inhalation for prevention, - not effective for acute disease.

• For maintenance, they are used in conjunction with

inhaled corticosteroids to allow minimal dosing. • little experience with their use in pregnancy (Bakhireva and colleagues, 2007)

Management of Chronic Asthma

• Cromolyn and nedocromil

- inhibit mast cell degranulation.

- ineffective for acute asthma and are taken chronically for prevention.

- not as effective as inhaled corticosteroids

- generally been replaced by leukotriene modifiers

(Fanta, 2009)

Management of Acute Asthma

• Treatment

- similar to that for the nonpregnant asthmatic.

- An exception

: significantly lowered threshold for hospitalization.

- Intravenous hydration may help clear pulmonary

secretions

- supplemental oxygen is given by mask.

Management of Acute Asthma

• The therapeutic aim

- to maintain the pO2 greater than 60 mm Hg

- preferably normal, along with 95-percent oxygen

saturation.

• Baseline pulmonary function

: FEV1 or PEFR

• Continuous pulse oximetry and electronic fetal monitoring : provide useful information.

Management of Acute Asthma

• First-line therapy

- a -adrenergic agonist

- terbutaline, albuterol, isoetharine, epinephrine, isoproterenol, or metaproterenol.

- given subcutaneously, taken orally, or inhaled.

- modulate bronchial smooth muscle relaxation.

- Long-acting preparations are used for outpatient therapy.

Management of Acute Asthma

• If not previously given for maintenance

- inhaled corticosteroids are commenced along with

intensive -agonist therapy.

• For severe exacerbations

- inhaled ipratropium bromide

• Corticosteroids should be given early to all patients with severe acute asthma.

Management of Acute Asthma

• Unless there is a timely response to treatment -> oral or parenteral preparations are given. • Intravenous methylprednisolone, 40 to 60 mg, every 6

hours is commonly used.

• Equipotent doses of hydrocortisone by infusion or prednisone orally can be given instead.

• Because their onset of action is several hours, corticosteroids are given initially along with -agonists for acute asthma.

Management of Acute Asthma

• If initial therapy with -agonists is associated with improvement of FEV1 or PEFR to above 70 percent of baseline -> discharge can be considered.

• for the woman with obvious respiratory distress,

or if the FEV1 or PEFR is less than 70 percent of

predicted after three doses of –agonist

-> admission is advisable.

Management of Acute Asthma

• Intensive therapy

- agonists

- intravenous corticosteroids

- close observation for worsening respiratory distress

or fatigue in breathing

Status Asthmaticus and

Respiratory Failure • Status asthmaticus.

- Severe asthma of any type not responding after 30 to 60 minutes of intensive therapy - Early intubation when maternal respiratory status worsens despite aggressive treatment - Fatigue, carbon dioxide retention, and hypoxemia : indications for mechanical ventilation.

Labor and Delivery

• Maintenance medications through delivery. • Stress-dose corticosteroids are administered to any

woman given systemic steroid therapy within the preceding 4 weeks.

• Usual dose is 100 mg of hydrocortisone given intravenously every 8 hours during labor and for 24 hours after delivery.

• The PEFR or FEV1 should be determined on admission, and serial measurements are taken if symptoms develop.

Labor and Delivery

• Oxytocin or prostaglandins E1 or E2 :

for cervical ripening and induction.

• A nonhistamine-releasing narcotic (fentanyl)

- preferable to meperidine for labor

- epidural analgesia is ideal

Labor and Delivery

• For surgical delivery

- conduction analgesia is preferred

- tracheal intubation can trigger severe bronchospasm.

• Postpartum hemorrhage

- treated with oxytocin or prostaglandin E2.

- Prostaglandin F2 or ergotamine derivatives

: contraindicated

: cause significant bronchospasm.

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