Case Study
A 27-year-old gravida 1, para 0 woman presented to labor and delivery at 35 weeks’ gestation for evaluation for dyspnea. Her pregnancy had been uncomplicated, but she had a known history of mild intermittent asthma for which she required an albuterol inhaler “occasionally.” She reported wheezing for 1 day that has not been responsive to her albuterol inhaler and a fever with chills that started that morning. She denied contractions and reported good fetal movement.
On physical examination, the patient had tachypnea with diffuse wheezing. Her vital signs were as follows: heart rate 125 beats/min, blood pressure 117/75 mmHg, respiratory rate 40 breaths/min, oxygen saturation 93 percent on room air, and temperature 38.0℃. Fetal heart rate tracing was Category I. An IV infusion was started, and fluids were administered. A chest x-ray was obtained and revealed “developing consolidation of the right lower lobe and evidence of mild air trapping.” The patient was given three treatments of nebulized albuterol and was started on ceftriaxone and azithromycin for treatment of possible community-acquired pneumonia.
After 1 hour of observation, the patient’s wheezing was slightly improved, but she continued to be tachypneic and uncomfortable. The obstetrician prescribed continued nebulized albuterol with ipratropium bromide every 20 minutes and admitted the patient to the antepartum unit for monitoring. She was stable initially but had increasing oxygen requirements to maintain her oxygen saturation at greater than 95 percent. Her work of breathing increased progressively despite continuous albuterol treatments. An arterial blood gas was remarkable for a respiratory acidosis with the following values: p. 7.29, PCO2 49 mmHg, PO2, 80 mmHg, and bicarbonate 28 mmol/kg. Fetal heart rate tracing was Category II with occasional deep variable decelerations.
The patient was transferred to the ICU for close monitoring and possible intubation and mechanical ventilation. Systemic IV steroids were added to her treatment regimen. Under close observation, her oxygen was gradually weaned to 4 liters/min via nasal cannula. Her care was gradually de-escalated, and she was discharged 5 days later on a steroid taper with close follow-up.
She remained stable for the remainder of her pregnancy and went into spontaneous labor at 38 weeks.
Key Points
Patients may experience exacerbation of previously mild to intermittent asthma in the setting of possible community-acquired pneumonia.
Subsequent hypoxia and hypercarbia despite aggressive therapy may result in the transfer to a higher level of care for further management.
Intubation and ventilation sometimes may be required.
Discussion
Acute respiratory failure (ARF) is rare during pregnancy but is one of the most common indications for ICU admission for parturients. Asthma is one of the most common comorbidities found in pregnancy and is a risk factor for pneumonia during pregnancy. Any respiratory insult during pregnancy may be more likely to lead to respiratory failure due to the normal changes in pulmonary physiology during pregnancy. Both maternal and fetal mortality rates from ARF are reported to be around 30 percent, with maternal rates being slightly higher. Optimizing oxygen delivery, maintaining euvolemia, and treating the underlying causes of lung injury are the primary goals of therapy.1
Respiratory Physiology during Pregnancy
During pregnancy, hyperventilation and a chronic respiratory alkalosis are normal, stimulated both by progesterone levels and by fetal CO2 in the maternal circulation. The diaphragm is pushed cephalad by the expanding uterus, and the anteroposterior and transverse diameters of the chest widen, leading to a stable total lung capacity (TLC). While vital capacity (VC) also remains stable, there is a significant increase in tidal volume (TV). Decreases in expiratory reserve volume (ERV) and residual volume (RV) lead to a significant reduction in functional residual capacity (FRC) by approximately 21 percent below the prepregnancy value. Given this reduction in FRC, there is a decrease in the difference between FRC and closing capacity (CC), making it more likely that small airway closure will occur during normal TV breathing. Obesity, multiple gestation, polyhydramnios, lung disease, and supine positioning all can exacerbate this problem, leading to increased ventilation-perfusion mismatch and hypoxia. The summation of these changes leads to poor tolerance of acute or chronic lung disease during pregnancy.
A normal pregnancy arterial blood gas determination reflects the above-mentioned changes with a fall in measured PaCO2 and a rise in PaO2. Generally, the PaO2 will be above 100 mmHg for the duration of pregnancy, and the PaCO2 will be approximately 30 mmHg. This respiratory alkalosis remains relatively stable for the duration of pregnancy and is accompanied by a compensatory increase in renal excretion of bicarbonate (normal HCO3– 21.7 mEq/liter).2, 3
Asthma
About 8 percent of pregnant women carry the diagnosis of asthma, making it one of the most common comorbidities encountered in pregnancy. The disease is characterized by airway inflammation with reactivity and reversible airway obstruction.3, 4 The National Asthma Expert Panel Report has defined four classes of asthma severity: intermittent, mild persistent, moderate persistent, and severe persistent. Well-controlled asthma can be defined by the following parameters: minimal or no chronic symptoms day or night, minimal or no exacerbations, no limitation of activities, maintenance of (near) normal pulmonary function, minimal use of short-acting inhaled beta2-agonist, and minimal or no adverse effects from medications. Disease course during pregnancy is known to be variable, with about 23 percent of women improving during pregnancy and 30 percent experiencing a worsening in their symptoms. Improvements in symptoms during pregnancy may be caused by progesterone-mediated bronchodilation and increased serum cortisol levels, but the exact mechanism is unknown. Worsening of symptoms may be due to increased stress, worsening of reflux symptoms, bronchitis, or medication noncompliance.3, 5
The National Asthma Education and Prevention Program published guidelines in 2004 on the pharmacologic treatment of parturients with asthma5 (Table 18.1). If asthma is uncontrolled, there is an increased risk of preeclampsia, intrauterine growth restriction, preterm delivery, congenital malformations, and perinatal death. For this reason, all parturients with asthma should undergo clinical evaluation and optimization of symptom control. The treatment of asthma in pregnancy should involve assessment of asthma with objective measures of pulmonary function on a monthly basis, control of factors contributing to asthma severity, patient education, and a stepwise approach to pharmacologic therapy. Should the parturient require an emergency room visit or hospitalization, therapy should be aggressive and focused on maintaining maternal O2 saturation above 95 percent. High-dose short-acting inhaled beta2-agonists, inhaled ipratropium bromide, and either oral or IV corticosteroids are a part of the inpatient treatment algorithm.6,7
Table 18.1 Pharmacologic Management of Asthma during Pregnancy Using a Stepwise Approach
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