Acute respiratory failure during pregnancy and the peripartum period

INTRODUCTION — Fewer than 2 percent of patients require admission to an intensive care unit (ICU) during pregnancy or the peripartum period, defined as the last month of gestation or the first few weeks following delivery [1-4]. Acute respiratory failure requiring mechanical ventilation is a rare complication of pregnancy affecting 0.1 to 0.2 percent of pregnancies [3].

The clinical presentation, differential diagnosis, most common causes, and management of acute respiratory failure during pregnancy and the peripartum period are reviewed here. Other critical illnesses associated with pregnancy are described separately. (See "Critical illness during pregnancy and the peripartum period".)

CLINICAL PRESENTATION — Pregnancy results in specific changes in respiratory physiology, including an increase in tidal volume and minute ventilation, while the respiratory rate remains relatively unchanged. (See "Maternal adaptations to pregnancy: Dyspnea and other physiologic respiratory changes".)

However, patients with acute respiratory failure during pregnancy or the peripartum period generally present with respiratory distress [5-7]. They are typically dyspneic and unable to speak in complete sentences. Confusion, somnolence, agitation, diaphoresis, and/or cyanosis are common. Most patients breathe more rapidly (tachypnea) and shallowly (small tidal volumes) than non-pregnant patients with acute respiratory failure and may be using their accessory muscles of respiration. Ausculatory findings vary according to the cause of the acute respiratory failure, but may include crackles, rhonchi, and/or wheezes. Consolidation may be evident, as indicated by bronchophony, egophony, or whisper pectoriloquy.

INITIAL EVALUATION AND MANAGEMENT — Initial management is the same regardless of the cause of the acute respiratory failure. It is focused on gas exchange and stabilization of the patient and undertaking a brief history and physical examination to determine the cause.

Supplemental oxygen should be administered. The preferred method of administering the oxygen depends upon the severity of the hypoxemia. For patients with mild hypoxemia, administration via nasal cannula may be sufficient. More severe hypoxemia generally requires administration via a facemask, high flow nasal cannula, or a nonrebreather mask. Oxygenation should be monitored continuously by pulse oximetry. A reasonable goal for pregnant patients is to maintain the oxyhemoglobin saturation ≥95 percent to optimize the fetal oxygen content. Adequate fetal oxygenation requires a maternal arterial oxygen tension (PaO₂) >70 mmHg, which corresponds to an oxyhemoglobin saturation of 95 percent [8].

Mechanical ventilation may be required. The decision about whether to intubate a patient should be considered in the context of pregnancy. Pregnant patients have hypocapnia due to hyperventilation at baseline. Thus, the arterial carbon dioxide tension (PaCO₂) tends to be lower in pregnant patients than in nonpregnant individuals with a similar degree of respiratory failure. The decision to intubate is discussed elsewhere. (See "The decision to intubate".)

Noninvasive ventilation (NIV) has been reported to be successful in the management of acute respiratory failure during pregnancy. The potential benefits of NIV include avoidance of endotracheal intubation and sedative medications used during and after intubation and institution of invasive mechanical ventilation. Pregnant patients are considered at higher risk for aspiration due to elevated intragastric pressure, slower gastric emptying and a reduction in the tone of the lower esophageal sphincter. NIV may increase gastric distention due to air insufflation of the stomach, potentially increasing the risk of vomiting and aspiration. Similar to non-pregnant patients, NIV should be initiated in a monitored setting and reserved for patients who are alert, have the ability to protect their airway, and have stable hemodynamics. The suggested starting pressures for NIV are inspiratory airway pressure (IPAP) 12 to 15 cm H₂O and expiratory airway pressure (EPAP) of 5 to 8 cm H₂O [9].

Intubation may be difficult during pregnancy and the peripartum period due to upper airway hyperemia, diminished airway caliber, and reduced oxygen reserve (as a result of reduced functional residual capacity and increased oxygen utilization). The failure rate of intubation is eight times higher than that of the general population [10]. Therefore, intubation should be performed by the most experienced provider available. Preoxygenation is essential. The process of intubation and the initiation of mechanical ventilation are also reviewed separately. (See "Approach to the difficult airway in adults for emergency medicine and critical care" and "Induction agents for rapid sequence intubation in adults for emergency medicine and critical care" and "Overview of advanced airway management in adults for emergency medicine and critical care" and "Rapid sequence intubation in adults for emergency medicine and critical care" and "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit".)

An arterial blood analysis (ABG) and chest radiograph should be obtained after initial stabilization:

●The ABG identifies and quantitates the severity of any ventilatory abnormalities. It also guides ventilator adjustments in mechanically ventilated patients. Ventilatory goals are different in pregnant patients. The target PaCO₂ is 30 to 32 mmHg, since this is the normal level during pregnancy. Marked respiratory alkalosis should be avoided because it may decrease uterine blood flow. Maternal permissive hypercapnia may also be deleterious to the fetus because of resultant fetal respiratory acidosis [11]. Arterial catheterization may be helpful if frequent arterial blood gases are likely to be needed. (See "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation".)

●The chest radiograph is used to narrow the differential diagnosis of the respiratory failure and, among intubated patients, to confirm that the endotracheal tube is in the correct position. (See "Diagnostic imaging in pregnant and lactating patients".)

A diagnostic evaluation for the etiology of the acute respiratory failure may include a complete blood count with differential, liver function tests, renal function tests (blood urea nitrogen and creatinine), respiratory viral panel including influenza and SARS-CoV-2, blood cultures, sputum Gram stain and culture, and urinary antigen testing for infectious etiologies.

Point of care ultrasound (POCUS) is a diagnostic tool used with increasing frequency in the ICU setting to diagnose cardiopulmonary pathology in critically ill patients. POCUS is being utilized in the assessment of acute respiratory failure to distinguish pneumonia, pneumothorax, pleural effusions, pulmonary edema and pulmonary consolidation. There are specific ultrasound patterns seen for a normal lung, a pneumothorax, interstitial edema, and pneumonia. POCUS was not specifically designed for use during pregnancy. However some data suggest that POCUS may be effectively utilized to assess acute respiratory failure during pregnancy [12]. (See "Indications for bedside ultrasonography in the critically ill adult patient" and "Bedside pleural ultrasonography: Equipment, technique, and the identification of pleural effusion and pneumothorax" and "Novel tools for hemodynamic monitoring in critically ill patients with shock".)

Extracorporeal membrane oxygenation (ECMO) utilization has increased in patients with refractory hypoxemia. There are case series and reports of ECMO utilization for refractory hypoxemia in pregnant patients [13,14]. According to a systematic review, the pooled prevalence of maternal and fetal survival was 77.2 and 69.1 percent, respectively. The most common maternal complication was bleeding (37.2 percent) [15]. In a separate study, the most common fetal complications were low Apgar score (0-6) and respiratory failure needing respiratory support in the ICU [16]. As these data are derived from observational studies, publication bias may exist. At this time, ECMO during pregnancy may be indicated in very select cases of refractory hypoxemia and should be provided in a designated ECMO center [17].

During maternal critical illness, obstetric consultation is required to assist in fetal monitoring, decision-making regarding the safety of continuing the pregnancy, and the method of delivery. During prolonged mechanical ventilation, it is recommended to measure and record the fetal heart rate tracing at least daily, to assess the umbilical artery by Doppler weekly, and to assess fetal growth by fetal ultrasound every two weeks [9].

DISEASE-SPECIFIC EVALUATION AND MANAGEMENT — The clinical features, diagnosis, and treatment of the major causes of acute respiratory failure during pregnancy and the peripartum period are reviewed in this section.

Pulmonary edema — Acute pulmonary edema occurs in approximately 0.08 percent of pregnancies, according to a retrospective cohort study of nearly 63,000 consecutive deliveries in a single medical center [18]. Approximately 50 percent of the cases of pulmonary edema were attributed to tocolytic therapy or cardiac disease. The remaining cases were ascribed to either preeclampsia or iatrogenic volume overload. Preterm labor increases the risk of pulmonary edema, likely due to the increased exposure of these patients to tocolytic therapy as outlined below. As an example, a case control study demonstrated pulmonary edema occurred in 6.7 percent of patients with preterm labor between 24 and 33 weeks gestation; among this population, exposure to antenatal corticosteroid therapy and tocolytic medications were major risk factors [19].

Tocolytics — The use of tocolytic beta-agonists (eg, terbutaline) to inhibit preterm labor is associated with pulmonary edema. This is more common among pregnancies complicated by multiple gestations or maternal infection [20], and among females who receive multiple tocolytic agents simultaneously [18,21]. (See "Inhibition of acute preterm labor", section on 'Beta-agonists (eg, terbutaline)'.)

Fluid overload is probably the major pathogenic factor in tocolytic-related pulmonary edema, although cardiac dysfunction and increased capillary permeability may also contribute [22]. Pregnant individuals are predisposed to fluid overload because they tend to receive a large amount of intravenous fluid in response to hypotension caused by peripheral vasodilation.

The clinical presentation of tocolytic-related pulmonary edema is nearly identical to that of other types of pulmonary edema: dyspnea, tachypnea, tachycardia, hypoxemia, and diffuse crackles. Chest pain and a cough may also be present. The chest radiograph reveals bilateral air space disease. A review of 58 case reports and case series found that the following findings were most frequent in tocolytic-related pulmonary edema [22]:

●Basilar crackles (100 percent)

●Bilateral air space disease on chest radiograph (81 percent)

●Shortness of breath (76 percent)

●Chest pain (24 percent)

●Cough (17 percent)

●Fever (14 percent)

The diagnosis of tocolytic-related pulmonary edema is made when these findings develop in a woman who is receiving tocolytic therapy with a beta-agonist in the absence of an alternative explanation for acute respiratory failure. There are no definitive diagnostic tests.

Most patients with tocolytic-related pulmonary edema respond well to discontinuation of the tocolytic beta-agonist, supplemental oxygen, fluid restriction, and diuresis. Mechanical ventilation may be necessary. Most cases resolve within 12 to 24 hours. Persistence of symptoms beyond this time period should prompt reconsideration of the diagnosis. Mortality is uncommon.

Alternative tocolytics that can be used after discontinuation of the beta-agonist are reviewed separately. (See "Inhibition of acute preterm labor".)

Pulmonary edema has occurred with magnesium sulfate tocolysis [23,24]. It appears to be associated with high magnesium and/or intravenous fluid infusion rate, as well as a large positive fluid balance. Thus, it is uncertain whether the etiology is the magnesium itself or volume overload.

Pulmonary edema has also been reported to occur with the tocolytic use of the calcium channel blockers nifedipine and nicardipine [25-27].

Cardiogenic — Surveillance data from the United States National Hospital Discharge Survey (2004 to 2006) found the rate of cardiogenic pulmonary edema was 23 and 11 per 1000 deliveries during delivery and the postpartum period, respectively [28]. Cardiogenic pulmonary edema can be a consequence of preexisting or new cardiac disease. This was illustrated by a case series of 51 patients who developed acute pulmonary edema during pregnancy or postpartum [18]. The pulmonary edema was attributed to heart disease in 13 patients (26 percent). Among these patients, six developed pulmonary edema prior to being diagnosed with valvular or myocardial dysfunction, while seven had known heart disease (aortic regurgitation, aortic stenosis, idiopathic subaortic stenosis, dilated cardiomyopathy).

The clinical presentation, diagnosis, and management of heart disease during pregnancy and the peripartum period are reviewed separately [29]. (See "Management of heart failure during pregnancy" and "Acquired heart disease and pregnancy" and "Peripartum cardiomyopathy: Etiology, clinical manifestations, and diagnosis".)

Preeclampsia or eclampsia — Pulmonary edema is an uncommon complication of severe preeclampsia and eclampsia. In a case series that included 1276 patients with severe preeclampsia or eclampsia, 3 percent developed pulmonary edema [30]. Among those with pulmonary edema, 70 percent developed this complication during the postpartum period (mean of 71 hours after delivery) and 11 percent died. Patients who were older or multigravid were at the greatest risk for pulmonary edema. Pulmonary edema was often accompanied by dysfunction of another organ system, such as disseminated intravascular coagulation, acute renal failure, hypertensive crisis, cardiopulmonary arrest, or cerebral edema.

Pulmonary edema associated with preeclampsia and eclampsia is multifactorial. Fluid overload, decreased plasma oncotic pressure, increased capillary permeability, and increased pulmonary capillary hydrostatic pressures all appear to play a role [31]. The increased hydrostatic pressure is probably due to arterial vasospasm causing elevated cardiac afterload [32,33].

The clinical presentation of severe preeclampsia- or eclampsia-related pulmonary edema is nearly identical to that of other types of pulmonary edema: dyspnea, tachypnea, tachycardia, hypoxemia, and diffuse crackles. These patients are hypertensive, and chest pain and/or cough may be present. The chest radiograph reveals bilateral air space disease.

The diagnosis is made when these findings develop in a woman who has severe preeclampsia or eclampsia in the absence of an alternative explanation for acute respiratory failure. There is no definitive diagnostic test. Recognition of both preeclampsia and eclampsia is reviewed elsewhere. (See "Preeclampsia: Clinical features and diagnosis" and "Eclampsia".)

Management of severe preeclampsia- or eclampsia-related pulmonary edema includes treatment of the severe preeclampsia or eclampsia, supplemental oxygen, and fluid restriction. Diuresis is indicated if there is fluid overload. However, clinicians must be careful to avoid compromising cardiac output and placental perfusion because many patients already have reduced cardiac preload due to intravascular depletion. Mechanical ventilation may be necessary. The treatment of preeclampsia and eclampsia is discussed separately. (See "Preeclampsia: Antepartum management and timing of delivery" and "Eclampsia".)

Pneumonia — Community-acquired pneumonia is a relatively common cause of acute respiratory failure in pregnant patients. The most common pathogens are the same as those found in nonpregnant patients: Streptococcus pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Legionella, Chlamydia pneumoniae, and influenza A [34-37]. However, the reduction in cell-mediated immunity that is associated with pregnancy (especially during the third trimester) also places pregnant patients at increased risk for severe pneumonia and disseminated disease from certain pathogens, such as herpesvirus, varicella, influenza A virus subtype H1N1, coccidioidomycosis, and coronavirus spectrum infection (ie, severe acute respiratory syndrome [SARS] and SARS-CoV-2) [38-43]. (See "Varicella-zoster virus infection in pregnancy" and "Primary pulmonary coccidioidal infection".)

The clinical features, diagnosis, and treatment of community-acquired pneumonia are the same for pregnant and nonpregnant patients:

●Clinical features include fever, a cough productive of mucopurulent sputum, dyspnea, tachycardia, and tachypnea. Many patients also have hypoxemia, chills, rigors, pleuritic chest pain, gastrointestinal symptoms (nausea, vomiting, diarrhea), and mental status changes. Auscultation may reveal focal crackles, rhonchi, and/or evidence of consolidation (eg, bronchophony, egophony, whisper pectoriloquy). Chest radiographs generally demonstrate focal air space disease. Gram stain of the sputum may reveal abundant polymorphonuclear leukocytes, while a culture of the sputum may grow the pathogen. The major blood test abnormality is leukocytosis with a leftward shift. Urinary antigen testing may also be a useful diagnostic tool for specific pathogens such as Streptococcus pneumonia and Legionella pneumophila serotype-1.

●Diagnosis requires a chest radiograph that reveals focal or multifocal airspace disease, as well as supportive clinical and microbiological features.

●Antibiotic therapy is necessary to treat community-acquired pneumonia. It is generally initiated empirically and then tailored to the microbiological results. Adjunctive therapies may include supplemental oxygen and suctioning. Mechanical ventilation may be necessary.

●CDC guidelines recommend that pregnant individuals (up until two weeks post-partum) receive treatment for influenza A if they have had a documented exposure to the influenza virus, or if they present with symptoms that are consistent with influenza infection and they are within the first 48 hours of illness. During the H1N1 pandemic, oseltamivir (75 mg twice a day for five days) was the recommended therapy, ideally begun within the first 48 hours. Therapy should not be delayed while awaiting confirmation of the diagnosis [35,44].

●An overview of the medical treatment in pregnant populations with symptomatic COVID-19, such as dexamethasone, antiviral drugs, and IL-6 inhibitors, is discussed elsewhere. (See "COVID-19: Antepartum care of pregnant patients with symptomatic infection".)

The clinical features, diagnosis, and treatment of community-acquired pneumonia are described in more detail elsewhere. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults" and "Treatment of community-acquired pneumonia in adults who require hospitalization".)

Some patients who have pneumonia progress to develop acute respiratory distress syndrome (ARDS) [45]; this disorder is discussed separately. (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults".)

Asthma exacerbation — Four to eight percent of pregnant individuals in the United States have asthma [46]. Among these individuals, 20 to 36 percent have an exacerbation during their pregnancy [47,48].

Asthma exacerbations are not uniformly distributed over the course of pregnancy. Two observational studies found that exacerbations were most frequently prior to week 24 of pregnancy, particularly during the preceding seven to ten weeks [48,49]. (See "Asthma in pregnancy: Clinical course and physiologic changes", section on 'Effects of pregnancy on asthma'.)

Pregnant individuals who have frequent or severe asthma exacerbations are more likely to have fetal complications (table 1) [50,51]. A meta-analysis of 40 studies demonstrated that maternal asthma is associated with an increased risk of low birth weight infants, intra-uterine growth retardation, pre-term delivery, and pre-eclampsia [52]. (See "Asthma in pregnancy: Clinical course and physiologic changes", section on 'Effects of asthma on pregnancy'.)

Clinical features of an asthma exacerbation include dyspnea, tachypnea, tachycardia, and wheezing. Many patients will have noticed a decrease in their peak flow rate and/or an increase in the use of their as-needed short-acting bronchodilator during the days prior to presentation. Pulsus paradoxus (ie, a fall in systolic blood pressure by at least 12 mmHg during inspiration), use of the accessory muscles of respiration, diaphoresis, and the inability to lie supine due to breathlessness are suggestive of severe airflow obstruction. Most patients are hypocapnic due to an increased respiratory drive; thus, eucapnia or hypercapnia are concerning findings and may be a sign of impending respiratory failure. Marked hypoxemia is unusual and chest radiographs are generally unrevealing.

Diagnosis of an asthma exacerbation is based upon the identification of compatible clinical features in a patient who has a history of asthma and no alternative explanation for their symptoms and signs.

The management of asthma exacerbations during pregnancy parallels that of non-pregnant individuals and is described separately. (See "Management of asthma during pregnancy" and "Management of asthma during pregnancy", section on 'Acute exacerbations'.)

Aspiration — Aspiration of gastric contents is most common during labor or soon after delivery. This is probably because the effects of sedation, analgesia, increased intraabdominal pressure, and recumbency are added to pre-existing factors that predispose pregnant individuals to aspirate. These factors include increased intra-abdominal pressure, relaxation of the lower esophageal sphincter, and delayed gastric emptying. Aspiration may also be a complication of general anesthesia and intubation during an emergent cesarean delivery.

Aspiration may induce chemical pneumonitis, airway obstruction, or acute bronchospasm:

●Chemical pneumonitis can be difficult to distinguish from pneumonia because the clinical manifestations are similar (see 'Pneumonia' above). Features that favor aspiration over pneumonia include an abrupt onset of symptoms and signs, a cough productive of material that resembles gastric contents, diffuse crackles, and chest radiograph infiltrates that are multifocal and predominate in the dependent portions of the lung. In addition, fevers tend to be low-grade. The diagnosis of pneumonitis is made when compatible symptoms and signs occur within the correct clinical context and there is no better explanation for the clinical findings. Treatment is supportive. This may include supplemental oxygen, suctioning, and, if necessary, ventilatory assistance. (See "Aspiration pneumonia in adults", section on 'Chemical pneumonitis'.)

●Airway obstruction typically presents with dyspnea and impaired ventilation and oxygenation. Physical findings vary depending upon the site of obstruction. Laryngeal, subglottic, or tracheal obstruction may cause stridor, while obstruction distal to the carina may induce asymmetric wheezing. These clinical findings are generally unresponsive to bronchodilators. The diagnosis is made by direct bronchoscopic visualization of the obstruction. Treatment is bronchoscopic removal of the obstructing foreign body. (See "Clinical presentation, diagnostic evaluation, and management of malignant central airway obstruction in adults".)

●Acute bronchospasm due to aspiration is difficult to distinguish from an asthma exacerbation because the symptoms and signs may be identical. Features that favor acute bronchospasm due to aspiration over an asthma exacerbation include an acute onset (ie, no prodrome) and coexisting evidence of aspiration (eg, witnessed aspiration, multifocal infiltrates in the dependent areas of the lung). The diagnosis is made when compatible symptoms and signs occur within the correct clinical context and there is no better explanation for the clinical findings. The treatment is the same as that for an asthma exacerbation. (See 'Asthma exacerbation' above.)

Some patients who have aspirated progress to aspiration pneumonia or acute respiratory distress syndrome (ARDS) [45]. These disorders are discussed separately. (See "Aspiration pneumonia in adults" and "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults".)

Pulmonary embolism — The risk of acute pulmonary embolism (PE) is increased five- to six-times during pregnancy [53]. This appears to be a consequence of several factors, including changes in the clotting factors and an increased likelihood of venous stasis. Predisposing factors include obesity, an older age, a personal or family history of thromboembolic disease, inherited thrombophilia, anti-phospholipid syndrome, trauma, cesarean delivery, and immobility [54]. (See "Inherited thrombophilias in pregnancy" and "Deep vein thrombosis in pregnancy: Epidemiology, pathogenesis, and diagnosis".)

The clinical features, diagnosis, and treatment of acute PE in individuals who are pregnant or peripartum are similar to those in nonpregnant individuals:

●Clinical features include dyspnea, pleuritic chest pain, cough, leg pain and/or swelling, tachypnea, tachycardia, and hypoxemia. Circulatory collapse can occur, but it is uncommon.

●The diagnosis is confirmed by imaging. Computed tomography pulmonary angiography (CT-PA) and low-dose ventilation perfusion (V/Q) scanning are appropriate imaging modalities, but conventional pulmonary angiography should be avoided. (See "Diagnostic imaging in pregnant and lactating patients" and "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism".)

●Anticoagulation is the mainstay therapy. Adjunctive therapies include supplemental oxygen and, if necessary, ventilatory assistance. Thrombolysis has been performed in the setting of circulatory collapse, but the risk of bleeding and its sequelae are high. (See "Use of anticoagulants during pregnancy and postpartum".)

The clinical features, diagnosis, and treatment of acute PE in pregnant and peripartum patients are described in more detail separately. (See "Deep vein thrombosis in pregnancy: Epidemiology, pathogenesis, and diagnosis" and "Venous thromboembolism in pregnancy and postpartum: Treatment".)

Amniotic fluid embolism — Amniotic fluid embolism is a rare but catastrophic illness of pregnancy and the peripartum period. It is reviewed in detail separately. (See "Amniotic fluid embolism".)

Air embolism — Venous air embolism is an uncommon complication of pregnancy. It usually occurs during the peripartum period as a result of caesarean delivery, uterine manipulation, or central venous catheterization [55,56]. Venous air embolism is discussed elsewhere. (See "Air embolism".)

Acute respiratory distress syndrome — Acute respiratory distress syndrome (ARDS) may occur in pregnant individuals due to conditions associated with pregnancy (eg, amniotic fluid embolism) or not associated with pregnancy (eg, trauma). In a database analysis of pregnant patients, the rate of mechanical ventilation for ARDS increased from 36.5 per 100,000 live births in 2006 to 59.6 cases per 100,000 live births in 2012 [57]. The mortality was at 9 percent, a rate that is lower than that reported in the general population (about 26 to 60 percent). There were obstetric and patient factors that were associated with a higher risk of death. These include prolonged mechanical ventilation, renal failure requiring hemodialysis, liver failure, amniotic fluid embolism, influenza infection, septic obstetric emboli, and puerperal infection. The ventilator management strategies for pregnant patients are similar to those for nonpregnant patients, except the target oxyhemoglobin saturation should be ≥95 percent, PaO₂ ≥70 mmHg, and PaCO₂ between 30 to 32 mmHg for proper fetal gas exchange (see 'Initial evaluation and management' above and "Acute respiratory distress syndrome: Ventilator management strategies for adults" and "Acute respiratory distress syndrome: Prognosis and outcomes in adults"). The indication for prone position ventilation is the same as the general population with severe ARDS. However, in late pregnancy, special attention should be paid to padding above and below the gravid uterus to prevent aortocaval compression [58].

Transfusion reactions — Transfusion related lung injury is rare but may be seen in those patients who receive blood products especially during labor and delivery. (See "Transfusion-related acute lung injury (TRALI)".)

GENERAL MEASURES — General measures refers to interventions that sustain life and prevent complications but do not treat the underlying cause of the critical illness. It includes oxygenation and ventilation (ie, supplemental oxygen or mechanical ventilation), sedation, pain control, hemodynamic support (ie, vasopressors), monitoring, volume management (ie, intravenous fluids or diuretics), nutritional support, glycemic control, stress ulcer prophylaxis, and venous thromboembolism prophylaxis. The supportive care of patients who are pregnant or peripartum is discussed separately. (See "Critical illness during pregnancy and the peripartum period", section on 'Supportive care'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Respiratory disease in pregnancy".)

SUMMARY AND RECOMMENDATIONS

●Presentation – Patients with acute respiratory failure who are pregnant generally present with respiratory distress. (See 'Clinical presentation' above.)

●Diagnostic evaluation – Initial management is the same regardless of the cause. It is focused on gas exchange and stabilization of the patient and undertaking a brief history and physical examination to determine the cause. (See 'Clinical presentation' above and 'Initial evaluation and management' above.)

●Management – Acute respiratory failure during pregnancy or the peripartum period may be due to a conventional respiratory insult or a pregnancy-specific disorder. (See 'Disease-specific evaluation and management' above.)

The usual differential diagnosis includes pulmonary edema, community-acquired pneumonia, aspiration, pulmonary embolism, asthma exacerbation, amniotic fluid embolism, and venous air embolism. Pulmonary edema is most often due to the treatment of preterm labor, heart failure, severe preeclampsia, or eclampsia.

●Supportive care – Once the patient has been stabilized and the cause of the acute respiratory failure has been determined, ongoing management includes supportive care and treatment of the etiology. Supportive care includes oxygenation and ventilation (ie, supplemental oxygen or mechanical ventilation), sedation, pain control, hemodynamic support (ie, vasopressors), monitoring, volume management (ie, intravenous fluids or diuretics), nutritional support, glycemic control, stress ulcer prophylaxis, and venous thromboembolism prophylaxis. (See 'General measures' above and 'Disease-specific evaluation and management' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Peter F Clardy, MD, who contributed to earlier versions of this topic review.