Table 2.
Factors contributing to decision to intubate and decision to initiate ECMO
| # | Peripartum status at time of ECMO initiation | Etiology/indication | Decision/parameters prompting providers to intubate | Decision/parameters prompting providers to initiate ECMO |
|---|---|---|---|---|
| A | Pregnant, 21 wk | Urosepsis, aspiration pneumonia, ARDS | Episode of hypoglycemia led to loss of consciousness and need for cardiopulmonary resuscitation, complicated by aspiration | Emergently initiated ECMO upon arrival from outside the hospital due to manual ventilation required to maintain SPO2 >90% |
| B | Pregnant, 22 wk | Malaria-induced ARDS | Worsening hypoxemia on continuous PAP support (pH 7.42, PO2 66, pCO2 27.6) | Persistent respiratory acidosis and hypoxemia (pH 7.24, pO2 64, pCO2 49) despite 100% FiO2, PEEP 18, VT 380, rate 30 on PRVC |
| C | Pregnant, 29 wk | Status asthmaticus, sepsis | Severe acidosis despite bilevel positive airway pressure (pH 7.08, pO2 83, pCO2 24.6) | Progressive hypoxemia (pH 7.34, pO2 67, pCO2 45) despite 100% FiO2, PEEP 5, VT 480, rate 24 on ACV |
| D | Pregnant, 30 wk | H1N1 influenza–induced ARDS | Significant increase in oxygen requirement, intubation done outside the hospital to secure airway before transport | Worsening subcutaneous emphysema, new left apical pneumothorax concerning for barotrauma, maximum ventilator settings with worsening hypoxemia (pH 7.38, pO2 73, pCO2 45.1) |
| E | Intraoperative, during cesarean delivery, 29 wk | Preeclampsia with severe features, flash pulmonary edema, ARDS | Intubated at start of cesarean delivery owing to loss of consciousness, persistent oxygen saturations of 60%, witnessed aspiration on induction | Persistent hypoxemia and hypercarbia, multiple modes of ventilation failed, manual ventilation required secondary to high peak airway pressures |
| F | Postpartum, day 0 | Septic abortion with septic shock, ARDS | Intubated at start of suction dilation and evacuation for septic abortion; developed florid pulmonary edema intraoperatively (aggressive fluid and blood product resuscitation) | Progressive hypoxia (pH 7.33, pO2 67, pCO2 40) despite FiO2 100%, PEEP 20, PIP 41 on pressure-controlled ventilation |
| G | Postpartum, day 1 | Cholecystitis with septic shock and multiorgan failure/ARDS and subsequent pneumonia | Worsening tachypnea on 4 L nasal cannula (pH 7.25, pO2 83, pCO2 37) with subsequent acute respiratory decline requiring intubation | Progressive hypoxemia (pH 7.26, pO2 48, pCO2 37) despite FiO2 100%, PEEP 15, PIP 50 on pressure-controlled ventilation |
| H | Postpartum, day 14 | Preeclampsia with pulmonary edema, ARDS (and subsequent pneumonia) | Presented with worsening shortness of breath on postoperative day 3 after cesarean delivery; found to be severely hypertensive (210/170 mm Hg) and hypoxic with pulmonary edema. Rapidly intubated for persistent hypoxia (SPO2 65% on room air, improved only to 80% on nonrebreather) | Following initial improvement on mechanical ventilation for 9 days (weaned to pressure support ventilation), respiratory status worsened over 48 h with progressive hypoxemia (pH 7.32, PO2 57, pCO2 47) despite aggressive ventilatory settings on high-frequency percussive ventilation with FiO2 95%, PEEP 8 |
| I | Postpartum, day 36 | Large lower extremity and inferior vena cava deep venous thrombus, pulmonary embolism, cardiac arrest | Acute decompensation intraoperatively during thrombectomy | Increasingly difficult to ventilate with increased airway pressures, cardiogenic shock, undergoing active cardiopulmonary resuscitation |
ACV, assist-control ventilation; ARDS, acute respiratory distress syndrome; ECMO, extracorporeal membrane oxygenation; PAP, positive airway pressure; PEEP, positive end expiratory pressure; PIP, peak inspiratory pressure; PRVC, pressure-regulated volume control.
Webster et al. Extracorporeal membrane oxygenation in pregnant and postpartum women. AJOG MFM 2020.