My residency program director once made the following statement:
At the time, I laughed when he said this, and I asked him to clarify this somewhat startling observation. We then had a brief discussion and came to the conclusion that pregnancy is associated with many comorbidities that otherwise would not typically occur in the non-pregnant patient. These include conditions of pregnancy that we commonly think of such as morning sickness and acid reflux disease. Diseases that are concerning for us clinicians practicing in the emergency department that pregnant patients may present with include diabetic ketoacidosis, preeclampsia and eclampsia, and thromboembolism.
This led me to wonder about the treatment of life-threatening thromboembolism, particularly massive pulmonary embolism (MPE), in the pregnant patient. We are familiar with the fact that pregnancy in and of it itself is a hypercoaguable state that puts patients at increased risk of thromboembolism. One of the worst-case scenarios I can envision is a young pregnant patient at 32 weeks’ gestation presenting to the emergency department after a syncopal episode with the classical picture of MPE: acute dyspnea, sudden chest pain, and signs of hemodynamic instability with a blood pressure of 83/46 mmHg, respiratory rate of 33 bpm, heart rate of 120 bpm, and 80% oxygen saturation upon room air. EKG reveals sinus tachycardia and evidence of right ventricular strain. An emergent transthoracic 2D echocardiogram is performed, which reveals a grossly enlarged right ventricle with severe tricuspid regurgitation and impaired right ventricular function. A VQ scan is highly suspicious for MPE, and a CT scan of the thorax shows a large saddle embolus that extends from the right to the left pulmonary arteries, confirming the diagnosis of MPE.
The ED attending physician orders alteplase 100 mg IV to be infused over 2 hours for this patient. Upon seeing this order, you state something to the following effect:
In terms of the choice of thrombolytic agent, it seems that alteplase would be the most ideal agent to use in this setting for now. Unlike urokinase, alteplase does not cross the placenta (although it is not clear whether this has any implications in inducing coagulopathy of the fetus). In addition, the “claim-to-fame” for alteplase when compared to streptokinase is the idea that the proposed incidence of immunogenic reactions is minimized (which has been previously discussed here). Perhaps there may be some interest in investigating the use of tenecteplase in pregnancy first, and then for the treatment of MPE in the setting of pregnancy, due to the fact that it can be given as an IV bolus with the added potential benefit of possessing a lower risk of bleeding compared to alteplase.
Although MPE is a difficult situation to manage, and even more so in the setting of pregnancy, there is no evidence to support the withholding of thrombolytic therapy in these patients. With two lives to potentially care for in this scenario, a rapid turnaround time can be expected with the administration of thrombolytic therapy that can salvage both the mother and baby. And as the saying goes, “Mama knows best.”