A 40-year-old male with a significant past medical history of schizoaffective disorder who was admitted to the intensive care unit with respiratory distress and fever secondary to RSV pneumonia and ARDS. He was intubated and mechanically ventilated with protective lung strategy and received supportive care. Condition improved and was extubated 8 days later. However, he required to be reintubated secondary to respiratory muscle weakness, prompting the decision to proceed with a tracheostomy. His hospital course was complicated with right upper extremity DVT requiring full anticoagulation with enoxaparin.
During the preparation for the tracheostomy procedure, the patient's oxygen saturation dropped as he was being transferred to the operating room table. Consequently, the procedure was aborted, and the patient was promptly returned to the ICU. Subsequently, his oxygenation improved, and he was placed back on a FiO2 of 50% and a PEEP level of 10, which were the same settings as before the aborted procedure. Of note, enoxaparin was placed on hold for the anticipated procedure.
The following day, in the morning, the patient encountered a sudden increase in oxygen demand, leading to the necessity of 100% oxygen supplementation. Moreover, there was a considerable surge in the patient's work of breathing, characterized by a notable increase his inspiratory efforts, respiratory rate, and in minute ventilation that increased from 8 liters per minute to approximately 16-17 liters per minute (see ventilator screenshot). His heart rate was 120-130 and BP 82/54 mm Hg requiring norepinephrine infusion.
Chest x-ray showed a mild infiltrate in the right lower lobe that does not explain the severity of his hypoxemia. Sputum gram stain and culture was obtained, and the patient was placed on cefepime and vancomycin empirically.
Arterial blood gas (ABG) analysis revealed a pH of 7.28, pCO2 of 62.7, and a PO2 of 52.5. His previous pCO2 was 47 on a minute ventilation of around 8 liters. Patient was deeply sedated, PEEP was increased, and he remained with FiO2 at 100%. The following screenshot shows progression of his blood gases over the next 4 hours.
Bedside echocardiography revealed dilated right ventricle and possible McConnel sign (right ventricular free wall hypokinesis with sparing of the apex).
Due to instability of the condition with severe hypoxemia and respiratory acidosis, we felt that obtaining CTA may not be safe for the patient at this point.
What would you do next?
0%Continue full anticoagulation
0%Give thrombolytic therapy with tPA
0%Start paralysis and place patient in proning position
0%Obtain CTA despite instability
Due to the presence of severe hypoxemia, dead space disease, right ventricular strain, positive d-dimers, and the absence of clear explanation on the chest-x ray, the diagnosis of massive pulmonary embolism was highly suspected, and the decision was made to give thrombolytic therapy with tPA.
After the infusion of tPA infusion, the patient continued to be severely hypoxemic without major improvement. The possibility of ECMO was entertained. Meanwhile, an ultrasound of the lower extremities revealed a nonocclusive thrombus in the right popliteal vein, making the diagnosis of pulmonary embolism more likely.
In the next 24 hours, oxygenation slightly improved and CTA of the chest was done confirming bilateral pulmonary emboli with possible infarction in the right lower lobe.
Catheter-directed thrombectomy was attempted with partial removal of the thrombi, however, oxygenation has improved remarkable and pO2 increased to 263 mm Hg and pCO2 was down to 60.1 mm Hg (see screenshot).
The following is an algorithm to guide thrombolytic therapy in confirmed pulmonary embolism.
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thanks for sharing , we had an almost similar case, but he had ICH also،small one ,multi-disciplinary team was involve in his managment ,anyway in the end he was anticoagulated near optimam dose with heparin infusion(easily can be revised) with regualr interval interval brain image , and in the end he fully recoved with no sequel