All the Red Herrings

My greatest fear is having a case I was involved in presented at M&M. Like the inevitability of a wet tap, I could not avoid the experience, but I still find myself wondering what exactly happened to this patient. 

68-year-old male with an incidentally found aortic aneurysm underwent a total arch repair with grafting of the innominate artery, left carotid, left subclavian artery, and a single vessel bypass grafting of the posterior descending artery. The patient had a past medical history of coronary artery disease, hypertension, hyperlipidemia, hepatitis-B, chronic kidney disease stage 3a, and prostate cancer status post prostatectomy. Total cardiopulmonary bypass time (CPB) was 151 min, with an aortic cross-clamp time of 104 min and a deep hypothermic circulatory arrest time of 49 min. His pre-operative echocardiogram showed a dilated ascending aorta and normal biventricular function with 1+ tricuspid regurgitation. Post-CPB TEE right ventricular inflow image below after chest closure on 0.125 mcg/kg/min milrinone showed normal RV function. In a Doppler image, tricuspid regurgitation was graded 1-2+.

The patient was fluid-resuscitated in the ICU and extubated on postoperative day 0. His right ventricular filling pressures remained in the 5-10 mmHg range. On POD1, after a posterior pericardiotomy chest tube was removed, he became hypoxemic and was found to have bilateral pneumothoraces on chest x-ray. 

Bilateral pigtails were placed, and the patient was stabilized on a nasal cannula. Later in his ICU course, he became acutely hypertension, requiring nicardipine and nitroprusside drips to maintain SBP < 130 mmHg. He was on nifedipine and gradually increased to his home dose of 90 mg. On postoperative day 2, he was transferred to the step-down unit with pigtails in place after being weaned from vasoactive support.

Within 4 hours in the step-down unit, the patient was hypotensive with systolic blood pressure in the 70’s. ABG showed hypoxemia with a PaO2 of 51 mmHg. POCUS was performed, showing robust LV function and mildly diminished RV function without dilation. An arterial line was placed and norepinephrine infusion was started stabilized at a dose of 12 mcg/min. The patient was noted to be volume responsive, and one liter IV crystalloid was administered, at which point the patient was transferred back to the ICU.

Central line and Swan Ganz catheter were inserted, and initial reading showed cardiac index of 2.55, flat CVP of 25, PA pressures of 37/20. chest x-ray for confirmation of line placement showed small right apical pneumothorax but no signs of pneumopericardium. Mean arterial pressure continued to fluctuate, at which point patient was started on a vasopressin infusion at 2.4 units/hr and epinephrine infusion at 2 mcg/min. Patient was noted to become increasingly hypoxemic and was intubated, at which point a TEE was performed. The TEE showed a collapsed right atrial wall and interatrial septum bowed towards the left. The decision was made to go back to the OR out of concern for cardiac tamponade.  

In the OR, with the chest opened, the CVP decreased from 23 to 11 in a matter of minutes, and mean arterial pressure improved. However, no fluid collections or clots were found in the pericardium or adjacent to the pericardium. Given the persistent pneumothorax, the pleural spaces were closely examined and bilateral 24 Fr tubes were placed. A bronchoscopy and an EGD were performed, and no evidence of aerodigestive disease was found.

Upon chest closure, TEE noted that the right ventricle function became moderately diminished and tricuspid regurgitation increased from 1+ to 3+. Nitric oxide was started and milrinone was started at 0.25 mcg/kg/min.

The patient was extubated by the following morning after takeback. His inotropes were gradually weaned, and his chest tubes were removed on sequential days, with no recurrence of pneumothorax. He was discharged from the ICU on POD7 and discharged from the hospital on POD10.

Was the persistent small pneumothorax relevant for this patient? Was it more significant than it appears on CXR? Though he showed signs of tamponade physiology, no tamponade etiology was found in the OR. Or was this a matter of tamponade of space given a relatively small chest size? The third theory is that the patient went into right ventricular failure from an inotropic wean and IV fluid administration. However, this explanation does not fully account for his decompensation on the floor.

Unfortunately, not every event has a denouement. Thankfully, the patient’s hemodynamics improved, and he was eventually able to return home. In the absence of signs of aerodigestive disease, it is hard to pinpoint a diagnosis, representing the unsatisfying part of this case. But perhaps that is part of the learning curve of being an early-career intensivist--that not everything fits into Occam’s razor after all. The second teaching point may be that we are not as alone as we think we are—when this patient decompensated, everyone from respiratory therapy to nursing to surgery was on board to help him. Because of a collaborative team effort, he survived.